Influenza, commonly known as the flu, is a highly contagious respiratory illness caused by influenza viruses. While it can affect people of all ages, infants are particularly vulnerable due to their underdeveloped immune systems. This makes understanding the risks, symptoms, and preventative measures crucial for protecting young children.

Increased Risk for Infants:

Compared to older children and adults, infants are at a higher risk for developing serious complications from the flu. This is because their immune systems are still maturing and haven’t yet developed full resistance to various viruses, including influenza. Additionally, infants have narrower airways than adults, making them more susceptible to respiratory problems that the flu can exacerbate.

Factors Contributing to the Risk:

Several factors further increase the vulnerability of infants to influenza:

  • Age: Infants under 6 months are at the highest risk, with the youngest, under 3 months, facing the greatest danger.
  • Underlying Medical Conditions: Infants with pre-existing medical conditions like chronic lung disease or congenital heart defects are more prone to severe complications.
  • Premature Birth: Prematurely born infants have weaker immune systems and underdeveloped lungs, making them highly susceptible.

Symptoms to Watch For:

While infants may not exhibit all the typical flu symptoms seen in adults, some key signs require immediate medical attention:

  • Fever: A high fever, especially above 102°F (38.9°C), is a major concern.
  • Respiratory Problems: Rapid breathing, wheezing, or difficulty breathing are alarming signs.
  • Lethargy: Excessive sleepiness or unusual fussiness can indicate the baby is feeling very unwell.
  • Poor Feeding: Refusal to feed or a significant decrease in feeding intake can be worrisome.
  • Dehydration: Signs of dehydration like sunken eyes, dry mouth, and fewer wet diapers require immediate medical attention.

Importance of Vaccination:

Fortunately, the most effective way to protect infants from the flu is through vaccination. While infants themselves cannot be vaccinated until they are 6 months old, those around them can get vaccinated, creating a cocoon of protection, also known as herd immunity. This includes:

  • Parents and caregivers: Getting vaccinated every year is crucial to protect their young and vulnerable babies.
  • Siblings and household members: Vaccinating everyone in close contact with the infant significantly reduces the risk of exposure.
  • Healthcare providers and other close contacts: Protecting those who interact with the infant is vital to minimize the risk of transmission.

Additional Preventive Measures:

Beyond vaccination, several preventive measures help further safeguard infants from the flu:

  • Frequent handwashing: Washing hands thoroughly with soap and water for at least 20 seconds is essential.
  • Avoiding close contact with sick individuals: Limiting interaction with anyone exhibiting flu symptoms protects the infant from potential exposure.
  • Maintaining a clean environment: Regularly disinfecting surfaces and toys can help prevent the spread of germs.

Conclusion:

Influenza can be a serious threat to infants. Recognizing the increased risk, understanding the symptoms, and prioritizing vaccination and preventive measures are crucial. By taking these steps, parents and caregivers can effectively shield their young ones from the dangers of the flu and ensure their healthy development.

Note: This information is intended for educational purposes only and should not be a substitute for professional medical advice. Always consult with a healthcare professional regarding any concerns or questions you may have about your infant’s health.

Source link

Introduction

Chronic obstructive pulmonary disease (COPD) is a prevalent respiratory disorder characterized by progressive airflow limitation and persistent respiratory symptoms. It presents a substantial global health burden and is a leading cause of morbidity and mortality.1 The development of COPD involves a complex interplay between genetic factors, such as predisposition, and environmental factors, including smoking, air pollution, and respiratory infections. Despite the diverse causes of COPD, current diagnostic and therapeutic approaches are limited, highlighting the need for a deeper understanding of its underlying mechanisms.2

In recent years, there has been growing interest in the role of the gut microbiota, which has been found to influence various aspects of human health, including immune regulation and systemic inflammation.3 Accumulating evidence suggests a potential link between the dysbiosis of the gut microbiota and the development of COPD.4,5 Observational studies have identified gut microbiome dysbiosis in COPD patients, and rodent models have demonstrated its contribution to COPD development.6,7 Furthermore, there have been reports on the associations between gut microbial dysbiosis and a decline in lung function in individuals with COPD.8–10

However, establishing a causal relationship between the gut microbiota and COPD remains challenging. The dynamic nature of the gut microbiome introduces challenges when attempting to characterize it through a single cross-sectional study design.11 This is due to the potential variability in microbial sequencing results, which can be influenced by various confounders and covariates. It is crucial to acknowledge that factors such as the use of inhalers, particularly inhaled corticosteroids (ICS), and antibiotics can act as confounding variables in these studies.12

Mendelian Randomization (MR) is an innovative and robust analytical approach that can provide insights into causal relationships between exposures and outcomes using genetic variants as instrumental variables (IV).13 By leveraging naturally occurring genetic variations unaffected by confounders, MR analysis circumvents some limitations of traditional observational studies, including confounding factors and reverse causality, and provides more reliable evidence for causal inference. The utilization of naturally occurring genetic variations in MR analysis offers a valuable approach to overcome limitations commonly encountered in traditional observational studies. MR analysis can effectively sidestep confounding factors and mitigate the issue of reverse causality.13

MR studies have been employed to establish genetic evidence supporting the causal link between gut microbiota and respiratory diseases.14–16 In a recent study conducted by Wei et al, they employed MR analysis to examine the causal connection between the gut microbiome and COPD. They identified 9 bacterial taxa associated with the risk of COPD. However, none of their MR results were found to be statistically significant after applying multiple testing corrections. This lack of significant findings may potentially be attributed to the relatively small sample size of the Genome-Wide Association Study (GWAS) utilized in their analysis.15 Additionally, while several observational studies have previously reported associations between the gut microbiota and lung function in COPD,8–10 the causal relationship involving the interplay between the gut microbiota, lung function, and COPD remains uncertain. Therefore, the objective of this study is to investigate the causal relationship between the gut microbiota, lung function, and COPD within the framework of MR analysis. To achieve this, we have incorporated the latest GWAS datasets, allowing for a more comprehensive analysis. By utilizing an extensive dataset and employing the MR approach, this research aims to shed light on the intricate causal relationships between these variables, providing insights into the pathogenesis and potential intervention strategies for COPD.

Method

Study Exposures

The summary statistics for gut microbiota abundance were obtained from a comprehensive GWAS conducted by the MiBioGen consortium. This study involved the analysis of host genetic variations in 18,340 participants from 24 cohorts, primarily of European descent. The study combined 16S rRNA gene sequencing profiles and human genotyping data from the participants. The dataset included a total of 211 taxa, encompassing 9 phyla, 16 classes, 20 orders, 35 families, and 131 genera, identified through 16S rRNA gene sequencing techniques (Supplementary Table S1).

Study Outcomes

The GWAS summary statistics for the outcomes were extracted from the large-scale biomedical databases of UK biobank and FinnGen biobank, both of which contain comprehensive health and genetic information from a large population of participants. The summary statistics for lung function, including FEV1 (forced expiratory volume in 1 second), FVC (forced vital capacity), and percentage of predicted FEV1, were extracted from the second analytical round of the UK biobank database. This extraction was performed on July 2, 2023. The GWAS summary statistics for COPD were obtained from the eighth analytical round of the FinnGen biobank database, accessed on April 29, 2023. It is worth noting that there was minimal overlap between the individuals included in the exposure and outcome samples. Supplementary Table S1 provides details about the GWAS summary statistics for reference.

Selection of Instrumental Variables

Human SNPs that were associated with the abundance of gut microbiota, which demonstrated genome-wide significance with a p-value of less than 1×10−5 were included. To assess potential confounding factors associated with the identified SNPs, we employed the Phenoscanner. SNPs found to be linked to confounding factors or outcomes were excluded from our analysis. (Supplementary Table S2) Clumping of these variants was performed to ensure the independence of the IVs. A clumping window of 10,000 kb and a pairwise linkage disequilibrium (LD) threshold of r2 < 0.001 were used for this purpose. To avoid weak instrument bias and ensure the strength of the IVs, we calculated the F-statistic. SNPs with an F-statistic below 10 were excluded from the analysis. Harmonization of variants was undertaken by aligning the effect alleles of different studies to the same reference allele using the TwoSampleMR package in R. Given the variability in genotyping platforms utilized in GWAS, it is possible that certain SNPs associated with the gut microbiota may not be present in the outcome dataset. Consequently, these missing SNPs were excluded from this study’s analysis.

Mendelian Randomization Analyses

The primary method used for causal inference in this study was the inverse variance weighted (IVW) method. This method combines the ratio estimates obtained from each genetic instrument in a meta-analysis model.17 To ensure the robustness of our findings, we employed additional analysis methods, including MR-Egger, weighted median, simple mode, weighted mode, and MR-PRESSO. MR-Egger detects violations of MR assumptions, such as horizontal pleiotropy, and provides an effect estimate that is not affected by these violations.18 The weighted median method combines the ratio estimates from genetic instruments using a median-based approach, which can provide reliable estimates even if up to 50% of the instruments are invalid. The simple mode and weighted mode methods consider the majority or weighted majority of genetic instrument estimates, respectively, to determine the direction and strength of the causal relationship.17 MR-PRESSO, a general test for the presence of outliers, was used to identify and remove genetic variants that significantly contributed to heterogeneity through a simulation approach.19 By incorporating these supplementary analysis methods, we can evaluate the consistency of the results and gain a more comprehensive understanding of the causal associations while considering potential violations of MR assumptions. For associations with an IVW-MR p-value < 0.05, we applied the Benjamini-Hochberg (BH) correction for multiple testing to reduce the likelihood of false-positive findings. Additionally, we conducted reverse analysis to examine the reverse causal association. All statistical analyses were performed using R version 4.2.3.

Sensitivity Analyses

In order to ensure the robustness of our primary causal estimate for associations with an IVW-MR p-value < 0.05, we performed sensitivity analyses. Cochran’s Q statistic was utilized with both the IVW and MR-Egger methods to assess the heterogeneity of effects. Additionally, we employed the MR-Egger intercept and MR-PRESSO Global test to evaluate the presence of horizontal pleiotropy. If any of these tests indicated the presence of pleiotropy with a significance level of p < 0.05, the corresponding results were excluded.18,19 Furthermore, a leave-one-out analysis was conducted to identify outliers and assess the stability of the results. These sensitivity analyses were crucial in ensuring the reliability and robustness of our findings.

Result

The purpose of this MR study was to investigate the causal effects of specific gut microbial taxa on lung function and COPD. (Figure 1) There are three main assumptions of MR analysis. First, the IVs should be strongly associated with the exposure. To address this assumption, we selected only exposures that had at least three independent genetic instruments at minimum p-value < 1×10−5. Additionally, we have excluded SNPs with mean F statistics < 10. The SNPs were then clumped by LD to ensure the independence of the IVs. Second, the genetic variants used as IVs are independent of any confounding factors that may influence both the exposure and outcome. Thus, we utilized the Phenoscanner to examine potential confounding factors associated with the SNPs. Any SNPs found to be related to confounding factors or outcomes were excluded from our analysis. The third assumption requires that the IVs only affect the outcome through their effect on the exposure and not through any alternative pathways. In order words, no pleiotropy should be presented. Any causal relationships that were detected to have pleiotropy would be excluded. After selecting SNPs according to the above criteria, we proceeded to harmonize the effect sizes of these variants on the exposure and the outcome for consistency and comparability. Among the MR results we obtained (Supplementary Table S3), a total of 64 potential associations were identified. These findings are summarized in Supplementary Table S4.

Figure 1 Overall MR framework and workflow of this study.

Effect of Gut Microbial Abundance on Lung Function

Fifteen potential causal relationships were identified between the genetically predicted abundance of gut microbial taxa and FEV1 in the IVW analysis. Six relationships remained significant after conducting multiple correction. (Figure 2) (Table 1) Order Erysipelotrichales (β = 0.031, CI = 0.009–0.053, p = 0.032), order Desulfovibrionales (β = 0.029, CI = 0.010–0.049, p = 0.031), order Clostridiales (β = 0.037, CI = 0.015–0.060, p = 0.020), class Clostridia (β = 0.044, CI = 0.020–0.067, p = 0.003), class Deltaproteobacteria (β = 0.034, CI = 0.015–0.053, p = 0.003) and class Erysipelotrichia (β = 0.031, CI = 0.009–0.053, p = 0.026) were positively associated with FEV1. No significant horizontal pleiotropy was detected in the MR-Egger intercept and MR-PRESSO analysis (p>0.05). (Supplementary Tables S5 and S6) Results from Cochrane’s. Q test showed no significant heterogeneity in the relationships (p>0.05). (Supplementary Table S7) All the results remained robust after excluding the SNP one by one in leave-one-out analysis. (Supplementary Table S8) The reverse analysis did not reveal any reverse correlations. (Supplementary Table S9)

Table 1 Causal Relationships Between Gut Microbiota and FEV1

Figure 2 Forest plot for the causal effects of genetically predicted abundance of gut microbial taxa on lung function and COPD.

In the IVW analysis, we identified sixteen potential causal relationships between the abundance of distinct gut microbiota and FVC. Following multiple correction, a significant association remained for four out of sixteen relationships. (Figure 2) (Table 2) Family Desulfovibrionaceae (β = 0.034, CI = 0.013–0.054, p = 0.033), order Desulfovibrionales (β = 0.032, CI = 0.013–0.051, p = 0.016), class Clostridia (β = 0.035, CI = 0.013–0.058, p = 0.016) and class Deltaproteobacteria (β = 0.034, CI = 0.016–0.053, p = 0.003) were all positively correlated with FVC. No significant heterogeneity and horizontal pleiotropy were detected in MR-Egger intercept, MR-PRESSO and Cochrane’s Q tests. (Supplementary Tables S5S7) Leave-one-out analysis revealed that some single SNPs might dominate the positive effects of class Clostridia. (Supplementary Table S8) No reverse correlations were found through reverse analysis. (Supplementary Table S9)

Table 2 Causal Relationships Between Gut Microbiota and FVC

IVW analysis unveiled eighteen potential causal relationships linking the abundance of gut microbiota and percentage of predicted FEV1. After conducting multiple corrections, two of these relationships remained statistically significant. (Figure 2) (Table 3) Order Selenomonadales (β = −0.073, CI = −0.120 – −0.026, p = 0.044) and class Negativicutes (β = −0.073, CI = −0.120–0.0026, p = 0.035) were negatively correlated with percentage of predicted FEV1. MR-Egger intercept, MR-PRESSO and Cochrane’s Q tests indicated no evidence of horizontal pleiotropy and heterogeneity. (Supplementary Tables S5S7) Furthermore, the stability and robustness of the results were confirmed through the leave-one-out analysis. (Supplementary Table S8) The reverse analysis indicated no reverse correlations. (Supplementary Table S9).

Table 3 Causal Relationships Between Gut Microbiota And percentage of Predicted FEV1

Effect of Gut Microbial Abundance on COPD

Our Mendelian randomization analysis revealed that genetically predicted abundance of fifteen microbial taxa exhibited potential causal effects on COPD. After implementing multiple corrections, two of these relationships remained statistically significant. (Figure 2) (Table 4) The abundance of genus Holdemanella (OR = 1.176, CI = 1.082–1.278, p = 0.015) were positively correlated with the risk of COPD, while FamilyXIII. (OR = 0.750, CI = 0.629–0.894, p = 0.042) exhibited a negative correlation with the risk of COPD. MR-Egger intercept, MR-PRESSO, and Cochrane’s Q tests did not detect any significant heterogeneity or horizontal pleiotropy in the analysis. (Supplementary Tables S5S7) The robustness and stability of the results were confirmed by the leave-one-out analysis. (Supplementary Table S8) The reverse analysis provided confirmation of the causal direction of the results. (Supplementary Table S9)

Table 4 Causal Relationships Between Gut Microbiota and the Risk of COPD

Discussion

To our knowledge, this study is the first to explore the causal relationship between gut microbiota, lung function, and COPD. Following a rigorous analysis that included sensitivity analysis, reverse analysis, and multiple corrections, a total of fourteen robust and stable causal relationships were identified. There was no overlap found between the microbial taxa influencing lung function and those impacting COPD. However, several microbial taxa were discovered to have a positive causal correlation with lung function, offering potential insights into the development of probiotics. Furthermore, the presence of microbial taxa negatively correlated with lung function and positively correlated with COPD emphasized the potential impact of gut microbiota dysbiosis on lung function and COPD development. This contributes to the expanding understanding of the gut-lung axis.

Based on our research, we found that our findings reinforced the existing body of observational evidence, lending further support to the established knowledge in this domain. In our results, the bacterial taxa that were positively associated with lung function were family Desulfovibrionaceae, order Erysipelotrichales, Desulfovibrionales, Clostridiales, class Clostridia, Deltaproteobacteria and Erysipelotrichia. On the other hand, order Selenomonadales and class Negativicutes were negatively correlated with lung function. Interestingly, various pulmonary disease states have been associated with the elimination of these taxa. Upon treating influenza-infected mice with either the Chinese herb formula GeGen QinLian or fecal microbiota transplantation, the intestinal flora was restored. This restoration led to an increase in the abundance of Desulfovibrio_C21_c20 and a subsequent decrease in both mortality and lung inflammation.20 Long-term consumption of allium tuberosum reduced inflammatory cell count, interleukin (IL)-5 and IL-13 in bronchoalveolar lavage fluid in asthmatic mice. This consumption also improved pulmonary histopathology. Additionally, Desulfovibrionaceae was revealed as a biomarker indicating the effectiveness of the treatment.21 Clinical observational studies have revealed a decrease in Clostridia within the gut microbial composition of adult asthma patients.22 Interestingly, among asthmatic patients, those with lower specific IgE levels to mites and Ascaris exhibited an enrichment of various members from the order Clostridiales.23 In a MR study, it was found that class Negativicutes and order Selenomonadales exhibited a notable association with COVID-19 hospitalization, susceptibility, and severity.14

Previous studies have provided evidence of the impact of gut microbiota on immune regulation, suggesting a potential mechanism by which dysbiosis of gut microbiota could affect lung function. Among the various mechanisms investigated, the role of short-chain fatty acids (SCFAs) has received significant attention. SCFAs are produced through the fermentation of dietary fibers and are released into the lumen and peripheral circulation. The binding of SCFAs to free fatty acid receptors on immune cells such as neutrophils and macrophages allows them to exert anti-inflammatory effects.24,25 This protective role of SCFAs has been observed in both animal models and clinical studies. In a mouse model of emphysema, SCFAs demonstrated notable preventive potential by reducing the progression and severity of emphysema.26–28 Furthermore, a comprehensive study revealed that individuals who consumed dietary fibers over a long term had a 30% reduced risk of developing COPD.29 Previous observational studies have also reported associations between changes in the gut microbiome and a decline in lung function in individuals with COPD. These associations may be linked to the loss of protective microbial taxa that are involved in SCFA pathways.8–10 In addition to the immune regulatory mechanisms associated with the secretion of SCFAs, the beneficial microbiota may be associated with the homeostasis of the gut microbiome, which attribute to the colonization of a more diverse microbiome, preventing the dominance of one potentially pathogenic microbiota. Furthermore, the maintenance of gut microbial homeostasis allows beneficial intestinal microorganisms to play a protective role. Therefore, the gut microbiota that exhibited positive associations with lung function in our study may potentially act as protective bacteria through similar mechanisms.

It is noteworthy that the bacterial taxa correlated with lung function in our study have not only been associated with pulmonary diseases in previous observational studies, but they have also been linked to inflammatory bowel diseases (IBD). In dogs with IBD, the abundance of Erysipelotrichia and Clostridia were notably diminished.30 Similarly, individuals with Crohn’s disease displayed a significant decrease in the abundance of Erysipelotrichales and Clostridiales within their gut microbial profile, which strongly correlated with their disease status.31 Interestingly, it has been reported that patients with COPD exhibit reduced integrity and function of the intestinal barrier, as well as a higher prevalence of IBD.32–35 Therefore, our results have offered insights into the intricate relationship between the gut and lungs, known as the gut-lung axis. The bacterial taxa that demonstrated positive causal correlations with lung function may potentially confer protective effects through this gut-lung axis.

In our MR results, the abundance of genus Holdemanella were positively correlated with the risk of COPD, while FamilyXIII exhibited a negative correlation with the risk of COPD. It is worth noting that previous findings have shown a intriguing negative correlation between the abundance of Holdemanella and propionate levels, one of the SCFAs, in individuals with diabetes and cognitive impairment.36 Furthermore, a recent MR analysis has observed a causal correlation between Holdemanella and the risk of developing asthma.16 These findings indicate that the genus Holdemanella could potentially play a role in the development of pulmonary diseases, possibly through the SCFA pathways. However, Holdemanella biformis, a specific strain belonging to the genus Holdemanella, has exhibited protective effect in mouse colitis.37 Therefore, it is important to note that different species within the same genus can have distinct impacts on health, though microbial taxa can only be classified up to the genus level when using 16S rRNA sequencing. As far as our knowledge goes, there have been no previous associations reported between FamilyXIII and either pulmonary or bowel diseases in animal or clinical studies. Therefore, the causal correlation we observed between FamilyXIII and COPD necessitates additional investigation. All in all, the causal relationships uncovered in our study likely involve intricate interactions between specific microbial taxa and host factors. To fully understand the mechanisms through which dysbiosis of the gut microbiota impacts lung function and COPD, future studies employing metagenomic and metabolic sequencing techniques are warranted. Further validation of the potentially beneficial bacteria we identified can be conducted in subsequent experiments. For instance, Lai et al conducted a study where they constructed a murine model of COPD, analyzed the intestinal bacterial profiles of COPD rats and normal rats, isolated a strain called Parabacteroides goldsteinii from the differing bacteria, and demonstrated that preparations of this strain had a beneficial effect in mitigating COPD. Thus, investigations into the functional capabilities of specific microbial taxa are necessary to gain further insights.

The inclusion of a MR design presents an advantage in our study. Through selection of SNPs significantly associated with the exposure, while excluding SNPs correlated with the outcome or potential confounders, we establish the validity of the IVs, thereby enhancing the reliability of our results. By conducting sensitivity analysis, multiple testing, and reverse analysis, we confirm the stability, robustness, and direction of the identified causal relationships in our MR results. Consequently, we overcome limitations commonly encountered in traditional observational studies, including confounding factors and reverse causality, and provide genetic evidence for causal inference. Furthermore, our study benefits from utilizing the largest publicly available GWAS datasets, ensuring a comprehensive and robust analysis. Incorporating these extensive datasets significantly enhances the statistical power of our MR analysis, enabling accurate estimation of causal effects.

It is important to acknowledge certain limitations in our study. Firstly, our analysis utilized GWAS data for microbiota that did not specifically target the complete 16S rRNA gene. This limitation poses a challenge in differentiating between microbial taxa with the desired taxonomic resolution. It is worth noting that within the same genus, microbial taxa can have opposing effects on the host, thus the absence of complete 16S rRNA gene sequencing data restricts our ability to identify potential therapeutic targets accurately. Furthermore, since 16S rRNA sequencing is not designed to target viruses and fungi, the impact of such microbiota components was not investigated in our study. Secondly, given the dynamic and complex nature of the gut microbiota, it is an exposure phenotype that influenced by numerous variants with relatively small effect size. To address this complexity and increase statistical power, we have used a less stringent p-value threshold of 1 × 10−5, thus incorporating a larger number of IVs into our analysis, consequently facilitating the use of sensitivity analysis and bolstering statistical power. However, this approach carries the risk of including false-positive variants. By only including SNPs with a F statistic above 10 and performing multiple correction, we have reduced the possibility of false-positive results. Thirdly, our study predominantly focused on European populations due to the availability of suitable genetic data. This limits the generalizability of our findings to other ethnic groups, and further investigations involving diverse populations are warranted. Lastly, our results only establish a limited causal relationship between one specific flora and the outcome. The intricate biological mechanisms, including the impact of short-term or long-term changes in this flora on the overall gut microbiome and the influence on microbial metabolites and host immunity remain unclear. These aspects require more comprehensive mechanistic studies to be conducted in the future.

In summary, our MR analysis presents genetic evidence supporting a causal link between alterations in gut microbiota, lung function, and COPD. Our findings highlight the potential involvement of the gut microbiota in the development and advancement of COPD. The findings of this study provide potential insights for future research, including the investigation of therapeutic approaches such as probiotics to modulate the gut microbiota and alleviate COPD progression. Further investigations, particularly utilizing metagenomic and metabolomic sequencing approaches, are warranted to elucidate the underlying mechanisms and enhance our understanding of the complex interplay within the gut-lung axis.

Abbreviations

COPD, Chronic obstructive pulmonary disease; ICS, inhaled corticosteroids; MR, Mendelian Randomization; IV, instrumental variables; GWAS, Genome-Wide Association Study; FEV1, forced expiratory volume in 1 second; FVC, forced vital capacity; LD, linkage disequilibrium; IVW, inverse variance weighted; BH, Benjamini-Hochberg; SCFA, short-chain fatty acid; IL, interleukin.

Data Sharing Statement

The datasets supporting the conclusions of this article are available in the MiBioGen [mibiogen.gcc.rug.nl/], FinnGen [www.finngen.fi/en/access_results] and UK biobank [www.nealelab.is/uk-biobank] repository.

Ethical Approval

Summary statistics for the studies used for analysis were composed and obtained from published studies. All studies have received prior approval from their respective institutional review boards (IRBs). The institutional Review Board of Zhongshan Hospital approved the protocol for this study, and as per their guidelines, this study exclusively utilized publicly available data without using any individual-level data. Therefore, no additional IRB approval was necessary.

Acknowledgments

We would like to extend our appreciation to the participants and investigators involved in the MiBioGen Consortium, UK biobank, and FinnGen study. Their invaluable contributions to the large-scale GWAS studies have significantly advanced our knowledge of the gut microbiome and its connection to lung function and COPD. We would also like to extend appreciation to Dr. Xicheng Gu from Huashan Hospital, Fudan University, for providing invaluable advices on code writing.

Funding

This work is supported by the Shanghai Science and Technology Committee (Project number 19DZ1920104).

Disclosure

The authors declare that they have no competing interests in this work.

References

1. Christenson SA, Smith BM, Bafadhel M, Putcha N. Chronic obstructive pulmonary disease. Lancet. 2022;399(10342):2227–2242. doi:10.1016/S0140-6736(22)00470-6

2. Stolz D, Mkorombindo T, Schumann DM, et al. Towards the elimination of chronic obstructive pulmonary disease: a Lancet Commission. Lancet. 2022;400:921–972.

3. Ruan W, Engevik MA, Spinler JK, Versalovic J. Healthy human gastrointestinal microbiome: composition and function after a decade of exploration. Dig Dis Sci. 2020;65(3):695–705. doi:10.1007/s10620-020-06118-4

4. Budden KF, Gellatly SL, Wood DLA, et al. Emerging pathogenic links between microbiota and the gut–lung axis. Nat Rev Microbiol. 2017;15(1):55–63. doi:10.1038/nrmicro.2016.142

5. Wypych TP, Wickramasinghe LC, Marsland BJ. The influence of the microbiome on respiratory health. Nat Immunol. 2019;20(10):1279–1290. doi:10.1038/s41590-019-0451-9

6. Lai H-C, Lin T-L, Chen T-W, et al. Gut microbiota modulates COPD pathogenesis: role of anti-inflammatory Parabacteroides goldsteinii lipopolysaccharide. Gut. 2022;71(2):309–321. doi:10.1136/gutjnl-2020-322599

7. Li N, Dai Z, Wang Z, et al. Gut microbiota dysbiosis contributes to the development of chronic obstructive pulmonary disease. Respir Res. 2021;22(1):274. doi:10.1186/s12931-021-01872-z

8. Chiu Y-C, Lee S-W, Liu C-W, Lan T-Y, Ls-h W. Relationship between gut microbiota and lung function decline in patients with chronic obstructive pulmonary disease: a 1-year follow-up study. Respir Res. 2022;23(1):10. doi:10.1186/s12931-022-01928-8

9. Chiu Y-C, Lee S-W, Liu C-W, et al. Comprehensive profiling of the gut microbiota in patients with chronic obstructive pulmonary disease of varying severity. PLoS One. 2021;16(4):e0249944. doi:10.1371/journal.pone.0249944

10. Wu Y, Luo Z, Liu C. Variations in fecal microbial profiles of acute exacerbations and stable chronic obstructive pulmonary disease. Life Sci. 2021;265:118738. doi:10.1016/j.lfs.2020.118738

11. Combrink L, Humphreys IR, Washburn Q, et al. Best practice for wildlife gut microbiome research: a comprehensive review of methodology for 16S rRNA gene investigations. Front Microbiol. 2023;14:1092216. doi:10.3389/fmicb.2023.1092216

12. Pragman AA, Kim HB, Reilly CS, Wendt C, Isaacson RE, Doern GV. Chronic obstructive pulmonary disease lung microbiota diversity may be mediated by age or inhaled corticosteroid use. J Clin Microbiol. 2015;53(3):1050. doi:10.1128/JCM.03320-14

13. Davies NM, Holmes MV, Davey Smith G. Reading Mendelian randomisation studies: a guide, glossary, and checklist for clinicians. BMJ. 2018;362:k601. doi:10.1136/bmj.k601

14. Song J, Wu Y, Yin X, Ma H, Zhang J. The causal links between gut microbiota and COVID-19: a Mendelian randomization study. J Med Virol. 2023;95(5):e28784. doi:10.1002/jmv.28784

15. Wei Y, Lu X, Liu C. Gut microbiota and chronic obstructive pulmonary disease: a Mendelian randomization study. Front Microbiol. 2023;14:1196751. doi:10.3389/fmicb.2023.1196751

16. Jin Q, Ren F, Dai D, Sun N, Qian Y, Song P. The causality between intestinal flora and allergic diseases: insights from a bi-directional two-sample Mendelian randomization analysis. Front Immunol. 2023;14:1121273. doi:10.3389/fimmu.2023.1121273

17. Bowden J, Holmes MV. Meta-analysis and Mendelian randomization: a review. Res Synth Methods. 2019;10(4):486–496. doi:10.1002/jrsm.1346

18. Bowden J, Davey Smith G, Burgess S. Mendelian randomization with invalid instruments: effect estimation and bias detection through Egger regression. Int J Epidemiol. 2015;44(2):512–525. doi:10.1093/ije/dyv080

19. Verbanck M, Chen C-Y, Neale B, Do R. Detection of widespread horizontal pleiotropy in causal relationships inferred from Mendelian randomization between complex traits and diseases. Nat Genet. 2018;50(5):693–698. doi:10.1038/s41588-018-0099-7

20. Deng L, Shi Y, Liu P, et al. GeGen QinLian decoction alleviate influenza virus infectious pneumonia through intestinal flora. Biomed Pharmacother. 2021;141:111896. doi:10.1016/j.biopha.2021.111896

21. Zheng H-C, Liu Z-R, Li Y-L, et al. Allium tuberosum alleviates pulmonary inflammation by inhibiting activation of innate lymphoid cells and modulating intestinal microbiota in asthmatic mice. J Integr Med. 2021;19(2):158–166. doi:10.1016/j.joim.2020.11.003

22. B-h G, Choi J-P, Park T, et al. Adult asthma with symptomatic eosinophilic inflammation is accompanied by alteration in gut microbiome. Allergy. 2023;78(7):1909–1921. doi:10.1111/all.15691

23. Buendía E, Zakzuk J, San-Juan-Vergara H, Zurek E, Ajami NJ, Caraballo L. Gut microbiota components are associated with fixed airway obstruction in asthmatic patients living in the tropics. Sci Rep. 2018;8(1):9582. doi:10.1038/s41598-018-27964-3

24. He J, Zhang P, Shen L, et al. Short-chain fatty acids and their association with signalling pathways in inflammation, glucose and lipid metabolism. Int J Mol Sci. 2020;21(17):6356. doi:10.3390/ijms21176356

25. Ney L-M, Wipplinger M, Grossmann M, Engert N, Wegner VD, Mosig AS. Short chain fatty acids: key regulators of the local and systemic immune response in inflammatory diseases and infections. Open Biol. 2023;13(3):230014. doi:10.1098/rsob.230014

26. Jang YO, Kim O-H, Kim SJ, et al. High-fiber diets attenuate emphysema development via modulation of gut microbiota and metabolism. Sci Rep. 2021;11(1):7008. doi:10.1038/s41598-021-86404-x

27. Jang YO, Lee SH, Choi JJ, et al. Fecal microbial transplantation and a high fiber diet attenuates emphysema development by suppressing inflammation and apoptosis. Exp Mol Med. 2020;52(7):1128–1139. doi:10.1038/s12276-020-0469-y

28. Lee SH, Kim J, Kim NH, et al. Gut microbiota composition and metabolite profiling in smokers: a comparative study between emphysema and asymptomatic individuals with therapeutic implications. Thorax. 2023;78(11):1080–1089. doi:10.1136/thorax-2021-217923

29. Szmidt MK, Kaluza J, Harris HR, Linden A, Wolk A. Long-term dietary fiber intake and risk of chronic obstructive pulmonary disease: a prospective cohort study of women. Eur J Nutr. 2020;59(5):1869–1879. doi:10.1007/s00394-019-02038-w

30. Minamoto Y, Otoni CC, Steelman SM, et al. Alteration of the fecal microbiota and serum metabolite profiles in dogs with idiopathic inflammatory bowel disease. Gut Microbes. 2015;6(1):33–47. doi:10.1080/19490976.2014.997612

31. Gevers D, Kugathasan S, Denson LA, et al. The treatment-naive microbiome in new-onset Crohn’s disease. Cell Host Microbe. 2014;15(3):382–392. doi:10.1016/j.chom.2014.02.005

32. Rutten EPA, Lenaerts K, Buurman WA, Wouters EFM. Disturbed Intestinal Integrity in Patients With COPD. Chest. 2014;145(2):245–252. doi:10.1378/chest.13-0584

33. Kirschner SK, Deutz NEP, Jonker R, et al. Intestinal function is impaired in patients with Chronic Obstructive Pulmonary Disease. Clin Nutr. 2021;40(4):2270–2277. doi:10.1016/j.clnu.2020.10.010

34. Ekbom A, Brandt L, Granath F, Löfdahl C-G, Egesten A. Increased risk of both ulcerative colitis and Crohn’s disease in a population suffering from COPD. Lung. 2008;186(3):167–172. doi:10.1007/s00408-008-9080-z

35. Lee J, Im JP, Han K, et al. Risk of inflammatory bowel disease in patients with chronic obstructive pulmonary disease: a nationwide, population-based study. World J Gastroenterol. 2019;25(42):6354–6364. doi:10.3748/wjg.v25.i42.6354

36. Du Y, Li X, An Y, Song Y, Lu Y. Association of gut microbiota with sort-chain fatty acids and inflammatory cytokines in diabetic patients with cognitive impairment: a cross-sectional, non-controlled study. Front Nutr. 2022;9:930626. doi:10.3389/fnut.2022.930626

37. Pujo J, Petitfils C, Le Faouder P, et al. Bacteria-derived long chain fatty acid exhibits anti-inflammatory properties in colitis. Gut. 2021;70(6):1088–1097. doi:10.1136/gutjnl-2020-321173

Source link

Introduction

Asthma and chronic obstructive pulmonary disease (COPD) are both common diseases diagnosed by the presence of chronic symptoms such as cough, sputum, shortness of breath, and airflow obstruction. Several clinical/inflammatory factors are commonly associated with the risk of developing asthma or COPD or with important clinical outcomes such as reduced lung function, exacerbations, reduced quality of life and mortality.1,2 They are characterized by their complex and heterogeneous nature, both clinically and in their molecular pathogenesis. Endotype is a dynamic molecular network that arises when an individual’s genetic factors interact with various environmental factors, such as infections, air pollution, tobacco smoke, antibiotics, and lung flora, driving the phenotype in a particular patient. Given the clinical and biological complexity and heterogeneity of the diseases, the development of therapeutic strategies targeting individual endotypes could help us enable early identification of disease risk with a high degree of accuracy and implementation of preventive strategies.3

Numerous genetic studies, including genome-wide association studies (GWAS), have found a number of loci that influence the development of asthma and COPD, and several genetic factors are common to both diseases. Genetic contribution of individual common variants to disease susceptibility is very small, especially in isolation, and the small proportion of heritability explained by these variants makes it difficult to predict disease onset in a practical clinical setting. At present, the more important significance of GWAS, however, is not to estimate individual risk, but rather to discover the biological pathways underlying complex diseases.4 The pathophysiological pathways identified by GWAS for a disease have important implications not only for carriers of a particular genetic polymorphism, but also in the origins of the disease itself.

This review describes representative endotypes indicated by genetic and molecular data to be commonly involved in both asthma and COPD, including chronic non-type 2 inflammation, type 2 inflammation, increased susceptibility to viral infections, and impaired lung development and repair/remodeling. Advances in genomic medicine in asthma and COPD are critically important for achieving precision medicine, allowing a departure from the current one-size-fits-all medicine according to disease labels or clinical symptoms, and population approach to disease incidence prevention that does not consider individual disease susceptibility.5

Overlap Between Asthma and COPD

Dutch hypothesis was proposed more than 50 years ago.6 In this hypothesis, asthma and COPD are two phenotypes of a syndrome called chronic nonspecific lung disease (CNSLD), where CNSLD is defined as the result of an interaction between intrinsic genetic factors and extrinsic factors such as viral infection, air pollution, tobacco smoke exposure, and allergen exposure. The timing of this interaction during an individual patient’s life stage determines which clinical syndrome develops (ie, asthma or COPD) or whether characteristics of both asthma and COPD appear. Thus, a particular genetic factor may combine with a particular environmental factor to cause asthma, or the same genetic factor may combine with another genetic or environmental factor to cause COPD.7 Several genes and loci have been reported as common factors in susceptibility to asthma and COPD.7,8 We performed a PubMed database search published through September 2012 for asthma, COPD, tuberculosis, and essential hypertension, respectively. For each disease, pathway-based analysis was performed to determine how the identified genes interacted with each other.8 In at least two independent reports, a total of 108 genes were found to be associated with asthma and 58 with COPD. These genes were grouped into multiple networks according to functional annotation. Twelve networks were found in asthma and 11 in COPD, and the overlapping network between the two diseases formed one complex network consisting of 229 common molecules (Figure 1). These overlapping molecules were significantly associated with aryl hydrocarbon receptor (AhR) signaling, the role of cytokines in mediating information transfer between immune cells, glucocorticoid receptor signaling, and pathways involved in IL-12 signaling and production in macrophages. At the network level, the Jaccard similarity index for asthma and COPD was 0.81, with an odds ratio of 3.62 for asthma/COPD pair in comparison to tuberculosis/essential hypertension pair. The overlap in the asthma and COPD gene networks indicated a high degree of pathobiological similarity between these two diseases.

Figure 1 Overlapping networks between asthma and COPD. The Ingenuity Pathway Analysis software program identified 229 overlapping molecules between 12 asthma networks and 11 COPD networks, and merged them into a single larger network. In total, 229 genes were common to both diseases, and 190 and 91 genes were unique to asthma and COPD, respectively. Each network is represented by a colored rectangle, and is labeled with its corresponding network number. Adapted with permission from Dove Medical Press. Kaneko Y, Yatagai Y, Yamada H, et al. The search for common pathways underlying asthma and COPD. Int J Chron Obstruct Pulmon Dis. 2013;8:65–78.8

Common Pathogenesis Characterized by Chronic Non-Type 2 Airway Inflammation

As discussed in the section above, AhR signaling is implicated in common pathologies of asthma and COPD; AhR acts as a regulator of mucosal barrier function and affects lung immunity by inducing changes in gene expression, intercellular adhesion, mucin production, and cytokine expression.9 Although the binding of this receptor to different ligands leads to what seems to be variable responses, AhR-regulated neutrophils and Th17 cells are involved in the responses to pro-inflammatory stimuli, including tobacco smoke and air pollutants.10 The AhR-ROS-NLRP3 inflammasome functional axis, which regulates Muc5ac expression and airway inflammation, may also be involved in airway inflammation in asthma and COPD.11

We performed a GWAS of adult-onset asthma that developed over the age of 40 and identified the HCG22 gene as a susceptibility gene.12 This gene was also associated with diffuse panbronchiolitis (DPB) and COPD. DPB is a chronic neutrophilic bronchiolitis with chronic cough, sputum, and shortness of breath on exertion as the main symptoms, and its prevalence increases after the age of 40 years. HCG22 is a novel mucin-like gene13 located at 6p21.3, the DPB susceptibility gene region. Furthermore, HCG22 has been reported to be associated with tree-in-bud pattern identified on chest computed tomography in asthmatic patients and with steroid refractoriness requiring high doses of corticosteroids.14 Based on its amino acid sequence, HCG22 has a chitin-binding protein-like structure.15 YKL-40, a chitinase-like protein similar to HCG22, has been reported to be associated with phenotypes characterized by neutrophilic inflammation in asthma and COPD.16,17 Chitin is a pathogen-associated molecular pattern found in mites and fungi, and it is of interest due to its involvement in infection immunity in the airway mucosa, and its association with the pathogenesis of middle-age-onset asthma, COPD, and DPB. Recently, the new disease category of muco-obstructive lung disease has been proposed, and it includes COPD, primary ciliary dyskinesia, and bronchiectasis.18 Mucus-derived obstruction is characterized by altered airway microbiota, mucociliary dysfunction, neutrophilic inflammation, and airway destruction, which are also important features in DPB and a subgroup of patients with non-type 2 asthma.

We have found a gene encoding HA synthase 2 (HAS2) as associated with asthma.19 HAS2 is a glycosaminoglycan found in the extracellular matrix and is highly expressed in the lung. Asthma-associated single nucleotide polymorphisms (SNPs) affected the expression levels of HAS2 mRNA. Hyaluronic acid (HA) is involved in many physiological and pathological processes, including cell migration, morphogenesis, tissue regeneration, wound repair, and tumor cell proliferation and invasion, and increased levels of HA in sputum have been reported in COPD patients.20 Patients with higher levels of hyaluronan had impaired lung function than patients with patients with normal hyaluronan levels. In addition, influx of neutrophil and levels of interleukin-8 and soluble tumor necrosis factor (TNF) receptors were higher in COPD patients with elevated HA levels. Decreased Has2 expression in mice enhanced ovalbumin (OVA)-induced airway inflammation, including increased neutrophils and eosinophils, airway hyperresponsiveness, and attenuated CD44 and transforming growth factor (TGF)-β signaling.21 CD44 is an HA binding protein and decreased CD44 downregulates TGF-β. In addition, lung mRNA sequencing and pathway analysis identified enriched terms “IL-17A signaling in fibroblasts”, “NRF2-mediated oxidative stress response”, and “glucocorticoid receptor signaling”. These terms were thought to be associated with severe asthma and COPD. Furthermore, in a chronic OVA sensitization and challenge-induced asthma model,22 IL-17A levels in lung homogenates were higher in Has2 heteroknockout OVA mice than in wild-type mice, and Has2 heteroknockout OVA mice showed goblet cell hyperplasia and excessive mucus production. Thus, chronic OVA stimulation induced a characteristic phenotype of airway remodeling through Has2-mediated attenuation of IL-17 and TGF-β signaling.

Taken together, neutrophil inflammation is recognized as an important pathogenic factor in asthma as well as COPD.

Common Pathogenesis Characterized by Type 2 Inflammation

Eosinophilic airway inflammation is found in patients with COPD as well as asthma, and the presence of eosinophilic inflammation is associated with exacerbations and responsiveness to inhaled corticosteroids. Overall, 612 (56%) of 1094 Japanese COPD patients had an absolute eosinophil number of 150 cells/mm3 or greater, and 902 (69%) of 1304 Japanese patients had an eosinophil fraction of 2% or greater23 (Figure 2). In a study comparing the comprehensive gene expression in the airway epithelial cells of asthma and COPD patients, the gene expression levels associated with type 2 inflammation were increased not only in asthma patients, but also in COPD patients.24 In particular, the expression of type 2-related genes in COPD patients was associated with stronger airflow limitation, airway eosinophil infiltration, and even the responsiveness to inhaled corticosteroid (ICS).

Figure 2 The distribution of blood eosinophil levels in a Japanese COPD clinical trial database. Distribution of (A) absolute blood eosinophil count and (B) percentage blood eosinophils among Japanese patients with COPD. Reprinted with permission from Dove Medical Press. Barnes N, Ishii T, Hizawa N, et al. The distribution of blood eosinophil levels in a Japanese COPD clinical trial database and in the rest of the world. Int J Chron Obstruct Pulmon Dis. 2018;13:433–440.23

In a large GWAS of 8068 patients with the overlapping asthma and COPD pathology in the UK Biobank and 4301 patients with the overlapping pathology from other cohorts, eight loci were identified,25 including the thymic stromal lymphopoietin (TSLP) gene. These eight loci were not clearly associated with smoking habits, but they were strongly associated with the peripheral blood eosinophil counts, immunoglobulin (Ig) E sensitization and asthma, suggesting the importance of type 2 inflammation in the overlapping pathology. Elevated TSLP protein and TSLP mRNA levels have been reported in bronchial epithelium in COPD patients.26 Multiple factors related to exacerbations of asthma and COPD, including respiratory viruses, cigarette smoke, and inflammatory cytokines, have been associated with increased TSLP production.27–30 TSLP gene was also identified as a potential susceptibility locus for impaired lung function in non-COPD, non-asthmatic healthy subjects, which supports the idea that TSLP is a genetic determinant of lung function that influences the risk of developing asthma and COPD.31

The ORMDL3/GSDMB gene located on chromosome 17q has been consistently associated with childhood-onset asthma, and most asthma patients associated with this gene are atopic. In addition, an association of the region with overlap between COPD and asthma without rhinitis has been reported.32 Susceptibility to rhinovirus (RV) infection is associated with this genetic region that affects transcription and protein expression of intercellular adhesion molecule 1 (ICAM1), a major receptor for human RV (HRV).33 ORMDL3/GSDMB has also been implicated in the development of childhood asthma related to indirect exposure to smoking at home.34 Furthermore, the importance of ORMDL3/GSDMB was indicated in susceptibility to early-onset adult asthma in Japanese. While the region was not associated with allergic sensitization, it was strongly associated with increased serum total IgE levels,35 and therefore, the region appears to act as a stress sensor in the airways caused by viral infections and smoking, and promotes airway inflammation through an enhanced innate type 2 immune response.

Common Pathogenesis Characterized by Increased Susceptibility to Viral Infections

HRV is an important risk factor for exacerbations both in asthma and COPD. RV induces several cytokines including IFNα, IFNγ, TNFα, CXCL10/11, and CC chemokine ligand 5 (CCL5) in airway epithelial cells. The airway epithelial cell responses to RV was overlapped with gene expression signatures reported in patients with asthma or COPD.36

We previously found that the gain-of-function −28G allele of a promoter SNP (rs2280788) in the CCL5 gene was a risk factor for adult-onset asthma who developed the disease at age 40 years or older, and also for COPD who had less emphysema lesions.37,38 Given that the CCL5 gene is a pathway involved in both the pathogenesis of older-onset asthma and COPD with less emphysema, it is interesting that CCL5 is shown to contributes to tissue-resident T cell-associated T1 neutrophilic inflammation in asthma and correlates with T2 inflammation and sputum eosinophilia as well.39

The CDHR3 gene, which was identified in GWAS of childhood asthma with frequent severe exacerbations, was found to encode a receptor for RV type C.40 We confirmed that the functional variant at CDHR3 has a significant genetic influence in Japanese adult asthma patients with onset by age 10 years, and that the association is stronger when restricted to allergen sensitization-positive individuals.41 In addition, a 10-year observational study was conducted to examine the genetic impact of the CDHR3 gene on the newly development of asthma or COPD in 1523 healthy adults with no pulmonary disease who had health checkups in 2008. During the 10-year period, a total of 79 cases and 25 cases newly developed asthma and COPD, respectively. The CDHR3 gene had a genetic influence on the development of asthma or COPD, especially in adults with allergen sensitization in 2008.42 A molecular network (endotypes) derived from the susceptibility to RV infection and allergen sensitization was found to be responsible not only for childhood-onset allergic asthma, but also for adult-onset asthma or COPD.

Common Pathogenesis Characterized by Impaired Lung Development and Repair/Remodeling in Asthma and COPD

The primary risk factor for COPD is smoking. However, there is growing evidence to suggest that lung disease in adults may originate from prenatal or early-life exposures to harmful stimuli.43 A whole genome sequencing study44 that compared 3181 moderate/severe asthmatics with 3590 non-asthmatic controls showed that asthma risk is genetically correlated with lung dysfunction. This genetic factor associated with asthma development was shown to be independent of genetic factors associated with eosinophilic inflammation that also contribute to asthma. The polygenic score for impaired lung function was also associated with early-onset of asthma. Thus, genes that influence lung development in utero and in early childhood, in combination with environmental exposure such as cigarette smoke and viral infections, all contribute to both childhood asthma and future COPD development.

Asthma and COPD are heterogeneous and complex diseases, because they are caused by multiple factors, and the impact of individual risk factors is small. A genetic risk score (GRS) has been applied to address the heterogeneity and complexity of these diseases.45 We developed a quantitative GRS according to genotypes at 16 SNPs implicated in impaired lung function in both Japanese and non-Japanese individuals.46 The modest effects of 16 SNPs were combined into a single variable, which was calculated as the weighted sum of the number of high-risk alleles at each SNP. The GRS with a reduced forced expiratory volume/forced lung capacity ratio was consistently associated with asthma or COPD in two independent Japanese populations. Clustering of patients with asthma according to their lung function GRS indicated that elevated GRS may be associated with the development of distinctive phenotype of asthma (early onset, atopy, and severe airflow obstruction). Analysis of the functional relevance of these 16 genes showed that lung function GRS is associated with molecular pathways involved in tissue repair and remodeling induced by lung injury. In addition, a study using UK Biobank data to examine the association of 391 genes known to regulate lung development and lung function in adults47 found that 55 genes were significantly associated with four biological categories including growth factors, transcriptional regulators, intercellular adhesion, and extracellular matrix. These results together showed the importance of lung growth-related genes in regulating lung function and influencing airflow obstruction in adults. Thus, respiratory function measurements from infancy through adolescence may facilitate early identification of individuals prone to lung growth failure, leading to early intervention and prevention of asthma and COPD development.

Several GWAS have indicated the hedgehog signaling pathway as an important pathway underlying lung function and COPD; hedgehog-interacting protein (HHIP) is a negative regulator of the hedgehog pathway and patched 1 (PCTH1) is a receptor that activates the pathway.48 In older adults with asthma, the PTCHD4 gene has recently been associated with the responsiveness to ICS, as indicated by the presence of oral corticosteroid bursts.49 PTCHD4 encodes patched domain-containing protein 4, which represses hedgehog signaling.50 Increased PTCHD4 mRNA expression was associated with aging, and enrichment of methylated CpG sites in the PTCHD4 gene was associated with COPD.51,52 Furthermore, COPD patients with larger lesion with airway smooth muscle cell of bronchial tissue responded better to ICS than those with smaller lesion with airway smooth muscle cell, suggesting that a detailed histological classification of COPD patients may reflect differences in endotypes and help determine treatment strategy.53 These results suggest that responsiveness to ICS in asthma and COPD patients may be strongly influenced by specific patient endotypes, and that patients with specific endotypes related to lung growth abnormalities or impaired injury repair may be less responsive to ICS.

Treatable Traits Approach in Patients with Asthma and COPD

Given the complexity and heterogeneity of chronic inflammatory pulmonary diseases, including asthma and COPD, their appropriate management requires a new approach that includes multidimensional assessment. Patients with chronic inflammatory pulmonary diseases should not be treated according to disease labels such as asthma, COPD, or asthma COPD overlap, but rather on what endotypes play a critical role in individual patients.54 In 2015, I had proposed a plausible approach for positioning ICSs and long-acting β2-agonists (LABAs)/long-acting muscarinic antagonists (LAMAs) in the treatment of COPD based on both the extent of airflow obstruction and the presence of type 2 airway inflammation55 (Figure 3). Thereafter, a management strategy based on the so-called treatable traits was proposed.56,57

Figure 3 Approach to COPD treatment based on the degree of airflow obstruction and peripheral blood eosinophil counts. This proposal for positioning ICSs and bronchodilators for the treatment of COPD in clinical practice follows a personalized medicine approach that is not based on the stratification of patients into subgroups, but rather is based on individual characteristics that consider the heterogeneity and complexity of the disease in patients. Reprinted with permission from Dove Medical Press. Hizawa N. LAMA/LABA vs ICS/LABA in the treatment of COPD in Japan based on the disease phenotypes. Int J Chron Obstruct Pulmon Dis. 2015;10:1093–1102.55

We attempted to identify a group of patients who were more prone to exacerbations beyond the name of the diseases using multiple risk factors common to asthma and COPD exacerbations.58 As a result, we identified five distinct clusters, each characterized by high eosinophil counts, smokers with reduced lung function, gastroesophageal reflux, non-allergic women, or allergic rhinitis with high total IgE levels. Clinical heterogeneity of disease exacerbations was shown to possibly indicate the presence of exacerbation-prone endotypes common to asthma and COPD, supporting the benefit of a trait-based approach for exacerbation prevention in patients with chronic inflammatory pulmonary disease.

Recently, it was reported that in COPD patients with type 2 inflammation, in whom both blood eosinophil counts and FeNO are elevated, dupilumab, an antibody against the IL4 receptor alpha chain, leads to a reduction in exacerbation frequency, improvement in lung function and quality of life, and even improvement in respiratory symptoms compared to placebo.59 Considering that patients with currently diagnosed asthma or a history of asthma were excluded from the study, these results appear to support the usefulness of a treatable trait approach.

Conclusion

Both asthma and COPD are syndromes with highly variable clinical manifestations (phenotypes), including severity and course over time, and are caused by complex interactions between individual genetic factors and various environmental factors such as viral infection, allergen exposure, and tobacco smoke exposure (endotype). In this review, I have described four representative endotypes common to asthma and COPD (Figure 4). These endotypes are involved in patient pathogenesis in varying proportions. Furthermore, while the interactions of individual endotypes shape each patient’s pathology, the relative contribution of each endotype in an individual patient may change over time. Clinical traits or biomarkers could be used to identify the presence of each endotype. We must consider that it is not one endotype per patient, but rather the interaction of multiple endotypes that drives individual patient pathologies. With the advancement of genomic medicine, our understanding of endotypes will advance, new therapeutic agents will be developed, and the diseases will be reclassified according to specific phenotypes and biomarkers that reflect differences in molecular pathobiology, ushering in an era of precision medicine that targets the molecular mechanisms underlying the diseases in individual patients.

Figure 4 Common endotypes underlying asthma and COPD. Asthma and COPD are syndromes caused by complex interactions between individual genetic factors and various environmental factors. At any given time, the interaction of multiple endotypes drives individual patient pathologies and phenotypes.

Disclosure

The author has received speaker fees and/or research funding from AstraZeneca, Boehringer Ingelheim, Kyorin Pharmaceutical, GlaxoSmithKline, Novartis, and Sanofi.

References

1. Suzuki M, Makita H, Konno S, Nishimura M. Clinical characteristics and natural course of chronic obstructive pulmonary disease and/or asthma in Japanese patients: a summary report of two Hokkaido-based cohort studies. Respir Investig. 2023;61(4):527–539. doi:10.1016/j.resinv.2023.05.002

2. Holtjer JCS, Bloemsma LD, Beijers RJHCG, et al. Identifying risk factors for COPD and adult-onset asthma: an umbrella review. Eur Respir Rev. 2023;32(168):230009. doi:10.1183/16000617.0009-2023

3. Hizawa N. The understanding of asthma pathogenesis in the era of precision medicine. Allergol Int. 2023;72(1):3–10. doi:10.1016/j.alit.2022.09.001

4. Hirschhorn JN. Genomewide association studies—illuminating biologic pathways. N Engl J Med. 2009;360(17):1699–1701. doi:10.1056/NEJMp0808934

5. Agustí A, Celli B, Faner R. What does endotyping mean for treatment in chronic obstructive pulmonary disease? Lancet. 2017;390(10098):980–987. doi:10.1016/S0140-6736(17)32136-0

6. Orie N, Sluiter H, DeVries K, et al. The host factor in bronchitis. In: Bronchitis: An International Symposium, 27–29 April 1960, Groningen. Assen, Royal Van Gorcum; 1961:43–59.

7. Weiss ST. What genes tell us about the pathogenesis of asthma and chronic obstructive pulmonary disease Am. J Respir Crit Care Med. 2010;181(11):1170–1173. doi:10.1164/rccm.201001-0069PP

8. Kaneko Y, Yatagai Y, Yamada H, et al. The search for common pathways underlying asthma and COPD. Int J Chron Obstruct Pulmon Dis. 2013;8:65–78. doi:10.2147/COPD.S39617

9. Beamer CA, Shepherd DM. DM Role of the aryl hydrocarbon receptor (AhR) in lung inflammation. Semin Immunopathol. 2013;35(6):693–704. doi:10.1007/s00281-013-0391-7

10. Veldhoen M, Hirota K, Westendorf AM, et al. The aryl hydrocarbon receptor links TH17-cell-mediated autoimmunity to environmental toxins. Nature. 2008;453(7191):106–109. doi:10.1038/nature06881

11. Hu X, Shen Y, Zhao Y, et al. Epithelial aryl hydrocarbon receptor protects from mucus production by inhibiting ROS-triggered NLRP3 Inflammasome in asthma. Front Immunol. 2021;12:767508. doi:10.3389/fimmu.2021.767508

12. Yatagai Y, Hirota T, Sakamoto T, et al. Variants near the HLA complex group 22 gene (HCG22) confer increased susceptibility to late-onset asthma in Japanese populations. J Allergy Clin Immunol. 2016;138(1):281–283. doi:10.1016/j.jaci.2015.11.023

13. Hijikata M, Matsushita I, Tanaka G, et al. Molecular cloning of two novel mucin-like genes in the disease-susceptibility locus for diffuse panbronchiolitis. Hum Genet. 2011;129(2):117–128. doi:10.1007/s00439-010-0906-4

14. Nomura N, Matsumoto H, Sunadome H, et al. Importance of mucus burden and mucociliary impairment in asthma. J Allergy Clin Immunol. 2023;151(5):1410–1411. doi:10.1016/j.jaci.2023.01.024

15. Jeong S, Patel N, Edlund CK, et al. Identification of a novel mucin gene HCG22 associated with steroid-induced ocular hypertension. Invest Ophthalmol Vis Sci. 2015;56(4):2737–2748. doi:10.1167/iovs.14-14803

16. Ober C, Tan Z, Sun Y, et al. Effect of variation in CHI3L1 on serum YKL-40 level, risk of asthma, and lung function. N Engl J Med. 2008;358(16):1682–1691. doi:10.1056/NEJMoa0708801

17. James AJ, Reinius LE, Verhoek M, et al. Increased YKL-40 and chitotriosidase in asthma and chronic obstructive pulmonary disease Am. J Respir Crit Care Med. 2016;193(2):131–142. doi:10.1164/rccm.201504-0760OC

18. Boucher RC, Drazen JM. Muco-obstructive lung diseases. N Engl J Med. 2019;380(20):1941–1953. doi:10.1056/NEJMra1813799

19. Yatagai Y, Sakamoto T, Yamada H, et al. Genomewide association study identifies HAS2 as a novel susceptibility gene for adult asthma in a Japanese population. Clin Exp Allergy. 2014;44(11):1327–1334. doi:10.1111/cea.12415

20. Dentener MA, Vernooy JHJ, Hendriks S, Wouters EFM. Enhanced levels of hyaluronan in lungs of patients with COPD: relationship with lung function and local inflammation. Thorax. 2005;60(2):114–119. doi:10.1136/thx.2003.020842

21. Tsunoda Y, Sherpa MT, Kiwamoto T, et al. Has2 deficiency enhances OVA- induced airway inflammation and hyperresponsiveness in mice. Allergy. 2021;76(7):2214–2218. doi:10.1111/all.14715

22. Sherpa MT, Kiwamoto T, Matsuyama M, et al. Has2 regulates the development of ovalbumin-induced airway remodeling and steroid insensitivity in mice. Front Immunol. 2022;12:770305. doi:10.3389/fimmu.2021.770305

23. Barnes N, Ishii T, Hizawa N, et al. The distribution of blood eosinophil levels in a Japanese COPD clinical trial database and in the rest of the world. Int J Chron Obstruct Pulmon Dis. 2018;13:433–440. doi:10.2147/COPD

24. Christenson SA, Steiling K, van den Berge M, et al. Asthma-COPD overlap Clinical relevance of genomic signatures of type 2 inflammation in chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2015;191(7):758–766. doi:10.1164/rccm.201408-1458OC

25. John C, Guyatt AL, Shrine N, et al. Genetic Associations and Architecture of Asthma-COPD Overlap. Chest. 2022;161(5):1155–1166. doi:10.1016/j.chest

26. Ying S, O’Connor B, Ratoff J, et al. Expression and cellular provenance of thymic stromal lymphopoietin and chemokines in patients with severe asthma and chronic obstructive pulmonary disease. J Immunol. 2008;181(4):2790–2798. doi:10.4049/jimmunol.181.4.2790

27. Lee HC, Headley MB, Loo YM, et al. Thymic stromal lymphopoietin is induced by respiratory syncytial virus-infected airway epithelial cells and promotes a type 2 response to infection. J Allergy Clin Immunol. 2012;130(5):1187–1196.e5. doi:10.1016/j.jaci.2012.07.031

28. Perez GF, Pancham K, Huseni S, et al. Rhinovirus infection in young children is associated with elevated airway TSLP levels. Eur Respir J. 2014;44(4):1075–1078. doi:10.1183/09031936.00049214

29. Nakamura Y, Miyata M, Ohba T, et al. Cigarette smoke extract induces thymic stromal lymphopoietin expression, leading to T(H)2-type immune responses and airway inflammation. J Allergy Clin Immunol. 2008;122(6):1208–1214. doi:10.1016/j.jaci.2008.09.022

30. Smelter DF, Sathish V, Thompson MA, Pabelick CM, Vassallo R, Prakash YS. Thymic stromal lymphopoietin in cigarette smoke-exposed human airway smooth muscle. J Immunol. 2010;185(5):3035–3040. doi:10.4049/jimmunol.1000252

31. Masuko H, Sakamoto T, Kaneko Y, et al. Lower FEV1 in non-COPD, nonasthmatic subjects: association with smoking, annual decline in FEV1, total IgE levels, and TSLP genotypes. Int J Chron Obstruct Pulmon Dis. 2011;6:181–189. doi:10.2147/COPD.S16383

32. Balantic M, Rijavec M, Flezar M, et al. A polymorphism in ORMDL3 is associated not only with asthma without rhinitis but also with chronic obstructive pulmonary disease. J Investig Allergol Clin Immunol. 2013;23(4):256–261.

33. Zhang Y, Willis-Owen SAG, Spiegel S, Lloyd CM, Moffatt MF, Cookson WOCM; WOCM. The ORMDL3 Asthma Gene Regulates ICAM1 and Has Multiple Effects on Cellular Inflammation. J Respir Crit Care Med. 2019;199(4):478–488. doi:10.1164/rccm.201803-0438OC

34. Bouzigon E, Corda E, Aschard H, et al. Effect of 17q21 variants and smoking exposure in early-onset asthma. N Engl J Med. 2008;359(19):1985–1994. doi:10.1056/NEJMoa0806604

35. Kitazawa H, Masuko H, Kanazawa J, et al. ORMDL3/GSDMB genotype as a risk factor for early-onset adult asthma is linked to total serum IgE levels but not to allergic sensitization. Allergol Int. 2021;70(1):55–60. doi:10.1016/j.alit.2020.04.009

36. Wronski S, Beinke S, Obernolte H, et al. Rhinovirus-induced human lung tissue responses mimic chronic obstructive pulmonary disease and asthma gene signatures Am. J Respir Cell Mol Biol. 2021;65(5):544–554. doi:10.1165/rcmb.2020-0337OC

37. Hizawa N, Yamaguchi E, Konno S, Tanino Y, Jinushi E, Nishimura M. A functional polymorphism in the RANTES gene promoter is associated with the development of late-onset asthma. Am J Respir Crit Care Med. 2002;166(5):686–690. doi:10.1164/rccm.200202-090OC

38. Hizawa N, Makita H, Nasuhara Y, et al. Functional single nucleotide polymorphisms of the CCL5 gene and nonemphysematous phenotype in COPD patients. Eur Respir J. 2008;32(2):372–378. doi:10.1183/09031936.00115307

39. Gauthier M, Kale SL, Oriss TB, et al. CCL5 is a potential bridge between type 1 and type 2 inflammation in asthma. J Allergy Clin Immunol. 2023;152(1):94–106.e12. doi:10.1016/j.jaci.2023.02.028

40. Bochkov YA, Watters K, Ashraf S, et al. Cadherin-related family member 3, a childhood asthma susceptibility gene product, mediates rhinovirus C binding and replication. Proc Natl Acad Sci U S A. 2015;112(17):5485–5490. doi:10.1073/pnas.1421178112

41. Kanazawa J, Masuko H, Yatagai Y, et al. Genetic association of the functional CDHR3 genotype with early-onset adult asthma in Japanese populations. Allergol Int. 2017;66(4):563–567. doi:10.1016/j.alit.2017.02.012

42. Shigemasa R, Masuko H, Hyodo K, et al. Genetic impact of CDHR3 on the adult onset of asthma and COPD. Clin Exp Allergy. 2020;50(11):1223–1229. doi:10.1111/cea.13699

43. Lange P, Celli B, Agustí A, et al. Lung-function trajectories leading to chronic obstructive pulmonary disease. N Engl J Med. 2015;373(2):111–122. doi:10.1056/NEJMoa1411532

44. Chang D, Hunkapiller J, Bhangale T, et al. A whole genome sequencing study of moderate to severe asthma identifies a lung function locus associated with asthma risk. Sci Rep. 2022;12(1):5574. doi:10.1038/s41598-022-09447-8

45. Moll M, Sordillo JE, Ghosh AJ, et al. Polygenic risk scores identify heterogeneity in asthma and chronic obstructive pulmonary disease. J Allergy Clin Immunol. 2023;152(6):1423–1432. doi:10.1016/j.jaci.2023.08.002

46. Yamada H, Masuko H, Yatagai Y, et al. Role of lung function genes in the development of asthma. PLoS One. 2016;11(1):e0145832. doi:10.1371/journal.pone.0145832

47. Portas L, Pereira M, Shaheen SO, et al. Lung development genes and adult lung function. Am J Respir Crit Care Med. 2020;202(6):853–865. doi:10.1164/rccm.201912-2338OC

48. Paré PD. The smoking gun: genetics and genomics reveal causal pathways for COPD. Can J Respir Crit Care Sleep Med. 2017;1(3):126–132. doi:10.1080/24745332.2017.1361203

49. Wang AL, Lahousse L, Dahlin A, et al. Novel genetic variants associated with inhaled corticosteroid treatment response in older adults with asthma. Thorax. 2023;78(5):432–441. doi:10.1136/thoraxjnl-2021-217674

50. Chung JH, Larsen AR, Chen E, Bunz F. A PTCH1 homolog transcriptionally activated by p53 suppresses Hedgehog signaling. J Biol Chem. 2014;289(47):33020–33031. doi:10.1074/jbc.M114.597203

51. Casella G, Munk R, Kim KM, et al. Transcriptome signature of cellular senescence. Nucleic Acids Res. 2019;47(14):7294–7305. doi:10.1093/nar/gkz555

52. Morrow JD, Cho MH, Hersh CP, et al. DNA methylation profiling in human lung tissue identifies genes associated with COPD. Epigenetics. 2016;11(10):730–739. doi:10.1080/15592294.2016.1226451

53. Stolz D, Papakonstantinou E, Pascarella M, et al. Airway smooth muscle area to predict steroid responsiveness in COPD patients receiving triple therapy (HISTORIC): a randomised, placebo-controlled, double-blind, investigator-initiated trial. Eur Respir J. 2023;62(1):2300218. doi:10.1183/13993003.00218-2023

54. Hizawa N. Clinical approaches towards asthma and chronic obstructive pulmonary disease based on the heterogeneity of disease pathogenesis. Clin Exp Allergy. 2016;46(5):678–687. doi:10.1111/cea.12731

55. Hizawa N. LAMA/LABA vs ICS/LABA in the treatment of COPD in Japan based on the disease phenotypes. Int J Chron Obstruct Pulmon Dis. 2015;10:1093–1102. doi:10.2147/COPD.S72858

56. Agusti A, Bel E, Thomas M, et al. Treatable traits: toward precision medicine of chronic airway diseases. Eur Respir J. 2016;47(2):410–419. doi:10.1183/13993003.01359-2015

57. Pavord ID, Beasley R, Agusti A, et al. After asthma: redefining airways diseases. Lancet. 2018;391(10118):350–400. doi:10.1016/S0140-6736(17)30879-6

58. Hyodo K, Masuko H, Oshima H, et al. Common exacerbation-prone phenotypes across asthma and chronic obstructive pulmonary disease (COPD). PLoS One. 2022;17(3):e0264397. doi:10.1371/journal.pone.0264397

59. Bhatt SP, Rabe KF, Hanania NA, et al. Dupilumab for COPD with type 2 inflammation indicated by eosinophil counts. N Engl J Med. 2023;389(3):205–214. doi:10.1056/NEJMoa2303951

Source link

New research on thoracic microbiome of healthy individuals could help treat those with respiratory illnesses.

Professors Miriam Moffatt and Bill Cookson have led a study at the National Heart and Lung Institute to further our knowledge on the bacteria that make up the microbiome in the lungs of healthy individuals. Their study, published in Communications Biology, provides a pathway to develop new treatments for respiratory disease including asthma. 

"By growing and sequencing most of the major species of the airway bacteria we have found many unexpected and exciting organisms. The stage is set to investigate each of these for their individual activities in keeping our airways healthy and pathogens at bay" Professors Moffatt and Cookson Lead authors

The internal (mucosal) surfaces of our airways and lungs are extensive and constantly challenged by inhaled microorganisms. Respiratory infections are consequently the leading cause of death in developing countries, resulting in 4 million deaths annually. Asthma and chronic obstructive pulmonary disease (COPD) each affect more than 300 million people worldwide. Acute attacks (exacerbations) of both diseases are driven by infection.   

The airways of healthy lungs are accompanied by a community of bacteria known as the commensal microbiome. Unlike their cousins in the gut, bacteria in the lungs are free of the task of digesting nutrients, and they play major parts in resisting infection and regulating immunity. Different from the healthy gut bacteria, those in the lung have been poorly studied and the roles of different species in maintaining health remain to be discovered. 

An unwanted effect of advancing civilisation is that the microbiome loses its natural diversity, and bad bacteria (pathogens) increase in number. This condition is known as dysbiosis. Airway dysbiosis is a factor in many respiratory diseases, particularly asthma and COPD.

Professors Moffatt and Cookson and their collaborators wanted to find out what causes dysbiosis and how it can be prevented or recovered from. To do this they set about capturing the microbiome of healthy people to see what could be learned.

Unchartered territory

This paper describes the systematic culture of bacteria gathered from the airways deep within the lung during bronchoscopy. It discovered 52 novel species amongst 126 organisms covering three quarters of the abundance of airway commensals. Analysis of all the genetic sequences of these bacteria was combined with gene expression and metabolomic data from respiratory epithelium and provided many completely new insights into the interactions between us (the hosts) and our respiratory microbiome. 

The findings of this study substantially add to what is known about individual airway bacteria and how they work in communities. Genome sequencing of the different bacteria found many clinically relevant genes, for example new sequences encoding antimicrobial synthesis, adhesion to the airways, and immune modulation.

The researchers identified dysbiotic features that may allow pathogens to grow and influence asthma and COPD. They also identified pathways that sustain healthy interactions between commensals and the lung mucosa. The results of this work provide a systematic basis for decrypting interactions between commensals, pathogens, and mucosa. 

Exciting new horizons

Treatments derived from healthy microbial communities are already established for inflammatory and metabolic bowel diseases, such as through faecal transplantation, administration of particular commensals, or dietary changes. This new research provides reason to believe this same concept could be applied in the lungs. The systematic collection of cultured and genetically sequenced healthy airway bacteria provided us with the exciting potential to develop microbial therapies for common respiratory diseases.

Professorss Moffatt and Cookson said "We are very pleased that this work has been published in such a good journal, because it represents a huge amount of work by many wonderful collaborators in different parts of the world. The bacteria that live in us and on us are known as the microbiome. They are essential for human health. It is commonplace for people to talk about "the microbiome" as a single entity, but that is like describing the immune system as "white cells". By growing and sequencing most of the major species of the airway bacteria we have found many unexpected and exciting organisms. The stage is set to investigate each of these for their individual activities in keeping our airways healthy and pathogens at bay".

The paper shows how continued research into the respiratory microbiome is crucial to provide treatments for the hundreds of millions of people worldwide effected by respiratory conditions.


‘Genomic attributes of airway commensal bacteria and mucosa’ by William Cookson, Miriam Moffatt, et al. is published in Communications Biology. DOI: doi.org/10.1038/s42003-024-05840-3

Source link

Estimates suggest that 17% of women and 34% of men in middle age suffer from sleep-disordered breathing (SDB), a condition that leads to upper airway obstruction during sleep. Results from the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) study suggests that certain metabolite risk scores (MRSs) may be associated with diabetes mellitus (DM), according to investigators who published their findings in Nature Communications.

“These MRSs have the potential to serve as biomarkers for SDB, guiding risk stratification and treatment decisions,” wrote the study authors.

SDB occurs when the airways become partially or completely obstructed during sleep (called apneas and hypopneas, respectively). This can worsen sleep quality, reduce oxyhemoglobin desaturation, and can lead to short-term snoring and excessive daytime sleepiness.

In addition, an increasing amount of evidence from epidemiological studies suggests that SDB can also increase a person’s risk of vascular and metabolic diseases (eg, stroke, coronary heart disease, hypertension, and DM).

Understanding metabolites (ie, products of metabolism) during SDB “may yield insights into the metabolic environment of the disorder, elucidate sex differences, and suggest SDB subtypes and related molecular mechanisms involved in the progression of cardiometabolic conditions,” study authors write in the paper.

Knowing this, investigators conducted a discovery-replication study to understand if combining SDB measures and changes in SBD-related metabolites could be used to identify new SDB biomarkers that predict metabolic risk.

Image credit: sbw19 | stock.adobe.com

The team used principal component (PC) analysis to look at the physiological phenotypes of different types of SDB, then evaluated the metabolites associated with SDB PCs to create SDB PC-specific metabolite risk scores.

Data were collected pertaining to the 3299 individuals who participated in the HCHS/SOL study.Individuals were characterized by phenotype of SDB—people with PC1 had frequent respiratory events and hypoxia events, and patients with PC2 had shorter respiratory events.

Metabolic scores were associated with accurate prediction of cardiometabolic outcomes. PC1 had a higher association with incident diabetes and hypertension over approximately 6 years on average. Individuals with PC1 were more likely to be men, while individuals with SDB PC2 were more likely to include younger women, people with severe insomnia, and self-reported poor sleep, increased awakenings, and longer sleep duration.

Among patients with PC1, higher concentrations of sulfated metabolites of progesterone and pregnenolone were associated with reduced risk of poor outcomes. Among patients with SDB PC2, the risk of incident outcomes was associated with concentration of 3 sphingomyelins (a component of plasma membrane), although it was not statically significant.

“Dysregulation of sphingomyelin has been implicated in immune regulation, inflammation and apoptosis, and acute and chronic lung pathology,” study authors wrote.

In a secondary analysis, investigators stratified patients by glucose regulation. Patients with SDB PC1 who had normal glucose regulation did not have an elevated risk of developing diabetes compared to those with impaired glucose regulation, according to the SDB PC1 MRS; however, patients with SDB PC2 and normal glucose regulation may have a higher risk of developing diabetes, according to the SDB PC2 MRS, which makes it a promising tool for identifying risk.

According to the study authors, come limitations of the study include not analyzing results in other populations, using PCA analysis, not basing phenotypes as new clinical measures, information loss, and using observational measures, which limits the ability to determine causation.

“These findings provide a strong basis for the use of metabolomics in studying SDB, including for clarifying and measuring risks for incident outcomes by different quantitative SDB phenotypes and dichotomous subtypes,” study authors wrote in the paper.

REFERENCE

Zhang Y, Yu B, Qi Q, et al. Metabolomic profiles of sleep-disordered breathing are associated with hypertension and diabetes mellitus development. Nat Commun 15, 1845 (2024). doi:10.1038/s41467-024-46019-y

Source link

Chronic obstructive pulmonary disease (COPD) is set to become a $10 billion challenge for Canada's healthcare system by 2030, the Lung Health Foundation (LHF) warns, marking a critical juncture for the nation. In an aggressive move to counteract this impending crisis, LHF has unveiled 'Breathe Change,' a groundbreaking series of virtual policy forums aimed at bolstering respiratory resilience through enhanced care, funding, and policy innovation starting March 7, 2024.

Understanding the COPD Crisis

COPD, a chronic lung condition that obstructs airflow and makes breathing difficult, is on the rise in Canada, adding stress to an already burdened healthcare system. LHF CEO Jessica Buckley highlights the dire need for increased diagnosis and care, noting that exacerbations of COPD are the leading cause of unplanned hospitalizations in Canada. This healthcare conundrum not only signifies a substantial economic strain but also underscores the urgent need for revamped federal and provincial health policy interventions.

The 'Breathe Change' Initiative

The 'Breathe Change' initiative by LHF is a series of three virtual policy forums, kicking off with 'Building Respiratory Resilience: Partnership for Improved Care & Funding in COPD.' The forum will dissect current policy efforts, identify gaps in COPD programming, and discuss the crucial role of early detection and treatment in managing the disease. It presents a unique opportunity for Canadians, including public and policy leaders, healthcare practitioners, and those affected by COPD, to engage in meaningful dialogue aimed at transforming the landscape of lung health in Canada.

Hope Amid Challenges

Despite the gloomy projections, LHF remains optimistic about the future of COPD management. Through initiatives like 'Breathe Change,' the foundation seeks to ignite a transformative shift in perceptions of lung disease, advocating for a comprehensive approach that includes early detection, effective management, and robust support for those affected. The foundation also offers a range of support programs and resources, available 24/7, aimed at assisting individuals in navigating the complexities of lung health.

As COPD continues to pose a significant threat to Canada's healthcare system, the 'Breathe Change' initiative emerges as a beacon of hope, aiming to galvanize public, policy, and healthcare sectors towards actionable solutions. With the right mix of policy intervention, awareness, and support, Canada can confront this looming crisis head-on, ensuring a healthier future for all citizens.



Source link

The first patient has been dosed in a Phase 2a clinical trial testing ReAlta Life Sciences’ RLS-0071 in adults with chronic obstructive pulmonary disease (COPD) who are experiencing acute exacerbations, or sudden symptom worsening.

The trial (NCT06175065) will evaluate the safety of RLS-0071 versus a placebo in as many as 24 hospitalized patients, ages 30 and older, who will continue to receive their standard COPD treatment. Patients are being recruited at Temple University, in Philadelphia.

The dosing announcement comes about four months after the study was cleared by the U.S. Food and Drug Administration. RLS-0071 is also being tested in a Phase 2 trial that’s enrolling newborns with hypoxic ischemic encephalopathy, or brain damage from lack of oxygen around time of birth.

“With two Phase 2 trials now actively enrolling patients, ReAlta today reached another important milestone as we explore the potential for RLS-0071 across multiple therapeutic areas,” Ulrich Thienel, MD, PhD, ReAlta’s CEO, said in a company press release.

In COPD, inflammation in the lungs blocks airflow, causing symptoms such as shortness of breath, wheezing, and persistent, chesty cough. Periods when symptoms suddenly worsen can occur, and are known as acute exacerbations or flares.

Acute exacerbations can be triggered by infection or exposure to an environmental irritant such as an allergen or air pollution. These flares can last for days or weeks, often leading to hospitalization and permanent lung damage.

Recommended Reading

Main banner for Caroline Gainer's column,

‘Few effective options’ for acute COPD exacerbations

While some COPD treatments may ease symptoms, there are “few effective options available today to address acute exacerbations,” said Kenji Cunnion, MD, ReAlta’s chief medical officer.

Cunnion called the Phase 2 trial “an important step forward in developing an effective therapy for patients.”

RLS-0071 is a peptide or small protein that’s designed to reduce inflammation in two ways. To start, it blocks C1, a protein key for the activation of the complement cascade, which helps the immune system mount an inflammatory response against foreign intruders. It’s administered directly into the bloodstream through infusions.

The therapy also reduces the activity of myeloperoxidase (MPO), an enzyme that helps a type of immune cells called neutrophils cast lacy structures called NETs. These trap foreign intruders and prevent them from spreading, sometimes at the expense of uncontrolled inflammation. Activated neutrophils are thought to enter the lungs and contribute to COPD symptoms.

Suppressing both complement and neutrophil activation is expected to ease inflammation and reduce the number of hospitalizations due to acute COPD exacerbations.

“The novel, dual mechanism of action of RLS-0071 that enables the rapid inhibition of both complement activation and neutrophil effectors … holds great promise to address the fundamental drivers of the acute exacerbations that are a pervasive threat,” Cunnion said.

Recommended Reading

Seasonal variation COPD

Phase 1 trial shows three doses halve number of neutrophils

In a Phase 1 trial (NCT05351671) involving 30 healthy people who were exposed to a lung inflammation trigger, three RLS-0071 doses were enough to reduce the number of neutrophils in the lungs by half and drop MPO levels compared with a placebo.

In the ongoing Phase 2a trial, COPD patients who have a history of smoking will be randomly assigned to either RLS-0071 or a placebo for up to five days.

RLS-0071 will be given at a dose of 10 mg/kg three times per day, for at least three days and up to five days total if patients are still hospitalized. Each infusion lasts about eight minutes.

The trial’s main goal is to monitor side effects in the two months after starting treatment. Researchers also will watch for changes in blood levels of RLS-0071 and inflammation biomarkers, as well as clinical progression and resolution.

Treating COPD acute exacerbations remains a “significant unmet need, threatening the lives and well-being of millions across the world, and burdening our healthcare systems with substantial economic costs,” Thienel said. “We believe RLS-0071 can have a significant role in addressing these problems.”

Source link

AIRWAYS DISORDERS NETWORK

Asthma and COPD Section

Remodeling of airways and destruction of parenchyma by immune and inflammatory mechanisms are the leading cause of lung function decline in patients with chronic obstructive pulmonary disease (COPD). Type 2 inflammation has been recognized as an important phenotypic pathway in asthma. However, its role in COPD has been much less clear, which had been largely associated with innate immune response.1

Activation of Interleukin (IL)-25, IL-33, thymic stromal lymphopoietin [TSLP] produces type 2 cytokines IL-4, IL-5, and IL-13, either by binding to ILC2 or by direct Th2 cells resulting in elevated eosinophils in sputum, lungs, and blood, as well as fractional exhaled nitric oxide.2 The combined inflammation from this pathway underpins the pathological changes seen in airway mucosa, causing mucous hypersecretion and hyperresponsiveness.

Prior trials delineating the role of biologics, such as mepolizumab and benralizumab, showed variable results with possible benefit of add-on biologics on the annual COPD exacerbations among patients with eosinophilic phenotype of COPD.3

More recently, the BOREAS trial evaluated the role of dupilumab as an add-on therapy for patients with type 2 inflammation-driven COPD established using blood eosinophil count of at least 300/mL at initial screening.4 Dupilumab is a human monoclonal antibody that blocks combined IL-4 and IL-13 pathways with a broader effect on the type 2 inflammation. It included patients with moderate to severe exacerbations despite maximal triple inhaler therapy with blood eosinophilia. Patients with asthma were excluded. This 52-week trial showed reduction in annual moderate to severe COPD exacerbations, sustained lung function improvement as measured by prebronchodilator FEV1, and improvement in patient-reported respiratory symptoms.4 Evaluation of sustainability of these results with therapy step-down approaches should be explored.

Maria Azhar, MD, Section Fellow-in-Training

Abdullah Alismail, PhD, RRT, FCCP, Section Member

Raghav Gupta, MD, FCCP, Section Member

References:

1. Scanlon & McKenzie. 2012.

2. Brussell, et al. 2013.

3. Pavord, et al. 2017.

4. Bhatt, et al. 2023.

CHEST INFECTIONS & DISASTER RESPONSE NETWORK

Disaster Response and Global Health Section

Viral infections frequently cause acute respiratory failure requiring ICU admission. In the United States, influenza causes over 50,000 deaths annually and SARS-CoV2 resulted in 170,000 hospitalizations in December 2023 alone.1 2 RSV lacks precise incidence data due to inconsistent testing but is increasingly implicated in respiratory failure.

Patients with underlying pulmonary comorbidities are at increased risk of severe infection. RSV induces bronchospasm and increases the risk for severe infection in patients with obstructive lung disease.3 Additionally, COPD patients with viral respiratory infections have higher rates of ICU admission, mechanical ventilation, and death compared with similar patients admitted for other etiologies.4

Diagnosis typically is achieved with nasopharyngeal PCR swabs. Positive viral swabs correlate with higher ICU admission and ventilation rates in patients with COPD.4 Coinfection with multiple respiratory viruses leads to higher mortality rates and bacterial and fungal coinfection further increases morbidity and mortality.5

Treatment includes respiratory support with noninvasive ventilation and high-flow nasal cannula, reducing the need for mechanical ventilation.6 Inhaled bronchodilators are particularly beneficial in patients with RSV infection.5 Oseltamivir reduces mortality in severe influenza cases, while remdesivir shows efficacy in SARS-CoV2 infection not requiring invasive ventilation.7 Severe SARS-CoV2 infection can be treated with immunomodulators. However, their availability is limited. Corticosteroids reduce mortality and mechanical ventilation in patients with SARS-CoV2; however, their use is associated with worse outcomes in influenza and RSV.7 8

Vaccination remains crucial for prevention of severe disease. RSV vaccination, in addition to influenza and SARS-CoV2 immunization, presents an opportunity to reduce morbidity and mortality.

Zein Kattih, MD, Section Fellow-in-Training

Kathryn Hughes, MD

Brian Tran, MD

References:

1. Troeger C, et al. Lancet Infect Dis. 2028;18(11):1191-1210.

2. WHO COVID-19 Epidemilogical Update, 2024.

3. Coussement J, et al. Chest. 2022;161(6):1475-1484.

4. Mulpuru S, et al. Influenza Other Respir Viruses. 2022;16(6):1172-1182.

5. Saura O, et al. Expert Rev Anti Infect Ther. 2022;20(12):1537-1550.

6. Inglis R, Ayebale E, Shultz MJ. Curr Opin Crit Care. 2019;25(1):45-53.

7. O'Driscoll LS, Martin-Loeches I. Semin Respir Crit Care Med. 2021;42(6):771-787.

8. Bhimraj A, et al. Clin Inf Dis. 2022.

CRITICAL CARE NETWORK

Palliative & End-of-Life Section

For providers caring for critically ill patients, navigating death and dying in the intensive care unit (ICU) with proficiency and empathy is essential. Approximately 20% of deaths in the United States occur during or shortly after a stay in the ICU and approximately 40% of ICU deaths involve withdrawal of artificial life support (WOALS) or compassionate extubation.

This is a complex process that may involve advanced communication with family, expertise in mechanical ventilation, vasopressors, dialysis, and complex symptom management. Importantly, surrogate medical decision-making for a critically ill patient can be a challenging experience associated with anxiety and depression. How the team approaches WOALS can make a difference to both patients and decision-makers. Unfortunately, there is striking variation in practice and lack of guidance in navigating issues that arise at end-of-life in the ICU. One study of 2814 hospitals in the US with ICU beds found that 52% had intensivists while 48% did not.2 This highlights the importance of developing resources focusing on end-of-life care in the ICU setting regardless of the providers’ educational training.

Important elements could include the role for protocol-based WOALS, use of oxygen, selection and dosing strategy of comfort-focused medications, establishing expectations, and addressing uncertainties. This would be meaningful in providing effective, ethical end-of-life care based on evidence-based strategies. While death may be unavoidable, a thoughtful approach can allow providers to bring dignity to the dying process and lessen the burden of an already difficult experience for patients and families alike.

Angela L. Birdwell, DO, MA, Section Chair

Nehan Sher, MD, Section Member

References:

1. Curtis JR, et al. Am J Respir Crit Care Med. 2012;186(7):587-592.

2. Halpern NA, et al. Crit Care Med. 2019;47(4):517-525.

SLEEP MEDICINE NETWORK

Nonrespiratory Sleep Section

Q: Are there interventions that can be readily implemented to improve sleep quality for hospitalized patients?

Dr. Arora: A patient’s first night in the hospital is probably not the night to liberalize sleep; you’re still figuring out whether they’re stable. But by the second or third day, you should be questioning – do you need vitals at night? Do you need a 4 AM blood draw?

We did an intervention called SIESTA that included both staff education about batching care and system-wide, electronic health record-based interventions to remind clinicians that as patients get better, you can deintensify their care. And we’re currently doing a randomized controlled trial of educating and empowering patients to ask their teams to help them get better sleep.

Q: Does hospital sleep deprivation affect patients after discharge?

Dr. Arora: Absolutely. “Posthospital syndrome” is the idea that 30 days after discharge, you’re vulnerable to getting readmitted – not because of the disease you came in with, but something else. And people who report sleep complaints in the hospital are more likely to be readmitted.

When people are acutely sleep deprived, their blood pressure is higher. Their blood sugar is higher. Their cytokine response and immune function are blunted. And our work shows that sleep deficits from the hospital continue even when you go home. Fatigue becomes a very real issue. And when you’re super fatigued, are you going to want to do your physical therapy? Will you be able to take care of yourself? Will you be able to learn and understand your discharge instructions?

We have such a huge gap to improve sleep. It’s of interest to people, but they are struggling with how to do it. And that’s where I think empowering frontline clinicians to take the lead is a great project for people to take on.

Vineet Arora, MD, MAPP, is the Dean for Medical Education at the University of Chicago and an academic hospitalist who specializes in the quality, safety, and experience of care delivered to hospitalized adults.

Alison Szabo, MD

Lisa Wolfe, MD, Section Member

THORACIC ONCOLOGY & CHEST PROCEDURES NETWORK

Lung Cancer Section

Lung cancer stands as the leading cause of cancer-related deaths globally, with its prevalence casting a long and challenging shadow. The most important risk factor for lung cancer is tobacco use, a relationship strongly substantiated by data. The impact of smoking cessation to reduce lung cancer incidence is underscored by the US Preventive Services Task Force (USPSTF), which mandates that smoking cessation services be an integral component of lung cancer screening programs.

However, beneath the surface of this overarching concern lies a web of factors contributing to racial and ethnic disparities in smoking cessation. Cultural intricacies play a pivotal role in shaping these disparities. Despite higher instances of light or intermediate smoking, racially ethnic minority groups in the general population often face greater challenges in achieving smoking cessation, as highlighted by Bacio, et al (Addict Behav. 2014). Adding another layer to this complex scenario is the profound impact of sustained smoking during cancer treatment. Research suggests that for individuals diagnosed with lung cancer, smoking cessation can markedly boost treatment efficacy, reduce the risk of secondary tumors, and even double the chances of survival.1

A study by Harris, et al. delving into the preferences of current smokers within a lung cancer screening setting uncovered noteworthy insights.2 White participants exhibited a fourfold greater likelihood of favoring a digital format for receiving smoking cessation information, while their Black counterparts expressed a preference for face-to-face support, phone assistance, or printed materials.

Moreover, a meta-analysis conducted by Jabari, et al. sheds light on the efficacy of culturally targeted smoking interventions.3 This comprehensive review describes a dual-level approach to tailoring smoking cessation health interventions: surface and deep. Surface adaptations encompass elements like language and imagery, which aim to enhance the acceptability of interventions within specific communities. Simultaneously, deep-tailored elements identify culturally significant factors that can fundamentally influence the behavior of the target population. The findings of this meta-analysis reveal that the integration of culturally tailored components into standard interventions significantly enhances their efficacy in facilitating smoking cessation.

In conclusion, sustained smoking cessation is a crucial element in combating the global burden of lung cancer. Recognizing the importance of individualized approaches in health care, it is imperative to tailor smoking cessation communications and interventions to diverse cultural influences and socioeconomic factors. Culturally tailored smoking cessation programs that account for nuances specific to each community have the potential to significantly enhance their effectiveness. This necessitates a shift towards individualized smoking cessation care, with a targeted focus on increasing cessation rates among racial and ethnic minority groups. In doing so, we take a step closer to a more equitable landscape in the battle against lung cancer.

Stella Ogake, MD, FCCP, Section Member

References:

1. Dresler, et al. Lung Cancer. 2003.

2. J Cancer Educ. 2018;33(5).

3. Addiction. 2023.

Source link

2023-2031] Computer and Gaming Glasses Market Current Trends and Growth  Opportunities

Report Ocean has published a new report on the COPD and Asthma Devices Market in diverse regions to produce a report with more than 250+pages. This market report is an excellent fusion of qualitative and quantitative data emphasizing major industry changes, business and competitor difficulties in gap analysis, and potential new possibilities in the COPD and Asthma Devices Market.

The global market for Chronic Obstructive Pulmonary Disease (COPD) and asthma devices is projected to experience substantial growth, with forecasts indicating a rise to $51,628.58 million by 2027, from a baseline established in 2020. This growth reflects a Compound Annual Growth Rate (CAGR) of 4.30% during the forecast period. This comprehensive report delves into the dynamics shaping this market, highlighting the drivers of growth, the challenges faced, and the burgeoning opportunities within the COPD and asthma devices sector.

Request To Download Free Sample of This Strategic Report@  reportocean.com/industry-verticals/sample-request?report_id=AMR1009

Market Overview:

COPD and asthma devices are crucial in the management and treatment of respiratory diseases, providing relief and improving the quality of life for patients. These devices range from inhalers to nebulizers and spirometers, each serving different needs and preferences of patients. The demand for these devices is on an upswing, driven by the rising prevalence of respiratory diseases globally, increased awareness about disease management, and technological advancements in device manufacturing.

Chronic obstructive pulmonary disease (COPD) and asthma devices, also known as pulmonary drug delivery devices, are used as a permanent treatment or rescue therapy for respiratory diseases and other related ailments. It is the most advanced mode of drug administration in which the drug is directly delivered to the lungs to provide a systemic effect. COPD and asthma have significant shares in the global respiratory diseases market. According to the Global Health Organization (WHO), in 2016, around 251 million cases of COPD were estimated globally. Thus, a variety of drug-delivery protocols, such as oral and parenteral delivery, are developed for the treatment of COPD and asthma. However, the pulmonary drug delivery system is the most effective treatment option as compared to the other conventional methods.

Growth Drivers and Opportunities:

The primary factors propelling the growth of the COPD and asthma devices market include the increasing global incidence of respiratory diseases such as asthma and COPD, attributed to factors like air pollution, smoking, and changing lifestyle patterns. Additionally, advancements in inhaler technologies, such as smart inhalers equipped with Bluetooth connectivity for monitoring usage and dosing, are anticipated to bolster market growth.

Download Free Sample of This Strategic Report with Industry Analysis@  reportocean.com/industry-verticals/sample-request?report_id=AMR1009

The market is also benefiting from heightened awareness and healthcare initiatives aimed at managing and treating respiratory conditions effectively. Moreover, the advent of portable and user-friendly devices has facilitated the adoption of homecare respiratory therapy, opening new avenues for market expansion.

Challenges:

Despite the optimistic growth trajectory, the COPD and asthma devices market faces several challenges. High costs associated with advanced respiratory devices and treatments can impede accessibility for a significant portion of the patient population, particularly in low- and middle-income countries. Moreover, the potential for side effects and complications arising from improper use of these devices remains a concern.

KEY BENEFITS FOR STAKEHOLDERS

– This report entails a detailed quantitative analysis along with the current global antihypertensive market trends from 2019 to 2027 to identify the prevailing opportunities along with the strategic assessment.
– The market size and estimations are based on a comprehensive analysis of key developments in the industry.
– A qualitative analysis based on innovative products facilitates strategic business planning.
– The development strategies adopted by the key market players are enlisted to understand the competitive scenario of the market.

Competitive Landscape:

The leading players profiled in this report include Aerogen, Inc., AstraZeneca PLC, Baxter International Inc., Boehringer Ingelheim International GmbH, 3M COMPANY, GF Health Products, GlaxoSmithKline Plc, Koninklijke Philips N.V., Novartis AG, PARI Medical Holding GMBH, and Smith’s Group Plc.

To Get More Business Strategies For Request Free Sample Report @  reportocean.com/industry-verticals/sample-request?report_id=AMR1009

Factors Affecting the Growth of the COPD and Asthma Devices Industry:

Increasing Prevalence of COPD and Asthma:

The growth of the COPD and asthma devices industry is significantly influenced by the increasing prevalence of chronic obstructive pulmonary disease (COPD) and asthma worldwide. COPD and asthma are chronic respiratory conditions characterized by airflow obstruction, inflammation, and respiratory symptoms such as coughing, wheezing, and shortness of breath. The global burden of COPD and asthma is substantial, with millions of people affected by these conditions, and the prevalence is projected to rise due to factors such as aging populations, environmental pollution, smoking, and urbanization. As the prevalence of COPD and asthma increases, there is a growing demand for devices and treatments that help manage symptoms, improve lung function, and enhance the quality of life for patients with these respiratory conditions, driving growth in the COPD and asthma devices industry.

Technological Advancements in Respiratory Devices:

Technological advancements play a crucial role in driving growth and innovation in the COPD and asthma devices industry. Manufacturers continually invest in research and development to innovate new respiratory devices and technologies that offer improved efficacy, convenience, and patient adherence. For example, advancements in inhaler devices include the development of dry powder inhalers (DPIs), metered-dose inhalers (MDIs), and soft mist inhalers (SMIs) with features such as dose counters, breath-actuated mechanisms, and compact designs for portability. Similarly, innovations in nebulizer technology include the development of ultrasonic nebulizers and mesh nebulizers that deliver medications more efficiently and with reduced treatment times. Moreover, the integration of digital health technologies, such as mobile apps, smart inhalers, and remote monitoring devices, enhances patient engagement, medication adherence, and disease management for patients with COPD and asthma. As manufacturers introduce advanced respiratory devices and technologies to address the evolving needs of patients and healthcare providers, they stimulate demand and drive growth in the COPD and asthma devices industry.

Healthcare Policy and Reimbursement Landscape:

The growth of the COPD and asthma devices industry is influenced by healthcare policy and reimbursement frameworks governing respiratory devices and treatments. Reimbursement policies set by government payers, private insurance companies, and healthcare systems impact patient access to respiratory devices and treatments and influence healthcare providers’ prescribing decisions. For example, favorable reimbursement rates for inhaler devices and medications may incentivize healthcare providers to prescribe these treatments to patients with COPD and asthma. Additionally, changes in healthcare policies, such as the implementation of value-based care models and initiatives to improve chronic disease management, drive the adoption of respiratory devices and technologies that support patient self-management and remote monitoring. As policymakers and payers prioritize initiatives to improve respiratory health outcomes and reduce healthcare costs associated with COPD and asthma, the COPD and asthma devices industry may experience changes in demand and growth opportunities.

For Further Information Regarding this Report: Request a Free Sample @  reportocean.com/industry-verticals/sample-request?report_id=AMR1009

Market Segmentation:

The report segments the global COPD and asthma devices market by product type (inhalers and nebulizers), disease indication (COPD and asthma), distribution channel (hospital pharmacies, retail pharmacies, and online pharmacies), and geography. It offers an in-depth analysis of each segment, providing insights into market size, growth trends, and future prospects.

Key Market Segments

By Product Type
– Inhalers
o Drug Powder Inhalers (DPIs)
o Metered Dose Inhalers (MDIs)
o Soft Mist Inhalers (SMIs)
– Nebulizers
o Compressor Nebulizers
o Ultrasonic Nebulizers
o Mesh Nebulizers

By Indication
o Asthma
o COPD

By Distribution Channel
o Retail Pharmacies
o Hospitals
o Online Pharmacies

– By Region
o North America
– U.S.
– Canada
– Mexico
o Europe
– Germany
– France
– UK
– Italy
– Russia
– Rest of Europe
o Asia-Pacific
– Japan
– China
– India
– Australia
– Rest of Asia-Pacific
o Middle East
– Saudi Arabia
– Brazil
– Argentina
– Colombia
– Turkey
– Rest of LAMEA

Get 30% Off On Various License Types When Buy Now At @  reportocean.com/industry-verticals/sample-request?report_id=AMR1009

Table of Contents

– Market Summary

– Economic Impact Competition Analysis by Players

– Production, Revenue (Value) by geographical segmentation

– Market Size by Type and Application

– Regional Market Status and Outlook

– Market Analysis and Outlook

– Market Forecast by Region, Type, and Application

– Cost Investigation, Market Dynamics

– Marketing Strategy comprehension, Distributors and Traders

– Market Effect Factor Analysis

– Research Finding/ Conclusion

– Appendix

– Continue……

Some of the Key Aspects that the Report Analyses:

  • Which regions in Market are witnessing rise in investments in the supply chain networks?
  • Which regions have witnessed decline in consumer demand due to economic and political upheavals in Industry?
  • Which countries in Market seem to have benefitted from recent import and export policies?
  • Which are some the key geographies that are likely to emerge as lucrative markets?
  • What are some the sustainability trends impacting the logistics and supply chain dynamics in the Market?
  • What are some of the demographic and economic environments that create new demand in developing economies?
  • Which regions in Market are expected to lose shares due to pricing pressures?
  • Which regions leading players are expected to expand their footprints in the near future in Industry?
  • How are changing government regulations shaping business strategies and practices?

Key Findings Market Reports:

  • Supply Chain Disruptions: Lockdowns, restrictions, and factory closures worldwide disrupted production and movement of goods, initially leading to reduced demand for this industry.
  • Shift in Demand: As consumer demand shifted, industry reports were increasingly used to transport essential goods such as medical supplies, PPE, pharmaceuticals, and groceries, while shipments of non-essential items declined.
  • Container Imbalances: Uneven trade flows and shipping disruptions caused imbalances in container availability, impacting pricing and availability across different regions.
  • Rising Shipping Costs: Increased demand for essential goods and disruptions in trade led to rising freight rates, affecting overall shipping costs and logistics.
  • Maintenance Challenges: Travel restrictions and lockdowns hindered maintenance activities for industry, potentially leading to longer-term maintenance challenges.
  • Supply Chain Resilience: Businesses recognized the need for greater supply chain resilience, leading to discussions and investments in robust container logistics and digital solutions.
  • Digital Adoption: The pandemic accelerated the adoption of digital solutions in logistics and supply chain management, including e-commerce and digital platforms for container booking and tracking.
  • Regulatory Impact: Governments implemented regulations and safety measures affecting shipping practices and container handling, impacting container operations.
  • Vaccine Transportation: Market played a vital role in transporting COVID-19 vaccines and related supplies, highlighting their importance in global health crises.
  • Supply Chain Strategies: Businesses reevaluated supply chain strategies, prioritizing risk mitigation and exploring alternatives for resilience against future disruptions.

Request full Report :- @  reportocean.com/industry-verticals/sample-request?report_id=AMR1009

About Report Ocean:

We are the best market research reports provider in the industry. Report Ocean is the world’s leading research company, known for its informative research reports. We are committed to providing our clients with both quantitative and qualitative research results. As a part of our global network and comprehensive industry coverage, we offer in-depth knowledge, allowing informed and strategic business conclusions to report. We utilize the most recent technology and analysis tools along with our own unique research models and years of expertise, which assist us to create necessary details and facts that exceed expectations.

Get in Touch with Us:
Report Ocean:
Email[email protected]
Address: 500 N Michigan Ave, Suite 600, Chicago, Illinois 60611 – UNITED STATES
Tel:+1 888 212 3539 (US – TOLL FREE)
Website: reportocean.com

Source link

COPD: A $10 Billion Threat to Canada's Healthcare System
by 2030, Warns Country's Leading Lung Health Non-Profit

Breathe Change Summons Public and Policy Leaders, Healthcare Professionals, Advocates
and those Affected by Lung Disease to Amplify Their Voices in Support of Driving Progress

LUNG HEALTH FOUNDATION LAUNCHES FIRST OF THREE LANDMARK POLICY FORUMS ON THURSDAY, MARCH 7 (CNW Group/Lung Health Foundation)LUNG HEALTH FOUNDATION LAUNCHES FIRST OF THREE LANDMARK POLICY FORUMS ON THURSDAY, MARCH 7 (CNW Group/Lung Health Foundation)

LUNG HEALTH FOUNDATION LAUNCHES FIRST OF THREE LANDMARK POLICY FORUMS ON THURSDAY, MARCH 7 (CNW Group/Lung Health Foundation)

TORONTO, March 4, 2024 /CNW/ - Chronic obstructive pulmonary disease (COPD) looms as a $10 billion healthcare crisis in Canada by 2030 and, according to the Lung Health Foundation ("LHF"), is poised to dismantle the Canadian healthcare system. LHF is the nation's leading non-profit organization dedicated to supporting and empowering individuals living with lung conditions across Canada.

In response to this crisis, LHF launches "Breathe Change", a landmark series of three virtual policy forums beginning on Thursday, March 7 at 1 pm to 2:30 pm ET with Building Respiratory Resilience: Partnership for Improved Care & Funding in COPD.

The inaugural forum will explore policy avenues to aid Canadians facing the most prevalent form of lung disease, scrutinize the impact of existing COPD interventions, probe access gaps in COPD programming and support mechanisms, champion the imperative role of spirometry in early COPD detection and treatment, and evaluate the influence of healthcare personnel on COPD care quality and outcomes. The session showcases the best-of-the-best in COPD and lung disease research, diagnosis and treatment modalities, and policy initiatives. Leading the expert COPD panel are Dr. Joshua Wald, Clinical Practice, Firestone Institute & Vice Co-Chair CTS COPD Assembly - COPD Steering Committee; Dr. Dawn Bowdish, Executive Director, Firestone Institute for Respiratory Health and Dr. Maya de Zoysa, Respirologist, West Nipissing General Hospital.

The session welcomes participation from all Canadians, spanning public and policy spheres, healthcare practitioners, advocates, media and the millions impacted by COPD. For further details and to register for this free virtual event, visit bit.ly/BreatheChange

"COPD in Canada remains a grossly underfunded lung condition, with only 1 in 5 afflicted individuals even receiving the necessary diagnosis and care," says LHF CEO Jessica Buckley. "COPD exacerbations currently rank as the number one cause of unplanned hospitalizations in Canada, creating a huge economic burden to our healthcare system. This serves as an urgent call-to-action for both federal and provincial health policy makers."

"We Aim to Activate Change and Ignite a Transformative Shift in Perceptions of Lung Disease"

Urgency underscores Buckley's message: "Through the largest series of policy forums on lung health in Canada, we aim to activate change and ignite a transformative shift in perceptions of lung disease, highlighting current policy efforts while propelling discussions toward new actionable solutions. The misconception that COPD solely stems from smoking must be dispelled, and our approach to caring for those impacted must evolve. Failing to do so risks compromising the quality of care for individuals dealing with this pervasive lung condition."

Yet amid the challenges, Buckley says there is a beacon of hope for COPD sufferers. "The Lung Health Foundation wages a daily battle for the respiratory well-being of all Canadians as incidences of COPD escalate in tandem with wildfires, climate change, radon and deteriorating air quality."

Attendees can also secure spots for upcoming lung health policy forums: Timely Triumph: Accelerating Lung Cancer Care – A Call to Action for Public and Policy Leaders (March 21) and Halt the Haze: A Strategic Approach to Ending Youth Vaping in Canada (April 18).

The Breathtaking Truth about COPD

  • Over half (53%) of COPD sufferers reside in long-term care or senior homes.

  • 1 in 4 Canadians will develop COPD during their lifetimes. COPD, while chronic and progressive, remains treatable.

  • An additional 1 million Canadians with COPD languish undiagnosed and untreated.

  • COPD ranks as the 5th leading cause of mortality in Canada.

  • Nearly 900,000 Ontarians were living with COPD in 2019.

  • COPD endures neglect, with merely 1 in 5 afflicted individuals receiving diagnosis.

  • The current tally of Ontarians who are needlessly suffering is intolerable.

  • 1 in 10 COPD patients confront hospitalization due to exacerbations annually.

  • Annual emergency department visits for COPD exacerbations plague 1 in 20 COPD patients in Ontario.

  • While overall hospital admission rates have waned since 2002, COPD patient admissions have surged by 9.6% during the same period.

Accessible Lung Health Foundation Support Programs and Resources Available 24/7

For those navigating the labyrinth of lung disease, LHF offers an expansive array of disease-specific support programs and resources. Visitors to LHF's digital portal enjoy free access to Canada's premier real-time repository of lung disease management, education, and awareness initiatives. Among the many programs offered: the popular and in-demand virtual Fitness for Breath, Smoking and Vaping Cessation Quash App, My Lung Coach and Lung Health Hotline, where callers can talk directly to Certified Respiratory Educators about a gamut of lung health-related issues and challenges, including asthma, COPD, lung cancer, pneumonia, RSV, immunizations, inhalers, medications, breathing conditions, and indoor and outdoor air quality.

About Lung Health Foundation

The Lung Health Foundation is dedicated to improving lung health for all Canadians. Through a range of community initiatives, grass-roots educational programs, research, and advocacy, the organization elevates awareness and fosters a compassionate environment for those affected by lung conditions, including their caregivers. Building on the legacy of the Ontario Lung Association, which for over a century served as the recognized leader, voice, and primary resource in lung health, LHF has expanded its efforts nationally. The Lung Health Foundation works tirelessly to prevent lung disease, help people manage their lung conditions, and promote policy change to create a world where everyone can breathe with ease. The Lung Health Foundation encourages individuals to connect with its Lung Health Hotline for one-on-one advice from Certified Respiratory Educators. For assistance, call 1-888-344-LUNG, email [email protected], or engage in live chat at www.lunghealth.ca. Visit us on Instagram @lunghealthfoundation, Facebook at lunghealthfoundation/, and on X at @LungHealthFdn.

SOURCE Lung Health Foundation

CisionCision

Cision

View original content to download multimedia: www.newswire.ca/en/releases/archive/March2024/04/c3364.html

Source link

2023-2031] Computer and Gaming Glasses Market Current Trends and Growth  Opportunities

Report Ocean has published a new report on the Mechanical Ventilator Market in diverse regions to produce a report with more than 250+pages. This market report is an excellent fusion of qualitative and quantitative data emphasizing major industry changes, business and competitor difficulties in gap analysis, and potential new possibilities in the Mechanical Ventilator Market.

The Global Mechanical Ventilator Market has experienced significant growth, expanding from a valuation of $2.94 billion in 2019 to an estimated $12.54 billion by 2027. This report provides an in-depth analysis of the market dynamics, emphasizing the factors contributing to an impressive Compound Annual Growth Rate (CAGR) of 16.5% during the forecast period from 2020 to 2027. It covers the current market trends, growth drivers, challenges, and potential opportunities within the mechanical ventilator industry.

Request To Download Free Sample of This Strategic Report @ reportocean.com/industry-verticals/sample-request?report_id=AMR1086

Market Overview:

Mechanical ventilators are critical life-support devices used in respiratory failures and other critical care conditions. They are essential in intensive care units (ICUs), emergency departments, and increasingly in home care settings. The demand for mechanical ventilators has surged, particularly highlighted by the COVID-19 pandemic, which significantly stressed healthcare systems worldwide.

Mechanical ventilation is a lifesaving intervention for patients with respiratory disorders or respiratory failure. It is a form of breathing assistance in which a patient is connected to a machine through an endotracheal tube directly applied to the airway or non-invasive (NIV) mask. It is also employed as a diagnostic tool to measure static compliance of airway resistance and irregular functioning of respiratory system. Currently, intensive care and portable mechanical ventilators are the two most widely used ventilators available in the market.

Growth Drivers and Opportunities:

The market’s growth is primarily driven by the increasing incidence of respiratory diseases, such as chronic obstructive pulmonary disease (COPD), asthma, lung cancer, and other acute respiratory infections. The COVID-19 pandemic has further underscored the vital role of mechanical ventilators in managing severe respiratory conditions, leading to a dramatic increase in demand.

Download Free Sample of This Strategic Report with Industry Analysis @ reportocean.com/industry-verticals/sample-request?report_id=AMR1086

Technological advancements in ventilator design, offering more patient-friendly, portable, and efficient devices, are propelling market growth. Additionally, the aging global population, susceptible to respiratory conditions requiring ventilatory support, and improvements in healthcare infrastructure across emerging economies present significant growth opportunities for the mechanical ventilator market.

Increase in incidences of chronic respiratory diseases, such as chronic obstructive pulmonary disease (COPD), asthma, bronchitis, and other lung disorders, and rise in number of accidental emergencies lead to substantial requirement of mechanical ventilators. In addition, growth in geriatric population prone to respiratory emergencies is one of the key drivers of the market. Moreover, technological innovations in respiratory care devices, namely, non-invasive ventilation technology and portable mechanical ventilators, further supplement the market growth.

Challenges:

Despite the optimistic growth outlook, the mechanical ventilator market faces several challenges. High costs associated with advanced ventilator systems can limit accessibility in low- and middle-income countries. Furthermore, the complexity of mechanical ventilators requires skilled healthcare professionals for operation and management, posing a challenge in regions facing healthcare workforce shortages.

KEY BENEFITS FOR STAKEHOLDERS

? This report provides a detailed quantitative analysis of the current market trends and future estimations from 2020 to 2027, which assists in identifying prevailing market opportunities.
? An in-depth analysis of various regions is likely to provide a detailed understanding of the current trends to the stakeholders to formulate region-specific plans.
? Comprehensive analysis of factors that drive and restrain growth of the mechanical ventilator market are provided.
? Key regulatory guidelines for the mechanical ventilator market are critically dealt according to region.
? A deep dive analysis of various regions provides insights that would allow companies to strategically plan their business moves.

To Get More Business Strategies For Request Free Sample Report @ reportocean.com/industry-verticals/sample-request?report_id=AMR1086

Competitive Landscape:

– Becton, Dickinson and Company
– Carl Reiner GmbH
– Draegerwerk AG & Co. KGaA
– Getinge AB
– General Electric Company (GE Healthcare)
– Hamilton Medical AG
– Koninklijke Philips N.V.
– Medtronic Plc.
– Mindray Medical International Limited
– Smiths Group Plc.
– Zoll Medical Corporation

Factors Affecting the Growth of the Mechanical Ventilator Industry:

Global Health Emergencies and Pandemics:

The growth of the mechanical ventilator industry is heavily influenced by global health emergencies and pandemics, particularly during outbreaks of respiratory diseases such as COVID-19. During public health crises, there is an increased demand for mechanical ventilators to support patients with severe respiratory failure, including those with acute respiratory distress syndrome (ARDS) caused by infectious diseases. The COVID-19 pandemic, in particular, has highlighted the critical role of mechanical ventilators in treating severely ill patients and preventing mortality. The surge in demand for mechanical ventilators during the pandemic has led to increased production, innovation, and investment in the mechanical ventilator industry to meet the growing needs of healthcare systems worldwide. As the frequency and severity of global health emergencies continue to impact healthcare infrastructure and resource allocation, the demand for mechanical ventilators remains a key driver of growth in the industry.

Technological Advancements and Innovation:

Technological advancements and innovation drive growth and competitiveness in the mechanical ventilator industry. Manufacturers continuously invest in research and development to improve the design, functionality, and performance of mechanical ventilators, aiming to enhance patient outcomes, user experience, and safety. Innovations in ventilation modes, such as pressure-controlled ventilation, volume-controlled ventilation, and dual-mode ventilation, offer clinicians greater flexibility and customization in tailoring ventilation strategies to individual patient needs. Moreover, advancements in ventilator monitoring and control systems, including real-time data analytics, remote monitoring capabilities, and integration with electronic health records (EHRs), enable more precise and personalized ventilation management. Additionally, the development of portable and transport ventilators enhances the mobility and flexibility of mechanical ventilation in various healthcare settings, including ambulances, intensive care units (ICUs), and home care settings. As manufacturers continue to introduce innovative features and technologies to meet evolving clinical requirements and regulatory standards, the mechanical ventilator industry experiences sustained growth and technological advancement.

For Further Information Regarding this Report: Request a Free Sample @ reportocean.com/industry-verticals/sample-request?report_id=AMR1086

Regulatory Landscape and Quality Standards:

The regulatory landscape and quality standards governing the manufacturing, distribution, and use of mechanical ventilators significantly impact the growth of the mechanical ventilator industry. Regulatory agencies such as the U.S. Food and Drug Administration (FDA) and the European Medicines Agency (EMA) establish guidelines and standards for the safety, efficacy, and quality of medical devices, including mechanical ventilators. Compliance with regulatory requirements, such as obtaining regulatory approvals or clearances, conducting clinical trials, and maintaining quality management systems, is essential for manufacturers to market their ventilators and ensure patient safety. Additionally, adherence to international quality standards, such as ISO 13485 certification for medical device quality management systems, demonstrates a commitment to quality and regulatory compliance. As regulatory requirements evolve and become more stringent, manufacturers invest in regulatory affairs and quality assurance processes to ensure compliance and market access for their mechanical ventilator products.

Market Segmentation:

The report segments the global mechanical ventilator market by product type (critical care ventilators, neonatal ventilators, portable ventilators, and others), mode (invasive and non-invasive), end-user (hospitals, ambulatory surgical centers, home care, and others), and geography. It provides a comprehensive analysis of each segment, detailing current market sizes, growth trends, and future projections.

KEY MARKET SEGMENTS
By Product Type
– Intensive care unit/critical care
– Transport/portable/ambulatory
– Neonatal care

By Component
– Devices
– Services

By Mode
– Non-invasive ventilation
– Invasive ventilation

By Age Group
– Pediatric & neonatal
– Adult
– Geriatric

By End User
– Hospital and clinic
– Home care
– Ambulatory surgical center
– Others

By Region
– North America
o U.S.
o Canada
o Mexico
– Europe
o Germany
o France
o UK
o Italy
o Spain
o Rest of Europe

Get 30% Off On Various License Types When Buy Now At @ reportocean.com/industry-verticals/sample-request?report_id=AMR1086

Table of Contents

– Market Summary

– Economic Impact Competition Analysis by Players

– Production, Revenue (Value) by geographical segmentation

– Market Size by Type and Application

– Regional Market Status and Outlook

– Market Analysis and Outlook

– Market Forecast by Region, Type, and Application

– Cost Investigation, Market Dynamics

– Marketing Strategy comprehension, Distributors and Traders

– Market Effect Factor Analysis

– Research Finding/ Conclusion

– Appendix

– Continue……

Some of the Key Aspects that the Report Analyses:

  • Which regions in Market are witnessing rise in investments in the supply chain networks?
  • Which regions have witnessed decline in consumer demand due to economic and political upheavals in Industry?
  • Which countries in Market seem to have benefitted from recent import and export policies?
  • Which are some the key geographies that are likely to emerge as lucrative markets?
  • What are some the sustainability trends impacting the logistics and supply chain dynamics in the Market?
  • What are some of the demographic and economic environments that create new demand in developing economies?
  • Which regions in Market are expected to lose shares due to pricing pressures?
  • Which regions leading players are expected to expand their footprints in the near future in Industry?
  • How are changing government regulations shaping business strategies and practices?

Key Findings Market Reports:

  • Supply Chain Disruptions: Lockdowns, restrictions, and factory closures worldwide disrupted production and movement of goods, initially leading to reduced demand for this industry.
  • Shift in Demand: As consumer demand shifted, industry reports were increasingly used to transport essential goods such as medical supplies, PPE, pharmaceuticals, and groceries, while shipments of non-essential items declined.
  • Container Imbalances: Uneven trade flows and shipping disruptions caused imbalances in container availability, impacting pricing and availability across different regions.
  • Rising Shipping Costs: Increased demand for essential goods and disruptions in trade led to rising freight rates, affecting overall shipping costs and logistics.
  • Maintenance Challenges: Travel restrictions and lockdowns hindered maintenance activities for industry, potentially leading to longer-term maintenance challenges.
  • Supply Chain Resilience: Businesses recognized the need for greater supply chain resilience, leading to discussions and investments in robust container logistics and digital solutions.
  • Digital Adoption: The pandemic accelerated the adoption of digital solutions in logistics and supply chain management, including e-commerce and digital platforms for container booking and tracking.
  • Regulatory Impact: Governments implemented regulations and safety measures affecting shipping practices and container handling, impacting container operations.
  • Vaccine Transportation: Market played a vital role in transporting COVID-19 vaccines and related supplies, highlighting their importance in global health crises.
  • Supply Chain Strategies: Businesses reevaluated supply chain strategies, prioritizing risk mitigation and exploring alternatives for resilience against future disruptions.

Request full Report :-  @ reportocean.com/industry-verticals/sample-request?report_id=AMR1086

About Report Ocean:

We are the best market research reports provider in the industry. Report Ocean is the world’s leading research company, known for its informative research reports. We are committed to providing our clients with both quantitative and qualitative research results. As a part of our global network and comprehensive industry coverage, we offer in-depth knowledge, allowing informed and strategic business conclusions to report. We utilize the most recent technology and analysis tools along with our own unique research models and years of expertise, which assist us to create necessary details and facts that exceed expectations.

Get in Touch with Us:
Report Ocean:
Email[email protected]
Address: 500 N Michigan Ave, Suite 600, Chicago, Illinois 60611 – UNITED STATES
Tel:+1 888 212 3539 (US – TOLL FREE)
Website: reportocean.com

Source link

(MENAFN- Straits Research) A spirometer measures the air volume inhaled and exhaled during a single breathing cycle. The device facilitates the occupational diagnosis of various respiratory problems, such as chronic obstructive pulmonary disease, emphysema, asthma, and other respiratory diseases. Spirometers are one of the respiratory laboratories and clinics' most commonly observed tools. Spirometers can create a profile of a user's lung health. Clinicians, therefore, utilize spirometers as both a diagnostic and monitoring tool. Numerous benefits are associated with personalized spirometers for patient use outside the clinic. Regular spirometry can detect a decline in lung health or the progression of the disease considerably earlier. This allows the patient and physician to prevent or treat the condition before it worsens.
The global growth in the prevalence of chronic obstructive pulmonary disease (COPD) is ultimately pushing higher demand for spirometers. According to the World Health Organization (WHO), around 300 million people worldwide have asthma, and 250,000 have died. In 2019, around 65 million people globally had COPD, including approximately 16 million Americans; this figure is projected to rise in the coming years. In addition, chronic obstructive pulmonary disease is one of the leading causes of morbidity and mortality in the United States. Numerous studies indicate that the general public is primarily uninformed of COPD. However, many individuals with respiratory symptoms are unaware that they require a diagnosis, which hinders the use of spirometers for identifying respiratory devices.
Market Dynamics
Growing Prevalence of Respiratory Diseases to Drive the Global Spirometer Market
Respiratory illnesses are one of the leading causes of death and disability worldwide. Several causes, including filthy air, outdoor and indoor pollution, tobacco usage through smoking, and dangerous particles emitted from workplaces, contribute to the increase in the prevalence of respiratory illnesses in the population. The incidence of cases ending in respiratory failure and death has climbed dramatically in recent years. The World Health Organization reported that around 65 million individuals suffered from chronic obstructive pulmonary disease in 2017, and approximately 3 million died as a result. Asthma is the most prevalent chronic disease affecting children, impacting 14% of children worldwide. It affects nearly 334 million people. As effective healthcare solutions, such as spirometers, are readily available, enhancing respiratory health through early identification and diagnosis can prevent, manage, and treat various illnesses. Hence, with the growing prevalence of respiratory illnesses, the worldwide spirometer market is predicted to rise rapidly in the upcoming years. Moreover, spirometers can identify chemical exposure in the workplace, shortness of breath, medicine side effects, lung performance assessment before surgery, and the progression of illness treatment. Thus, it is projected that such spirometers' advantages will help expand the global spirometer market.
Furthermore, lifestyle behaviors such as smoking and alcohol consumption have led to respiratory issues and are among the key drivers driving the growth of the worldwide spirometer market. As spirometers aid in the early detection of several respiratory disorders, it is anticipated that the prevalence of these conditions would rise, hence driving demand. In addition, an increase in the older population, susceptible to a variety of respiratory diseases, stimulates the expansion of the spirometer market. In addition, technological developments in spirometry and an increase in regulatory approvals contribute to the growth of the spirometer market.
Regional Insights
North America will command the market with the largest share and a CAGR of 3.2% during the forecast period. Increasing asthma, COPD, and cystic fibrosis incidences are primarily accountable for the region's predominance. The American Lung Association reports that COPD is the third leading cause of death in the United States. Additionally, around 20.4 million people in the United States have asthma. As a result, there is a growing preference among Americans and physicians for pulmonary function testing for the early detection of lung illnesses to avoid future expensive medical expenses. In addition, technical advancements in the production of user-friendly and portable spirometers and greater patient awareness are expected to fuel the growth of the U.S. spirometer market throughout the forecast period.
In addition, North America is considered an early adopter of new medical innovations. This is mainly attributed to raising awareness of the numerous respiratory medicines in hospitals and expanding government and non-governmental organization (NGO) programs. Consequently, it is projected that the need for spirometers will increase among individuals afflicted with various respiratory illnesses.
Asia-Pacific will hold the second-largest share of USD 539 million with a CAGR of 4.5%.
Due to its large population, multiple chronic and lifestyle disorders, and rapid increase in the frequency of respiratory diseases, the Asia-Pacific region provides market participants in the spirometer industry lucrative opportunities. During the forecast period, the market for spirometers is likely to be propelled by an increase in the proportion of geriatric patients susceptible to a variety of respiratory disorders and an increase in the use of spirometers in general healthcare settings, such as hospitals. Moreover, using artificial intelligence (AI) in spirometers will create opportunities for key market participants.
Increasing demand for modern medical devices, healthcare reforms, and the prevalence of chronic respiratory diseases like asthma, COPD, cystic, and pulmonary fibrosis all lead to the expansion of the spirometer market. In addition, an increase in programs, grants, and initiatives connected to the availability of medical equipment in the region is anticipated to propel further the growth of the spirometer market in the region.
Key Highlights

The global spirometer market had a share value of USD 1,221 million in 2021, which is expected to grow to USD 1,608 million with a CAGR of 3.5% during the forecast period.
Based on type, the segment of table-top spirometer is expected to hold the largest share with a CAGR of 3.7% during the forecast period.
Based on technology, the segment of flow measurement is estimated to have the largest market share with a CAGR of 4.1% during the forecast period.
Based on end-user, the segment of hospitals & clinics is expected to have the largest market share with a CAGR of 3.9%.
Based on regional analysis, the North American region is expected to command the market with the largest share and a CAGR of 3.2%.

Competitive Players in the Market

SCHILLER
Hill-Rom, Inc.
Midmark Corp.
FutureMed
COSMED Srl
MGC Diagnostics Corporation
Smiths Medical
Vyaire Medical
Teleflex
NSPIRE HEALTH INC.

Market News

In 2022, Midmark Corp. announced a strategic partnership with Bien-Air Dental SA.
In 2022, Midmark Corp. announced the launch of its Synthesis Wall-Hung Cabinetry to provide animal health teams with enhanced visibility and access to supplies.
In 2022, MGC Diagnostics Corporation announced the global distribution agreement with BedfontÒ Scientific Ltd.

Global Spirometer Market: Segmentation
By Type

Hand-Held
Tabletop

By Technology

Volume Measurement
Flow Measurement

By Application

COPD
Asthma
Others

By End-User

Hospitals & Clinics
Home Care Settings
Others

By Region

North America
Europe
Asia-Pacific
LAMEA

MENAFN04032024004597010339ID1107929961


Legal Disclaimer:
MENAFN provides the information “as is” without warranty of any kind. We do not accept any responsibility or liability for the accuracy, content, images, videos, licenses, completeness, legality, or reliability of the information contained in this article. If you have any complaints or copyright issues related to this article, kindly contact the provider above.

Source link

OSHA Cites Brick Manufacturer for Exposing Workers to Respiratory Hazards

OSHA Cites Brick Manufacturer for Exposing Workers to Respiratory Hazards

Selma, Alabama-based Henry Brick Co. faces proposed penalties of $124,212.

OSHA has cited Henry Brick Co. Inc.—a clay brick manufacturer based in Selma, Alabama—for serious violations, for exposing workers to silica crystalline respiratory hazards

According to a release dated Feb. 27, OSHA found multiple infractions at the company, including failure to implement engineering controls and provide adequate training on crystalline silica. Workers were exposed to airborne concentrations up to six-and-a-half times the permissible level without proper respiratory protection, potentially leading to lung diseases. 

“Crystalline silica can be deadly. Workers who are overexposed to it can contract incurable, progressively disabling and sometimes fatal illnesses. This is why employers must take every precaution to protect employees from this danger,” OSHA Area Office Director Jose Gonzalez in Mobile, Alabama, said in a statement. “Employers with questions about how to develop respiratory protection programs can contact our trained professionals for assistance.”

OSHA’s investigation concluded with the identification of 11 serious citations and the proposal of penalties totaling $124,212. Henry Brick Co. now has 15 business days to comply, request an informal conference, or contest the agency’s findings before an independent commission.

About the Author



Robert Yaniz Jr. is the Content Editor of Occupational Health & Safety.





Source link

LOS ANGELES, CA - DECEMBER 30: Drive thru COVID-19 testing administered by Total Testing Solutions (TTS) in front of White Memorial Medical Center in Boyle Heights on Thursday, Dec. 30, 2021 in Los Angeles, CA. The long-feared winter coronavirus wave reached new heights Thursday as Los Angeles County reported more than 20,000 new cases, fueled in part by the highly transmissible Omicron variant that is washing over the region. (Gary Coronado / Los Angeles Times)

A healthcare professional with Total Testing Solutions stands under an umbrella in the rain at a drive-through coronavirus testing site in front of White Memorial Medical Center in Boyle Heights on Thursday. (Gary Coronado / Los Angeles Times)

With California's coronavirus surge worsening, the state has issued new recommendations for when people infected with the virus can end their isolation, guidance that is stricter than what was made earlier this week by the U.S. Centers for Disease Control and Prevention.

California is now recommending that asymptomatic, coronavirus-infected people can exit isolation after the fifth day following a positive test, but only if they get a negative test result.

By contrast, the CDC's recommendations don't ask for a follow-up negative test; the CDC only recommends that those ending isolation continue wearing a mask around other people for five additional days.

Dr. Robert Wachter, chair of the UC San Francisco Department of Medicine, praised California's stricter guidelines. "Kudos," Wachter wrote. "Safer than [CDC's] version."

The move comes as the Omicron surge is reaching new highs.

Los Angeles County on Thursday reported more than 20,000 new cases, fueled in part by the highly transmissible Omicron variant.

Overall, California’s reported average daily coronavirus caseload has more than quadrupled in the last two weeks — an astonishing rise that has pushed infection levels significantly higher than during the summer surge linked to the Delta variant.

“The risk for virus transmission has never been higher in our county,” Los Angeles County Public Health Director Barbara Ferrer said Thursday.

The Los Angeles County Department of Public Health endorsed California's new isolation recommendations and will codify them in its latest local mandatory health order.

The new California recommendations still largely mirror the CDC's guidelines. Both shorten the minimum time recommended for isolation from 10 days to five for asymptomatic people.

Both the CDC and California also suggest the quarantine of people who are not up-to-date on their booster shots if they have been exposed to someone who tests positive for the coronavirus.

Officials recommend calling 911 if you have difficulty breathing, chest pain or pressure on the chest; bluish lips or face; are confused or hard to wake; or have other emergency symptoms.

The Omicron variant is believed to be two to four times as contagious as the previously dominant Delta. People who are eligible for booster shots but haven't yet received them are at increased risk for infection.

"Data from South Africa and the United Kingdom demonstrate that vaccine effectiveness against infection for two doses of an mRNA vaccine is approximately 35%. A COVID-19 vaccine booster dose restores vaccine effectiveness against infection to 75%," the CDC said in a statement.

Here's a summary of California's new guidelines to exit isolation:

If you test positive for the coronavirus:

  • Stay home for at least five days after the onset of symptoms or after you were tested, regardless of vaccination status, even if you have no symptoms.

  • After the fifth day, you can exit isolation if a test shows you are negative, and you have no symptoms or symptoms are resolving. (Officials recommend getting a rapid antigen test for this purpose, as PCR tests — which require saliva or nasal swabs be sent to a lab for processing and take a day or two to get results — are so sensitive that they can show a positive test result for several months, long after you've stopped being contagious.)

  • These state guidelines will be requirements in L.A. County. "You can't be a 'positive' person and decide on Day 6, you're leaving isolation in L.A. County. You can leave if you've had a negative test on Day 5, you're asymptomatic or your symptoms have dramatically improved, and you're fever-free," Ferrer said.

  • If you can't get a test or choose not to test, you can exit isolation after the 10th day, as long as you have no symptoms or the symptoms are resolving.

  • If a fever is present, stay isolated until the fever resolves.

  • If symptoms other than fever are not resolving, continue to isolate until symptoms resolve or until after the 10th day.

  • Wear a well-fitting mask around other people for 10 days, especially indoors. Surgical masks or higher-grade masks, such as N95, KN95 and KF94, are recommended.

  • Cooperate with local contact tracing staffers with your local health department, who will notify people you've been around while you were infectious.

If you've been exposed but haven't fallen ill or tested positive:

Recommendations on how to act following an exposure to someone who tests positive for the coronavirus differ depending on your vaccination status and whether you're up-to-date on booster shots.

If you're recently vaccinated or had a booster shot and you've been exposed:

  • Get tested on the fifth day after being exposed to a coronavirus-positive person.

  • Wear a well-fitting mask such as an N95, KN95 or KF94 around others for 10 days, especially indoors.

  • If you test positive, follow isolation recommendations.

  • If symptoms develop, test and stay home.

If you're unvaccinated or haven't been boosted and have been exposed:

  • Stay home for at least five days after your last contact with a person who has tested positive for the coronavirus.

  • Test on the fifth day.

  • The quarantine can end after the fifth day if symptoms are not present and a test taken on the fifth day or later is negative.

  • If you're unable to test or choose not to and have no symptoms, the quarantine can end on the 10th day.

  • Wear a well-fitting mask around others for 10 days, especially inside.

  • If you test positive, follow the isolation recommendations.

  • If symptoms develop, test and stay home.

Vaccinated people are eligible for booster shots six months after their second dose of the Pfizer-BioNTech or Moderna shots, and two months after the primary dose of the Johnson & Johnson shot.

A close contact is when someone has spent at least 15 minutes over a 24-hour period within six feet of someone who has tested positive for the coronavirus.

What does it mean to stay at home during isolation?

  • Stay home except to get medical care.

  • Get food delivered to you or have someone drop off food.

  • Don't have visitors.

  • Wear a face covering around others, including family members and housemates.

  • Disinfect a shared bathroom after each use, or use a separate bathroom if possible.

  • Open windows if you must be in a shared space.

  • Stay at least six feet away from other people, especially higher-risk people such as those 65 and older; are severely overweight; have a chronic disease such as cancer, diabetes and heart or lung disease; or have a weak immune system.

This story originally appeared in Los Angeles Times.



Source link

Published: Mon 4 Mar 2024, 6:00 AM

Doctors in the UAE are highlighting at least a 10 per cent surge in patients seeking medical attention for persistent coughs.

They said weather fluctuations commonly act as triggers for conditions such as asthma, allergies, and bronchitis, leading to an escalation in chronic cough during these changes.

Medics explained chronic cough often stems from respiratory issues like asthma, Chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, bronchiectasis, and various other respiratory causes.

Stay up to date with the latest news. Follow KT on WhatsApp Channels.

Dr Jimmy Joseph, Specialist Internal Medicine and Diabetologist, Aster Clinic, International City said, “There is a surge in cases of cough. I get to see 8-10 patients daily in OPD with disturbing coughs lasting more than 10 days. We see persistent coughs greater than three weeks with nearly 20-30 per cent of daily cases. Persistent cough means when the cough lasts between three to eight weeks.”

Dr Jimmy Joseph

Dr Jimmy Joseph

Acid reflux-induced cough

Even Gastroesophageal reflux disease (GERD) is a condition where stomach acid regularly flows back into the esophagus, irritating the lining. When this acidic fluid reaches the throat and respiratory tract, it can lead to irritation and trigger a cough.

“Causes include post viral/ post-infective cough, postnasal drip, GERD/ acid reflux, asthma, and smoking. Other causes include chronic bronchitis/COPD, Covid 19 and post-infection, ACE inhibitors (blood pressure medication), congestive heart failure, and lung cancer,” he added.

Medics stressed the substantial increase in cough cases can be attributed significantly to the changing seasons, the flu, influenza, cold weather, rain, and dust.

“Patients should approach a doctor when a cough lasts more than 7-10 days, a person loses weight rapidly, coughs out blood, has continuous fever, night sweats, chest pain, and shortness of breath. If your doctor prescribes an antibiotic, complete the full antibiotic course. Avoid OTC medications,” Joseph added.

Dr Bassam Abdelmonem, consultant Emergency Care with Prime Hospital, also reiterated that they’ve recently observed an increased number of patients with chronic coughs.

Dr Bassam Abdelmonem

Dr Bassam Abdelmonem

He said, “Around 10 per cent of patients visiting the Emergency Room (ER) present themselves with chronic cough. Weather changes are common asthma triggers; allergies and bronchitis then chronic cough will increase by these changes. Patients with chronic cough should seek medical advice when they have had a cough for more than three weeks persistently or they're losing weight for no reason. Other reasons include if one has a weakened immune system – for example, because of chemotherapy or diabetes.”

Multiple underlying causes

They emphasised determining the cause of chronic cough is crucial to effective treatment. In many cases, more than one underlying condition may cause a chronic cough.

Healthcare professionals pointed out a persistent cough sometimes goes beyond being a mere inconvenience, as it can disrupt one’s sleep and lead to feelings of exhaustion. In more severe instances, chronic coughing may induce vomiting and dizziness, and even rarely result in rib fractures.

Dr Zaid Mahdi Mohammed, Canadian Specialist Hospital Dubai, said, “The most common causes of chronic cough are postnasal drip, asthma, and acid reflux from the stomach. These three causes are responsible for up to 90 per cent of all cases of chronic cough. Honey and saltwater gargling, using a humidifier, or taking steam can be some of the effective home remedies.”

Dr Zaid Mahdi Mohammed

Dr Zaid Mahdi Mohammed

ALSO READ:

Source link

An asthma drug has been placed under review after young children suffered severe side effects, the medicines regulator has confirmed.

Children as young as three have suffered traumatic side effects from montelukast with families of asthma patients saying they were not properly warned of the risks of the commonly prescribed drug, also known as Singulair.

The drug has been associated with night terrors, depression and in rare cases hallucinations or suicidal behaviour.

The montelukast UK action group, which represents nearly 3,500 members, is campaigning for more prominent warnings, stricter controls and support for those affected. It said patients should first consult a doctor if they have any concerns.

Graham and Alison Miller’s son Harry took his life aged 14 in February 2018 while on the drug. They learned of montelukast’s possible side effects two years after their son’s death and want his inquest to be reopened and are among the families calling for action.

Mrs Miller said she was convinced the drug had led to her son’s death and the couple would like to see their son’s inquest re­opened. “A perfectly healthy, happy kid dies after taking this drug and there has been no change,” she told the Observer. “It’s unacceptable.”

The Millers said the changes they are campaigning for, including a warning on the drugs packet of the risk and better monitoring of patients on the drug, have still not been implemented.

Montelukast is used to prevent the symptoms of asthma. It is usually prescribed when asthma is mild and can stop it from getting worse. It can also help people with asthma who have breathing difficulties when they exercise and seasonal allergies, such as sneezing, itchiness and a blocked or runny nose, according to the NHS website.

The drug was launched by the pharmaceutical giant Merck in 1998. The side effects of the drug, including behaviour and mood changes, are listed in the patient information sheet, but campaigners say the warnings should be printed on the packet and flagged by health professionals.

There were 4.3 million montelukast prescriptions in 2022/23 in England, at a cost of £6.69m. The action group estimates that about 350,000 patients are prescribed the drug in England, including more than 35,000 children, based on an analysis of NHS data. It can be given to babies as young as six months old, but should not be given to anyone who has ever had an allergic reaction to montelukast or any other medicine, or to people who have a rare hereditary problem of galactose intolerance.

In the US, the drug has had a black box warning since 2020, the highest safety warning drugs can be assigned by the Food and Drugs Administration. The agency has highlighted animal studies which suggest the drug can cross the blood-brain barrier, a membrane that acts as a filter and keeps out harmful substances and pathogens.

The Medicines and Healthcare products Regulatory Agency (MHRA) said clearer warnings were included in the product information about the risk of neuropsychiatric effects following a European review in 2019. It also highlighted at that time the risks of neuropsychiatric reaction, with some side effects more frequently reported in children.

A spokesperson said: “We are conducting a further review to consider any new data on the risk, indicators of lack of awareness with patients, carers and healthcare professionals and whether any further regulatory action is required. We are now in the final stages of our review. We continue to closely monitor reports of suspected neuropsychiatric adverse drug reactions with montelukast and have initiated our current review following identification of further concerns.”

Organon, a Merck spinoff responsible for montelukast in the UK, said: “Nothing is more important to Organon than the safety of our medicines and the people who use them. We continually monitor safety. We are confident that, in conjunction with the MHRA, we have communicated to healthcare professionals and patients complete and appropriate information regarding the safe and effective use of monetelukast.”

Dr Andy Whittamore, clinical lead at Asthma+Lung UK, said: “Montelukast is usually a very safe medication. It is important that doctors explain its possible side effects.”

Source link

After Flovent, one of the most popular inhalers for treating childhood asthma, was discontinued this past January, some parents are reporting challenges in obtaining the generic versions of the medication.

Both versions are identical medications and manufactured by the same pharmaceutical company, GSK, which is based in London.

"Effective Jan. 1, 2024, and subsequent to the availability of these authorized generics, GSK will discontinue manufacturing branded Flovent HFA (all strengths) and branded Flovent Diskus (all strengths) for the U.S. market," GSK said in a statement in the fall of 2023.

WITH POPULAR ASTHMA INHALER NOW DISCONTINUED, WHAT OTHER OPTIONS DO PATIENTS HAVE?

"It’s important to understand that the transition from branded to authorized generics will not have an impact on our ability to supply the market, and we expect minimal disruption for patients," the company added.

Most insurance plans likely will replace Flovent with a generic version, but some customers may experience delays if their insurance doesn’t cover the generic, the Asthma and Allergy Foundation of America (AAFA) says on its website.

Flovent

GSK discontinued manufacturing the Flovent inhaler in the U.S. as of Jan. 1, 2024. (Getty Images / Getty Images)

"The U.S. has a complicated drug pricing ecosystem," said Kenneth Mendez, president and CEO of AAFA, in a statement the foundation shared with FOX Business. 

"The U.S. has a complicated drug pricing ecosystem."

"Drug manufacturers, pharmacy benefit managers, insurance companies, employers and federal policies can create situations that reduce access to critical medications for patients," he added.

Here’s what to know about the transition from the brand name to the generic version of Flovent.

Generic versions vs. Flovent

Asthma is a chronic lung condition characterized by narrowing and inflammation of the airways, according to the National Institutes of Health (NIH).

Bronchodilators, such as albuterol, help dilate the airways, while inhaled steroids like Flovent help control lung inflammation.

Some patients with asthma need to take inhaled steroids daily to prevent worsening of respiratory symptoms.

Person using inhaler

Asthma is a chronic lung condition characterized by narrowing of the airways and inflammation surrounding the airways, according to the National Institutes of Health. (iStock / iStock)

GSK noted that the authorized generic versions of Flovent contain the same medicine – in the same device and with the same instructions – as the name-brand version.

"We have seen the price of Flovent increase. The price of Flovent HFA, fluticasone propionate HFA and Flovent Diskus has risen 47% since 2014," Tori Marsh, director of research at GoodRx, who is based in Colorado, told Fox News Digital.

"Usually when we see brand drugs discontinued in favor of generics, it’s to create lower prices for consumers."

PFIZER SCRAPS TWICE-DAILY WEIGHT LOSS PILL DANUGLIPRON AFTER STUDY SHOWS ‘HIGH RATES’ OF ADVERSE SIDE EFFECTS

When medications become generics, multiple manufacturers can produce them, which creates more competition, she said.

Yet consumers don’t always see these savings because insurance coverage plays a big role in determining what they will actually pay at the pharmacy, Marsh added.

If the insurance plan doesn’t cover the generic fluticasone, AAFA recommends requesting a "formulary exception" to determine whether the provider will opt to cover the inhaler. 

Flovent

GSK noted that the authorized generic versions of Flovent contain the same medicine, in the same device and with the same instructions as the name-brand version. (Getty Images / Getty Images)

If the insurance plan still will not cover the generic, providers will look for alternative brands of inhalers, like ArmonAir Digihaler and Arnuity Ellipta, according to AAFA.

When insurance only covers a different generic inhaler, but not generic Flovent, this is when customers typically see large price discrepancies, Marsh said.

Reactions to the switch

Some users are discussing on social media how the switch is affecting their children.

One reported that a pharmacy had difficulty maintaining a consistent supply of the drug.

"And as a bonus, my insurance still charges me the same copay as a brand-name medication," a frustrated user wrote on Reddit.

NARCAN NASAL SPRAY IS AVAILABLE FOR OVER-THE-COUNTER PURCHASE IN US: ‘LIFESAVING DRUG’

Other parents have not noticed any difficulties with the switch.

One user said they're using the generic version, while another "just noticed that my son has actually been on the generic [version] for a while … He has not noticed a difference."

Another parent expects her child’s doctor to switch the child to Arnuity, "which is basically the same thing."

"I expect this to have minimal effect on her."

Differences between inhaler types

"The type of device and type of medicine can impact effectiveness on individual patients," Mendez told Fox News Digital.

Two common types of inhalers are meter dose inhalers (MDIs) or dry powder inhalers (DPIs) — but they are not used the same way, AAFA cautioned.

If children are switched to a different brand of inhaler, they may be forced to use a different type, an expert noted. (iStock / iStock)

An MDI sprays a pre-set amount of medicine through the mouth into the airway, according to Cleveland Clinic’s website.

When the canister is pressed down, a propellant helps the medicine get into the lungs.

Some children have difficulty with this step because they must take a deep breath right as they press down on the canister, so the medicine may stay at the back of the throat instead of entering the lungs, Cleveland Clinic stated.

DELTA AIR LINES BACKS FLIGHT ATTENDANT WHO DENIED PASSENGER’S ALLERGY ACCOMMODATION

Children often have an easier time using an MDI attached to a small cylinder-shaped tube known as spacer, according to the American Lung Association.

After the inhaler is attached to the end of the spacer, the child seals the lips tightly around the rubber ring on the other end.

Instead of having to synchronize a deep breath while pressing down on the inhaler, the child can take more normal breaths after the inhaler is pressed.

GSK building

GSK, the pharmaceutical company that made Flovent, is based in London. (iStock / iStock)

The spacer whistles to warn the child when they are breathing too fast to get the medicine to their lungs.

If a child is switched to a different brand of inhaler, he or she may be forced to use a DPI inhaler instead of an MDI, Mendez noted.

"A DPI is breath-actuated, meaning that a patient needs to be able to adequately breathe in the medicine and properly use the diskus device," he said.

CLICK HERE TO SIGN UP FOR OUR HEALTH NEWSLETTER

Pulmicort, an inhaler in the same class of inhaled corticosteroids but with a different active ingredient than Flovent, only comes as a DPI.

The medicine is stored as a powder, but the inhaler does not contain a propellant to push the medicine into the lungs, so the patient must take a deep breath to use the inhaler properly, according to Cleveland Clinic.

GET FOX BUSINESS ON THE GO BY CLICKING HERE

"DPIs can be challenging to use for children, seniors who may lack dexterity, or those with severe asthma who cannot breathe deeply enough to get the medicine into their lungs," Mendez said. 

Fox News Digital reached out to GSK, maker of Flovent, requesting comment.

For more Health articles, visit www.foxnews/health.

Source link

Chronic Obstructive Pulmonary DiseaseChronic obstructive pulmonary disease or COPD, ranks as the third leading cause of death worldwide, trailing only behind heart disease and strokes. The condition impedes breathing by damaging the airways and/or lungs. It may cause chronic coughing, mucus and wheezing and permanently disable the affected individual. In affluent countries, one can easily avoid it by self-care, especially by avoiding smoking.

On the other hand, in developing countries, air pollution and the living environment are much more significant factors. Interestingly, estimates suggest that 50% of COPD cases in Sub-Saharan Africa occur in individuals who have never smoked and it often remains undiagnosed. It is a silent killer of so much of the population simply because they are impoverished.

Chronic Obstructive Pulmonary Disease in Nigeria

The lifestyle of the people in Nigeria likely causes chronic obstructive pulmonary disease in the country. Whether or not people smoke tobacco, most African kitchens suffer from poor ventilation due to biomass smoke. Biomass fuel includes anything from a living thing, mostly wood or animal waste. Fires, often fueled by more biomass or kerosene, are also constant for heating or light. Although women are less likely to smoke than men, they have the same amount of COPD cases because they spend far more time inside the house.

COPD prevalence in Nigeria is attributable to factors beyond solely toxic air. Malnourishment at birth is a high-risk factor, potentially leading to weaker or misshapen lungs. Unborn and newborn infants, sharing environmental exposures with their mothers, may also encounter lung defects. Moreover, in economically disadvantaged African communities, high rates of HIV and tuberculosis persist. These diseases, if causing lung damage, contribute to the risk factors for COPD.

Prevention

COPD remains incurable, with survival strategies centered around removing oneself from potential dangers, such as tobacco use, engaging in regular exercise and maintaining optimal lung health. Ideally, addressing this concealed epidemic involves preventive measures to stop it before it begins.

However, the World Health Organization has implemented multiple steps to protect Africans from chronic obstructive pulmonary disease. The first is the WHO Framework Convention on Tobacco Control, approved by 180 countries, including Nigeria, which aims to help protect people from tobacco smoke. The second is the Global Alliance against Chronic Respiratory Diseases (GARD), a network aimed solely at eliminating respiratory illnesses like COPD and asthma in low- and medium-income countries.

Various other proposals have been suggested to prevent illnesses caused by indoor air pollution. One approach involves the construction of homes equipped with chimneys or flues, allowing smoke to exit the living spaces efficiently. Creating infrastructure to provide homes with electricity or gas for cooking could eliminate the use of biomass fuel and its associated smoke.

Enhancing housing conditions goes beyond improving living standards; it has the potential to not only create better living environments but also to save lives.

– Varsha Pai
Photo: Pixabay

Source link

SUFFOLK, Va. — A Hampton Roads mother and a non-profit foundation are raising awareness for cystic fibrosis after she lost her daughter to the debilitating disease.

"Martina was the life of every party. She had a double lung transplant when she was 17 and another double lung transplant when she was 29," Tina Natoli said.

Tina Natoli’s daughter, Martina Natoli Lagman, was 30-years old when she lost her battle to cystic fibrosis in 2021.

Cystic fibrosis is a life threatening disorder that damages the lungs and digestive system.

It affects mucus, sweat and digestive juices, causing the fluids to become too thick.

"She had to do breathing treatments constantly. Lots of medicine. She took about 40 pills a day she took prescribed," Natoli said.

Since Martina’s death, her family started the Martina Natoli Lagman Foundation to raise awareness and money for individuals with cystic fibrosis.

"We raise money for children with cystic fibrosis and adults. Initially we started off with scholarships, thousand dollar scholarships. But then we thought some kids with cystic fibrosis are too sick to go to school so we turned it into a medical as well," Natoli said.

Natoli says last year, they raised more than $15,000 for 5 families.

"You all helped our family out financially through your scholarships and took the time to host a fundraiser for my daughter when she was in the hospital. Truly are making a big difference in the CF world," Holly Goetz, a mother whose daughter had cystic fibrosis, said.

Natoli says the Martina Natoli Lagman Foundation donated to Goetz's daughter medical expenses.

Now the non-profit is putting on its annual womanless pageant to raise money for individuals with the disease.

At the womanless pageant, men will put on dresses to raise money for a good cause.

Non-profit raises awareness for Cystic Fibrosis with womanless pageant

Martina Natoli Lagman Foundation

Non-profit raises awareness for Cystic Fibrosis with womanless pageant

"Martina loved people. She was very nonjudgmental. And her foundation is based on that. Whatever your lifestyle is, we don’t care," Natoli said.

The pageant will be on March 23rd at 7 p.m. at The Hub 757 in Suffolk.

You can purchase a ticket by clicking here.

If you're interested in donating or helping, you can visit Martina Natoli Lagman Foundation's Facebook page.



Source link

Coleen Nolan has revealed how a severe chest infection left her fearing she would die before finally deciding to kick her 40-year smoking habit.

The Loose Women star, 58, recalled becoming so unwell she was left 'gasping for air' and 'struggling to breathe.' 

Now 12-weeks cigarette free, Coleen told of how she suffered a panic attack as a result of her breathing troubles, when she was unable 'to walk a few feet' without having to stop due to feeling 'constantly winded.' 

Despite warnings whilst on the Loose Women set she continued to film and later returned to her hotel with her partner Michael Jones, 60, where things only got worse. 

In quotes obtained by The Mirror, she explained: 'I had a full-scale panic attack and the more stressed I got and the more I cried, the less able I was to breathe.' 

Coleen Nolan, 58, has revealed how a severe chest infection left her fearing she would die before finally deciding to kick her 40-year smoking habit

Coleen Nolan, 58, has revealed how a severe chest infection left her fearing she would die before finally deciding to kick her 40-year smoking habit

The Loose Women star recalled becoming so unwell she was 'gasping' for air and 'struggling to breathe' (pictured in 2010)

The Loose Women star recalled becoming so unwell she was 'gasping' for air and 'struggling to breathe' (pictured in 2010)

She added: 'I genuinely thought ‘I’m going to die in my hotel room, away from home’. It was really frightening. The whole thing lasted two minutes but it felt like an hour.'

After finally deciding to visit her doctor Coleen was warned if she carried on smoking she could suffer further attacks.

The presenter continued: 'I was going to bed at night, saying to Michael, "I’ve got COPD or lung cancer... what an idiot!" When I went back to get the results and was told my X-ray had come back clear, it was a massive relief.'

Explaining how her chest will 'never fully recover', Coleen said the scare felt like her 'last chance' to alter her lifestyle in order to 'still be around for her kids.'

Back in 2020, Coleen admitted she 'wasn't yet ready' to give the habit up in a fiery on-air clash with Loose Women co-host Denise Welch. 

Denise had admitting that she wanted the 'horrible' habit to be banned outdoors, sparking a heated debate. 

At the time, the former actress from Tynemouth, said that after quitting smoking seven-years ago, she could no longer walk past a group of smokers without 'feeling sick'. 

She went on to tell host Coleen, that after 'saying it for years' now was the perfect opportunity to quit her vice, insisting that she 'has to get her head around it and stop'. 

Now 12-weeks cigarette free, Coleen told of how she suffered a panic attack as a result of her breathing troubles, when she was unable 'to walk a few feet' without having to stop

Now 12-weeks cigarette free, Coleen told of how she suffered a panic attack as a result of her breathing troubles, when she was unable 'to walk a few feet' without having to stop 

Explaining how her chest will 'never fully recover', Coleen said the scare felt like her 'last chance' to alter her lifestyle in order to 'still be around for her kids'

Explaining how her chest will 'never fully recover', Coleen said the scare felt like her 'last chance' to alter her lifestyle in order to 'still be around for her kids'

Back in 2020, Coleen admitted she 'wasn't yet ready' to give the habit up in a firey on-air clash with Loose Women co-host Denise Welch

Back in 2020, Coleen admitted she 'wasn't yet ready' to give the habit up in a firey on-air clash with Loose Women co-host Denise Welch 

Coleen replied that she 'wasn't ready' to give the habit up, saying it feels unfair for smoking outdoors to be banned when there's no such restriction on drinkers.

When asked whether she felt the ban was a good idea, Coleen said: 'To have taken that away from me [especially] yesterday, as a smoker, that would just finish me off. 

'If you don't like it move away. And the amount of people when I say "I'm going for a fag" and they say "I'll come too"...' 

However Denise disagreed, insisting: 'I smoked for years and gave up seven years ago, and now if I just walk past a group of people smoking the smell makes me feel sick. 

'I never thought I would be that way but I am, and it's like I can't stand being around drunk people now I don't drink, and I can't stand being around the smoke. 

'Selfishly I would love it to be banned outside, if I was still a smoker I'd be furious. But I would love it to be banned,  

'I think it's horrible and Coleen this is your opportunity now, to stop. You have been saying it for years and you have to get your head around it and you have to stop.' 

When quizzed by host Kéllé Bryan on whether walking past smokers makes her fear she'll fall back into the habit, Denise went on: No, I just feel so much healthier and it's mainly the smell of it. 

'I understand with the rules more people will be outside and if you have more people outside, it is annoying.' 

Coleen went on to say that while she 'admires' Denise for giving up, she herself isnt ready to quit smoking. 

Denise had admitting that she wanted the 'horrible' habit to be banned outdoors, sparking a heated debate - after she quit seven years prior

Denise had admitting that she wanted the 'horrible' habit to be banned outdoors, sparking a heated debate - after she quit seven years prior 

Denise told Coleen that after 'saying it for years' now was the perfect opportunity to quit her vice, insisting that she 'has to get her head around it and stop'

Denise told Coleen that after 'saying it for years' now was the perfect opportunity to quit her vice, insisting that she 'has to get her head around it and stop'

She said: 'It is annoying, I admire you, you've given it all up and you've been amazing and you look fabulous.

'But here's my thing, I'm not ready to give up yet to be honest. I don't drink, it is kind of my only vice and I hate drinkers and when people say "ban smokers", I want to ban drinks then. I hate being around drunks, that's why I don't go sit outside in a pub.'  

Viewers clashed over the issue, with some feeling annoyance towards smokers is no different to disliking heavy drinking while others branded smokers 'utterly disgusting' and 'selfish'. 

Meanwhile, others lashed out: 'TOTALLY ban smoking! Don't project your bad habits on other people and get a healthy life, it KILLS YOU. It is UTTERLY DISGUSTING. Don't be so selfish.'

Source link