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Washington (AFP) – Coronavirus survivors have twice the risk of developing dangerous blood clots that travel to their lungs compared to people who weren't infected, as well double the chance of respiratory symptoms, a large new study said Tuesday.

The research by the Centers for Disease Control and Prevention found that as many as one in five adults aged 18-64 years and one in four of those over 65 went on to experience health conditions that could be related to their bout of Covid -- a finding consistent with other research.

Among all conditions, the risk of developing acute pulmonary embolism -- a clot in an artery of the lung -- increased the most, by a factor of two in both adults younger and older than 65, as did respiratory symptoms like a chronic cough or shortness of breath.

Pulmonary embolisms usually travel to the lungs from a deep vein in the legs, and can cause serious problems, including lung damage, low oxygen levels and death.

The study was based on more than 350,000 patient records of people who had Covid-19 from March 2020 - November 2021, paired with 1.6 million people in a "control" group who had sought medical attention in the same month as a corresponding "case" patient, but weren't diagnosed with Covid.

The team assessed the records for the occurrence of 26 clinical conditions previously associated with long Covid.

Patients were followed one month out from the time they were first seen until they developed a subsequent condition, or until a year had passed, whichever came first.

The most common conditions in both age groups were respiratory symptoms and musculoskeletal pain.

In patients under 65, risks after Covid elevated for most types of condition, but no significant differences were observed for cerebrovascular disease, mental health conditions, or substance-related disorders.

"Covid-19 severity and illness duration can affect patients' health care needs and economic well-being," the authors wrote.

"The occurrence of incident conditions following infection might also affect a patient's ability to contribute to the workforce and might have economic consequences for survivors and their dependents," as well as placing added strain on health systems.

Limitations of the study included the fact that data on sex, race, and geographic region were not considered, nor was vaccination status. Because of the time period, the study also didn't factor in newer variants.

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A large study of adults in the United States who survived COVID-19 during the first 2 years of the pandemic found that they had twice the risk of developing pulmonary embolism or respiratory conditions in the year following infection.

In other developments, US Centers for Disease Control and Prevention (CDC) tracking today shows that the more transmissible BA.2.12.1 Omicron subvariant is now the dominant strain, as illness levels continue a steady rise across the country.

Seniors had higher risk of neuro, mental conditions

The new findings on post COVID-19 conditions come from a CDC analysis of a large electronic health record database that compared outcomes in people ages 18 and older who received a COVID-19 diagnosis in a clinic, emergency department, or hospital with people from the same settings who weren't sick with the virus.

The study included 353,164 COVID-19 patients and 1,640,776 controls. The findings appear today in an early online edition of Morbidity and Mortality Weekly Report (MMWR).

Researchers looked at 26 clinical conditions that had been previously linked to post-COVID illness. Patients were followed until their first occurrence of one of the 26 conditions or until Oct 31, 2021.

Of patients ages 18 to 64 years old, one in five COVID survivors experienced a condition linked to previous infection. Of those 65 and older, one in four experienced one of the conditions.

For both groups, the highest risk were for pulmonary embolism and respiratory symptoms. However, seniors had a higher risk of neurological conditions and four mental health conditions, which included mood disorders, other mental conditions, anxiety, and substance-related disorders. Researchers said those findings were concerning, because older people are already at higher risk for stroke and neurocognitive impairment.

The authors wrote that the findings are consistent with earlier studies showing that post-COVID problems occur in 20% to 30% of patients, with some requiring follow-up care. They said COVID prevention strategies and routine assessment for post-COVID conditions are critical for reducing the impact of the disease and its longer-term complications.

They also said more research is needed to better understand the physiologic mechanisms that contribute to the post-COVID conditions.

BA.2.12.1 becomes dominant in US

In its updated variant tracking today, the CDC estimated that the BA.2.12.1 Omicron subvariant, first spotted in New York, is now the nation's dominant strain, making up an estimated 58% of sequenced specimens. Last week, the variant made up 49.4% of sequenced samples.

BA.2.12.1 is thought to be more transmissible than BA.2, but so far, there's no evidence that it causes more severe disease.

In other US developments:

  • The CDC today issued a Health Advisory Network alert to clinicians about COVID-19 rebound after treatment with Paxlovid. Symptoms can recur 2 to 8 days after Paxlovid treatment, and patients can test positive again after having tested negative. The CDC said Paxlovid treatment helps prevent hospitalization and deaths and said a brief return of symptoms might be part of the natural history of SARS-CoV-2 infection, regardless of treatment or vaccination status. So far, rebound infections are reported to be mild and the condition can be managed with isolation and masking.
  • For the week ending May 17, more than 107,000 COVID-19 infections were reported in kids, up 72% from 2 weeks ago, the American Academy of Pediatrics said in its latest update.
  • The nation's 7-day average for daily COVID-19 cases is 107,316, with 312 daily deaths, according to an analysis from the New York Times.

WHA shores up WHO funding

The World Health Assembly is meeting this week in-person in Geneva today for the first time since the start of the pandemic, and today the group adopted a more sustainable funding mechanism to support the World Health Organization (WHO).

The plan gradually increases member contributions to eventually make up 50%—up from 16% currently—of the WHO's core budget by 2030-2031. It also includes measures to replenish funds to broaden financing and strengthened WHO governance to add transparency, efficiency, and accountability.

The WHA, made up of health leaders from 194 member states, is the decision-making body of the WHO.

In other WHA developments, the group re-elected the WHO's Director-General Tedros Adhanom Ghebreyesus, PhD, to serve a second 5-year term. He was the only candidate.

In other global developments:

  • The European Medicines Agency has approved the use of AstraZeneca-Oxford COVID-19 for third-dose boosters in both those who got the vaccine as their primary series and in those who got an mRNA vaccine.
  • North Korea says its "fever cases" are starting to decline, but global health officials say it's extremely difficult to gauge the country's COVID-19 surge situation, according to Reuters. So far, North Korea hasn't responded to offers from other nations to help. At the World Economic Forum this week, South Korea is expected to press for help for North Korea.

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A pulmonary embolism (PE) occurs when blood flow to an artery that supplies blood to the lungs has become blocked, typically due to a blood clot. Complications can develop from either the clot or the treatment for the PE.

PE may begin with a blood clot, or thrombus, that forms in another part of the body, such as the leg. The blood clot can travel to the lung through the circulatory system and lodge in an artery.

Symptoms may include breathlessness, chest pain, cough, fainting, rapid breathing, or an irregular heartbeat.

PE can permanently damage the lungs or result in blood oxygen levels so low that other organs become damaged.

If the clot is small, there may be no complications. However, if the clot is large, it can lead to issues with the lungs or heart or an increased risk of sudden death.

This article discusses the complications that can occur as a result of a PE.

Complications of a pulmonary embolism.Share on Pinterest
Photography courtesy of James Heilman, MD/Wikimedia & gilaxia/Getty Images

PE is a type of venous thromboembolism (VTE). A 2015 article notes that the likelihood of recurrence after a person first develops VTE is 5–7% each year.

Treatment

After a PE diagnosis, a healthcare professional will prescribe anticoagulants, or blood-thinning medications. This helps prevent future blood clots.

However, anticoagulants can lead to side effects, such as excessive bleeding. People should contact a healthcare professional to discuss the best course of treatment for them.

Approximately 5% of individuals with PE develop chronic thromboembolic pulmonary hypertension (CTEPH), or high blood pressure in the arteries of the lungs, as a result.

Scarring of the blood vessels in the lung narrows their passageways, resulting in labored breathing.

If a person develops persistent or progressive shortness of breath between the first 3 months to 2 years after receiving a PE diagnosis, a doctor may investigate further.

The doctor may order:

Treatment

People may need to undergo a surgical procedure health experts call pulmonary thromboendarterectomy. This is a complex procedure to remove blood clots from the pulmonary arteries.

A person with CTEPH may need to take anticoagulant medication for the rest of their life.

Pulmonary infarction (PI) occurs when a blood clot blocks the peripheral arteries, preventing some of the lung tissue from receiving enough blood and oxygen. The lung tissue then dies.

According to research from 2021, 30% of people with PE show signs of PI.

Individuals may experience:

Treatment

There is no specific treatment for PI. Healthcare professionals will focus on treating the PE using anticoagulants and supportive care.

PE is one of the most common causes of pleural effusion, which affects 20–55% of people with PE.

Pleural effusion is when there is a buildup of fluid between the tissues that line the lungs and the chest, called the pleura.

Symptoms can include:

  • sharp chest pain
  • shortness of breath
  • cough

Treatment

Alongside treating the PE, a healthcare professional may perform surgery to drain the fluid. They may also prescribe diuretics.

For 10–15% of individuals with PE, the heart is unable to pump enough oxygen and blood to the brain and other organs in the body. This can cause a drop in blood pressure and slow down a person’s pulse.

A person may experience:

Cardiogenic shock is a life threatening emergency, as it can result in brain injury or organ failure.

Treatment

The National Heart, Lung, and Blood Institute notes that treatment focuses on protecting the organs from damage and getting the blood flowing properly.

People may require a heart transplant.

A PE can lead to a cardiac arrest, which increases the risk of death by 95%. Healthcare professionals would classify this as a massive PE.

A cardiac arrest is when the heart suddenly stops beating.

Treatment

Healthcare professionals may administer a drug called tissue plasminogen activator. This will help break up the blood clots.

A person may also require surgery called venoarterial extracorporeal membrane oxygenation, which is a type of cardiopulmonary bypass surgery.

According to a 2019 article, a PE is the third most common cause of death related to the heart. Approximately 45% of those with acute PE will experience right ventricular failure.

The authors note that the right ventricle is designed to deal with a low resistance afterload. Afterload refers to the pressure that the heart works against in order to eject blood from the chambers and into the arteries.

An increase in the afterload can negatively affect the right ventricle’s ability to function, resulting in right heart failure.

Symptoms can include:

Treatment

A doctor will first assess the severity of the condition.

Treatment may involve:

Treatment for blood clots involves anticoagulants. If the blood becomes too thin, and a cut or abrasion occurs, an individual can bleed too much.

Symptoms can include:

Treatment

The American College of Cardiology notes that if the bleeding events are minor, a healthcare professional may recommend missing a few doses of the blood-thinning medication.

In more severe cases, however, they may suggest reversal agents, such as andexanet alfa.

Without treatment, 30% of individuals with PE will die. If a person is able to get treatment, this number reduces to 8%.

If a person experiences any symptoms of a PE, they should seek immediate medical attention.

People may have an increased risk of developing a PE if they have been in any of the following situations:

  • They have recently had a surgery, especially joint replacement surgery.
  • They have experienced physical trauma, such as a broken leg.
  • They have taken hormone-based medicine, including oral birth control.
  • They have been pregnant or given birth.
  • They have had cancer or heart or lung disease.
  • They have not moved for a long period, for instance, due to bed rest or a long trip.

Other factors that increase risk include:

  • being over 40 years of age
  • having a family history of blood clots
  • having obesity

To prevent complications from PE, early diagnosis is essential. If any symptoms of PE arise, a person should seek medical attention immediately.

These symptoms include:

Some complications develop due to underlying heart or lung conditions. To prevent PE complications, a person can try the following:

PE can be a serious condition if the blood clot is large or if there are many blood clots.

If any symptoms of PE develop, a person should seek medical attention right away. If a PE has already occurred, and any new symptoms, such as shortness of breath, develop, people should contact a doctor immediately.

If an individual takes blood thinners, and they experience excessive bleeding, a healthcare professional may need to adjust their treatment.

PE is a serious condition that occurs due to a blood clot traveling to an artery in the lung. It may first form in the leg, abdomen, or pelvis and travel to the lung via the circulatory system.

PE may lead to complications. These may include excessive bleeding from treatment with blood thinners, recurring blood clots, pulmonary hypertension, or cardiogenic shock.

Some factors increase the risk of a PE, such as bed rest, long travel, recent trauma, pregnancy or giving birth, and taking hormone-based medication.

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Introduction

Chronic obstructive pulmonary disease (COPD) is a clinical syndrome that features chronic respiratory symptoms and structural pulmonary abnormalities leading to lung function impairment with persistent airflow limitation.1 A recent study indicated that the overall prevalence of spirometry defined for COPD was 8.6% of adults in China, including 11.9% of men aged 40 years or older. The acute exacerbation of COPD (AECOPD) is a key factor that affects the disease prognosis and leads to hospitalization. Thus, AECOPD-related morbidity and mortality should be given more attention.2,3 Pulmonary hypertension (PH) is a common and severe comorbidity of COPD that results in an increased risk of hospitalization, reduced exercise capacity, and shorter survival. Right-heart catheterization (RHC) is the “gold standard” for the diagnosis of PH. However, RHC related significant risks and its difficulty of placement limits this procedure in patients with PH. Echocardiography is a noninvasive method that is widely used to assess PH in patients with AECOPD.4 A tricuspid regurgitant jet ≥3 m/s tested by echocardiography is diagnosed as PH, which may lead to underdetermined diagnoses of PH.5 Moreover, pulmonary artery systolic pressure detected by echocardiography is poorly correlated with the mean pulmonary artery pressure (mPAP) in severe COPD. A main pulmonary artery to ascending aorta diameter ratio (PA/A) of greater than one has been reported to be a promising indicator for revealing PH.6,7 Furthermore, an increased ratio of PA/A was closely associated with the poor survival of patients with COPD, particularly in individuals with moderate-to-severe cases.8 Nevertheless, the impact of the PA/A ratio in AECOPD remains to be elucidated. In this present study, we aim to disclose the associations between the PA/A ratio and clinical outcomes in hospitalized patients with AECOPD.

Patients and Methods

Study Population

This retrospective observational study was conducted at the Yijishan Hospital affiliated with the Wannan Medical College and was approved by the Research Ethics Committee of Yijishan Hospital. The clinical data of patients was maintained with confidentiality and in compliance with the Declaration of Helsinki. Written informed consent from patients was waived due to the retrospective nature of this study. Consecutive AECOPD patients admitted to the Department of Respiratory Medicine and Respiratory Intensive Care Units (RICU) were reviewed from September 2017 to July 2021. Patients with advanced lung cancer, pneumothorax, stroke, pneumonia, diffuse interstitial lung disease, hemodialysis, or left-heart failure, as well as those who only accepted palliative therapy, or had a lack of chest computed tomography (CT) images, were excluded from the final analysis.

AECOPD is defined as COPD with an acute worsening of respiratory symptoms (typically cough, dyspnea, increased sputum volume, and/or sputum purulence) requiring additional treatments.9 Indications for RICU admission were made according to the expert consensus released in 2014 on AECOPD in China.10 In brief, these consisted of a significant increase in symptom intensity (severe dyspnea, changes in mental status, moderate or severe hypoxemia with or without hypercapnia), failure of an exacerbation to respond to initial medical management, hemodynamic instability, and a patient requiring mechanical ventilation (MV). The treatment success of AECOPD patients was defined as improvement in the clinical condition when discharged from the hospital. Conversely, treatment failure was thought to occur as an event of in-hospital death or deterioration of the clinical condition prior to discharge.

Demographic characteristics, including gender, age, the age-adjusted Charlson Comorbidity Index (aCCI), length of stay, body mass index (BMI) and in-hospital death, were collected. Laboratory tests, including an arterial blood gas analysis (pH value, oxygenation index, the ratio of arterial partial pressure of oxygen to the fraction of inspired oxygen), PaCO2, and the blood lactate level), hemoglobin, blood red cell distribution width (RDW), D-dimer, brain natriuretic peptide (BNP), fibrinogen (Fib), and blood platelet (PLT), were initially recorded after admission. The percentage of ICU admissions requiring invasive MV (IMV) was also calculated. A chest CT was performed when the patient was admitted to the hospital. The procedure for measuring the pulmonary artery (PA) diameter and PA/A ratio determined by the chest CT conformed to a previous study.6 Briefly, the PA diameter and ascending aorta diameter were averaged from two perpendicular measurements at the PA bifurcation level collected from the same chest CT images, as shown in Figure 1.

Figure 1 Diameters of the PA and A were determined by CT scan at the PA bifurcation. (A) PA/A ratio < 1; (B) PA/A ratio > 1.

Abbreviations: A, aorta; PA, pulmonary artery.

Statistical Analysis

Continuous data were analyzed using a normal distribution test prior to further analysis. Continuous data are indicated as the mean (standard deviation [SD]) or median (inter-quartile range [25,75]). Categorical variables are presented as the number (n) or percentage. Continuous variables were analyzed using the independent t-test or the Mann-Whitney U-test, and categorical variables were analyzed using a Chi-square test. The logistic regression model was used as a multivariate analysis to reveal the independent risk factors of in-hospital worst outcomes in patients with AECOPD. The Kaplan–Meier survival method was used to analyze the effect of the PA/A ratio on outcomes of AECOPD patients. A Log rank test was applied to appraise the statistical differences between the two survival curves. A receiver operating characteristic (ROC) curve analysis was conducted to evaluate factors predicting an in-hospital worst outcome. A P value less than 0.05 was considered statistically significant. The statistical analyses were performed using SPSS for Windows (release 22.0, IBM Corporation, USA).

Results

As indicated in Figure 2, a total of 229 patients with AECOPD were reviewed. According to the inclusion criteria and exclusion criteria, 111 patients were excluded due to the condition being combined with advanced lung cancer (n = 10), pneumothorax (n = 4) stroke (n = 5), pneumonia (n = 29), diffuse interstitial lung disease (n = 7), hemodialysis (n = 6), left-heart failure (n = 19), palliative therapy (n = 23), and a lack of CT images (n = 10). Ultimately, 118 eligible individuals were reviewed in this study: 74 individuals with a PA/A ratio <1 and 44 individuals with PA/A ratio ≥1. The outcomes of 21 patients were treatment failures, and 97 patients were treatment successes when discharged from the hospital.

Figure 2 A flowchart of this study.

Characteristics of the AECOPD Patients with a PA/A Ratio <1 or a PA/A Ratio ≥1

The pH value in the PA/A ratio ≥1 group was significantly lower than that in the PA/A ratio <1 group (p = 0.026). Remarkably, the PA/A ratio ≥1 group had a significantly higher value of PaCO2, RDW, BNP, PA diameter, and RICU admissions, as well as worse outcomes than the PA/A ratio <1 group (P < 0.05). However, there were no significant statistical differences for the other indicators between the two groups (Table 1).

Table 1 Characteristics of AECOPD Patients with Different PA/A Ratio

Clinical Features of the AECOPD Patients with Treatment Failure

As indicated in Table 2, compared to the treatment success group, the treatment failure group had a much lower pH value (7.34 ± 0.11 vs 7.28 ± 0.13, respectively, p = 0.040) and less count of PLT (median 167 × 109/L vs 130 × 109/L, respectively, p = 0.018). The treatment failure group had higher levels of D-dimer and BNP compared with the improved group (P < 0.05). In addition, the percentage of RDW, rate of RICU admissions, and the proportion of IMV in the treatment failure group were significantly higher than that in the improved group (P < 0.05). Notably, the PA diameter and PA/A ratio were significantly increased in the treatment failure group than in the improved group (mean PA diameter: 3.71 vs 3.22, p = 0.001; mean PA/A ratio: 1.09 vs 0.89, p < 0.001).

Table 2 Characteristics of Treatment Success Group and Treatment Failure Group in Severe AECOPD

A PA/A Ratio ≥1 Was an Independent Risk Factor for Treatment Failure in AECOPD

The multivariate analysis indicated that the PA/A ratio ≥1 (OR value = 6.129, 95% CI: 1.665–22.565, p = 0.006) and IMV (OR value = 10.798, 95% CI: 2.072–56.261, p = 0.005) were two independent risk factors for treatment failure in patients with AECOPD. Although the RDW, D-dimer, PLT, and RICU admissions had observed significant differences between the two groups according to the univariate analysis, they did not reach significant statistical differences according to the multivariate analysis (Table 3). Additionally, the Kaplan–Meier survival analysis indicated that patients with a PA/A ratio ≥1 had worse outcomes than patients with a PA/A ratio <1 during hospitalization (HR = 5.277, 95% CI: 2.178–12.78, p < 0.001) (Figure 3).

Table 3 Multivariate Analysis for Risk Factors of Treatment Failure in AECOPD

Figure 3 Effect of the PA/A ratio on the outcomes of AECOPD patients.

Abbreviation: PA/A ratio: main pulmonary artery to ascending aorta diameter ratio.

Note: A Kaplan–Meier survival curve analysis was performed, and a Log rank test was used, and a P < 0.05 was considered statistically significant.

Predictors of Treatment Failure in Hospitalized Patients with AECOPD

Figure 4 displays the diverse ROC curve of the PA/A ratio, the PA value, the BNP, and the RDW for predicting treatment failure in hospitalized patients with AECOPD. Even though there were no significant statistical differences observed, the area under the curve (AUC) value of the PA/A ratio was numerically larger than that of the other indicators. The best cut-off value of the PA/A ratio for predicting treatment failure was 0.925. The sensitivity was 81.82%, and the specificity was 66.67% (Table 4).

Table 4 ROC Curve Analysis for Factors Predicting Treatment Failure

Figure 4 PA/A ratio, PA value, BNP, and RDW for predicting treatment failure in hospitalized patients with AECOPD.

Abbreviations: PA/A ratio, main pulmonary artery to ascending aorta diameter ratio; PA, main pulmonary artery; RDW, blood red cell distribution width; BNP, brain natriuretic peptide.

Note: The receiver operating characteristic (ROC) curve analysis was conducted to evaluate factors predicting in-hospital worst outcomes.

Discussion

The strengths of this study were its primary findings. First, patients with a PA/A ratio ≥1 had significantly higher PaCO2, RDW, BNP, PA diameters, RICU admission rates, and proportions of treatment failure. Second, the PA diameter and PA/A ratio were significantly increased in the treatment failure group compared with the treatment success group. Third, a PA/A ratio ≥1 was an independent risk factor for treatment failure in patients with AECOPD. The Kaplan–Meier survival analysis indicated that patients with a PA/A ratio ≥1 had worse outcomes than patients with a PA/A ratio <1 during hospitalization. Finally, the PA/A ratio may be a promising factor for predicting treatment failure in hospitalized AECOPD patients.

A previous study indicated that the relative pulmonary arterial enlargement (PA/A ratio >1 on CT scanning) predicted hospitalization for AECOPD, and a PA/A ratio >1 with increased blood troponin levels shared close associations with increased respiratory failure, ICU admission, and in-hospital mortality.11 Iliaz et al reported that the PA/A ratio was related to the frequency of hospitalizations and exacerbations due to COPD in one year after hospital discharge.12 However, the relationships between a PA/A ratio >1 alone and ICU admission or in-hospital mortality are still unclear. In the present study, we found that AECOPD patients with a PA/A ratio ≥1 had a decreased pH value and increased PaCO2 compared with patients with a PA/A ratio <1, implicating increased type II respiratory failure in patients with a PA/A ratio ≥1. A decreased pH value and increased PaCO2 may contribute directly to pulmonary vasoconstriction leading to a rise in pulmonary vascular resistance and pulmonary arterial pressure.13 In addition, we also disclosed a higher percentage of RICU admissions and a markedly increased rate of treatment failure in hospitalized AECOPD patients with a PA/A ratio ≥1. Thus, an increased PA/A ratio was associated with severity and worse outcomes in inpatients with AECOPD. Many studies have revealed that the RDW is a valuable biomarker for predicting pulmonary hypertension and its associated prognosis.14–16 In a previous study performed by our group, we indicated that the RDW shared positive relationships with the PA/A ratio in patients with pH secondary to COPD.17 Similar to previous studies, we found an increase in the RDW in AECOPD patients with a PA/A ratio ≥1. Likewise, the serum level of BNP was drastically elevated. BNP is an important indicator for identifying risk categories in PH. Increased BNP is related to a worse outcome of PH.18

In this study, we demonstrated that there was a decreased pH value, lower number of PLTs, and increases in the RDW, D-dimer, BNP, PA diameter, and PA/A ratio in AECOPD patients with treatment failure compared with the improved group. Patients with treatment failure also required more IMV supports and intensive care. It was reported that lower pH values were associated with short or long mortality in hospitalized AECOPD patients.19,20 RDW is an indicator that reflects the heterogeneity of red blood cell volume. Recently, RDW was found to be an independent negative prognostic factor closely associated with adverse outcomes in hospitalized AECOPD patients.21,22 Dysregulation of erythrocyte homeostasis and metabolic imbalance may account for significant changes in the RDW in AECOPD patients. However, the underlying pathophysiological mechanisms remain unknown.23 A hypercoagulable state is a feature of hospitalized AECOPD patients. An increased D-dimer level is not only an important independent risk factor for pulmonary embolism in inpatients with AECOPD but also a predictor of higher mortality in stable COPD patients.24,25 Cardiac failure is a frequent complication of AECOPD, deeply affecting exercise tolerance and life span in patients with COPD. BNP is widely used to evaluate heart function. BNP can be used to risk-stratify, and an elevated BNP is associated with a higher MV use and worse outcomes in AECOPD patients.26 An increased PA/A ratio is positively correlated with COPD severity. Previous studies have reported that pulmonary artery enlargement detected by CT is a risk predictor for a severe exacerbation of COPD.27,28 Intriguingly, the PA/A ratio is an important determinant of mortality in moderate-to-severe COPD.8 In our present study, we found that a PA/A ratio ≥1 was a strong independent risk-factor of in-hospital treatment failure in patients with AECOPD. In addition, the PA/A ratio might be a better predictor of in-hospital treatment failure compared with other indicators including the PA value, BNP, and RDW. Taken together, the results of the present study provide additional evidence for a close association between the PA/A ratio and the outcome of AECOPD.

In this study, AECOPD patients with a PA/A ratio ≥1 had markedly higher values of PaCO2, RDW, BNP, the PA diameter, ICU admission rates, and proportions of treatment failure and had worse outcomes during hospitalization. A PA/A ratio ≥1 was an independent risk factor for treatment failure in patients with AECOPD. The PA/A ratio may be a promising predictor for treatment failure. It is worth noting that there are several limitations in this study. First, the sample size was small, and this might lead to an interpretation bias in the final analysis. Further work is required to validate the initial conclusion for a larger sample size. Second, the PA/A ratio partially reflects a change in the pulmonary artery pressure. However, the association between the PA/A ratio and the pulmonary artery pressure was not assessed in this study. Finally, to reduce the chance of radioactive exposure, a dynamic change in the PA/A ratio during hospitalization was unclear.

Acknowledgments

We thank LetPub for its linguistic assistance during the preparation of this manuscript.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Funding

The design of the study and collection, analysis, and interpretation of data were supported by the Anhui Provincial Key projects of the Natural Science Foundation for Colleges and Universities (KJ2021A0834).

Disclosure

The authors report no conflicts of interest in this work.

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18. Hoeper MM, Pausch C, Olsson KM, et al. COMPERA 2.0: a refined 4-strata risk assessment model for pulmonary arterial hypertension. Eur Respir J. 2021;2102311. doi: 10.1183/13993003.02311-2021

19. Gayaf M, Karadeniz G, Guldaval F, et al. Which one is superior in predicting 30 and 90 days mortality after COPD exacerbation: DECAF, CURB-65, PSI, BAP-65, PLR, NLR. Expert Rev Respir Med. 2021;15:845–851. doi:10.1080/17476348.2021.1901584

20. Chen L, Chen L, Zheng H, et al. Emergency admission parameters for predicting in-hospital mortality in patients with acute exacerbations of chronic obstructive pulmonary disease with hypercapnic respiratory failure. BMC Pulm Med. 2021;21:258. doi:10.1186/s12890-021-01624-1

21. Hu GP, Zhou YM, Wu ZL, et al. Red blood cell distribution width is an independent predictor of mortality for an acute exacerbation of COPD. Int J Tuberc Lung Dis. 2019;23:817–823. doi:10.5588/ijtld.18.0429

22. Epstein D, Nasser R, Mashiach T, et al. Increased red cell distribution width: a novel predictor of adverse outcome in patients hospitalized due to acute exacerbation of chronic obstructive pulmonary disease. Respir Med. 2018;136:1–7. doi:10.1016/j.rmed.2018.01.011

23. Salvagno GL, Sanchis-Gomar F, Picanza A, et al. Red blood cell distribution width: a simple parameter with multiple clinical applications. Crit Rev Clin Lab Sci. 2015;52:86–105. doi:10.3109/10408363.2014.992064

24. Wang J, Ym D. Prevalence and risk factors of pulmonary embolism in acute exacerbation of chronic obstructive pulmonary disease and its impact on outcomes: a systematic review and meta-analysis. Eur Rev Med Pharmacol Sci. 2021;25:2604–2616. doi:10.26355/eurrev_202103_25424

25. Husebo GR, Gabazza EC, D’Alessandro GC, et al. Coagulation markers as predictors for clinical events in COPD. Respirology. 2021;26:342–351. doi:10.1111/resp.13971

26. Vallabhajosyula S, Haddad TM, Sundaragiri PR, et al. Role of B-type natriuretic peptide in predicting in-hospital outcomes in acute exacerbation of chronic obstructive pulmonary disease with preserved left ventricular function: a 5-year retrospective analysis. J Intensive Care Med. 2018;33:635–644. doi:10.1177/0885066616682232

27. Yang T, Chen C, Chen Z. The CT pulmonary vascular parameters and disease severity in COPD patients on acute exacerbation: a correlation analysis. BMC Pulm Med. 2021;21:34. doi:10.1186/s12890-020-01374-6

28. Wells JM, Washko GR, Han MK, et al. Pulmonary arterial enlargement and acute exacerbations of COPD. N Engl J Med. 2012;367:913–921. doi:10.1056/NEJMoa1203830

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Spontaneous pneumomediastinum (SPM) is a rare and self-limiting condition characterized by the presence of air in the mediastinum not related to trauma or surgical procedures [1]. Described by Laennec in 1819 as a complication of trauma, Hamman 120 years later published his case series of SPM. This condition typically affects young adults aged 20-30 years, with a male preponderance of 8:1. SPM is associated with other medical conditions, including asthma, connective tissue disease, interstitial lung disease, diabetic ketoacidosis, chronic obstructive airway disease, and influenza-like syndrome. [1] SPM is reported to develop in 10% of cases of intubated COVID-19 with acute respiratory distress syndrome (ARDS) even with low tidal volume strategies [2,3]. One unmatched case control study of 271 patients showed the incidence of SPM among non-intubated acute COVID-19 patients at 3.3%, similar to our patient [4]. The case we described would fit into this group. 

The cause of COVID-19, SARS-CoV 2, is a novel coronavirus associated with wide heterogeneity in clinical presentation ranging from asymptomatic to critical illness. The first infection was detected in late 2019 in Wuhan, China, after which it rapidly spread worldwide. Mortality was high among those with advanced age and significant comorbidities. The acute phase of COVID-19 infection lasts approximately three to four weeks. After four weeks of infection, SARS-CoV 2 no longer has the capability to replicate, and residual illness in this stage is called the post-acute COVID-19 syndrome [5]. Symptoms associated with the infection may persist, such as lethargy, easy fatigability, and shortness of breath, with some requiring prolonged supplemental oxygenation. To our knowledge, the incidence and risk factors of SPM among patients who have recovered from COVID-19 infection, i.e., patients in the post-acute phase, is yet to be studied.

We present a case of SPM in a patient with post-acute COVID-19 syndrome who received high flow nasal oxygen therapy in the acute stages of the disease.

The patient was a 58-year-old Chinese gentleman who never smoked. He had a BMI of 29.4kg/m2 and was fully vaccinated for COVID-19 (last dose was given three months prior to admission). He was admitted to the emergency room complaining of a productive cough accompanied by shortness of breath. A nasal pharyngeal swab for polymerase chain reaction (PCR) detecting SARS‐CoV‐2 ribonucleic acid (RNA) resulted in a positive. His significant medical history included hypertension and hyperlipidemia. He had no prior trauma, asthma history, diabetes, pulmonary tuberculosis, or connective tissue disease.

On admission, physical examination showed decreased breath sounds on both lungs and diffuse systolic murmur. He was febrile at 38 degrees Celsius, with a blood pressure of 114/77mmHg, heart rate of 143 per minute, and respiratory rate of 35 per minute. Oxygen saturation was at 89% on 100% non-rebreather mask. Arterial blood gas showed type 1 respiratory failure with a P/F ratio of 46. Therefore, we decided to start oxygen therapy with a high-flow nasal cannula (HFNC) (FiO2: 100%, flow: 60 L/min with SpO2: 96%). Initial chest X-ray (CXR) revealed right middle and lower zone patchy airspace opacities without pleural effusion or pneumothorax (Figure 1).

The full blood count showed a white blood cell count (WBC) of 6.95x10^9/L, hemoglobin 15.2g/dL, platelets 191x10^9/L, C-Reactive protein (CRP) 151.1mg/L (N=1.0-5.0mg/L), procalcitonin 1.2ng/mL (N=0.5 to 2.0ng/mL), serum lactate 1.9mmol/L (N=0.6-1.4mmol/L), serum urea 6.8mmol/L (N=2.4 to 6.6mmol/L) and beta-hydroxybutyrate 0.35mmol/L (N=0.02-0.27). His International Severe Acute Respiratory and Emerging Infection Consortium (ISARIC) 4C score was nine, signifying high risk and an in-hospital mortality of 31.4 to 34.9%. The patient was prescribed intravenous dexamethasone before transferring to medical intensive care unit (MICU).

In the medical intensive care unit, he received empiric intravenous amoxicillin-clavulanic acid and oral doxycycline. Blood cultures and sputum cultures, which were taken from endotracheal tube (ETT), were all reported as no bacterial growths. Fever persisted, and a repeat chest X-ray showed worsening bilateral airspace opacities. Antibiotics were escalated to intravenous piperacillin-tazobactam while on intravenous dexamethasone therapy. Blood cultures and sputum cultures were repeated and were negative. On day six of illness, he received the first dose of a five-day course of intravenous remdesivir. Due to persistent hypoxia, he received two doses of intravenous tocilizumab on day six and day 26 of illness.

He also developed starvation ketosis and revealed newly diagnosed diabetes mellitus with HbA1c of 8.1%. Subcutaneous (SC) intermediate-acting insulin (Insulatard) was prescribed. Thromboprophylaxis with subcutaneous enoxaparin was given during the pulmonary phase of the illness. The HFNC setting for the first 15 days was on maximum flow of 60L/min, with a taper to 40L/min on the remaining seven days. Initial FiO2 on HFNC was at 100%, with subsequent gradual weaning to 40% on day 28 of illness. On day 10 of illness, he received a trial of continuous positive airway pressure ventilation (CPAP), but HFNC was resumed as no significant improvement was seen on oxygenation. CRP levels improved from 151mg/L to 72.8mg/L, and by day 28 of illness, the CRP was at 4.4mg/L. The patient performed awake prone positioning to improve oxygenation.

On day 30 of illness, he was weaned off to a non-rebreather mask and managed to sustain adequate oxygen saturation on nasal cannula oxygenation at 5-liter oxygen. He was transferred to the general ward for rehabilitation. He remained afebrile and normotensive with a resting tachycardia at 100-110/min. Despite mild dyspnea and easy fatigability, oxygen saturations were at 98% on 4-liter oxygen nasal cannula. Intravenous dexamethasone was gradually tapered down.

On day 34 of illness, COVID-19 PCR with cycle threshold (CT) ratio was 33.34/33.37. Despite this, his saturations dropped to 77% while on 4-liter oxygen nasal cannula. He was put on 100% non-rebreather mask, and oxygen saturations increased to 96-99%. Repeat CXR showed stable bilateral diffuse airspace opacities with no evidence of pneumothorax. Repeat arterial blood gas revealed type 1 respiratory failure with a P/F ratio of 119 and CRP of 0.7mg/L. An electrocardiogram showed normal sinus rhythm at 73/min. A computed tomography pulmonary angiogram (CTPA) was arranged to rule out acute pulmonary embolism. SC enoxaparin was restarted at a therapeutic dose. The scan was negative for pulmonary embolism but detected a pneumomediastinum (PM), pneumopericardium (PP), and subcutaneous emphysema (Figure 2, 3). Respiratory medicine service recommended keeping him on non-rebreather mask oxygenation, and he was deemed a poor candidate for positive pressure ventilation in the event of current deterioration. On examination, he was alert tachypneic with bilateral scattered crackles in the middle and lower zones on auscultation. He developed subcutaneous emphysema at the neck but no change in the quality of his voice. After discussion with the patient and his family, he opted for maximum ward management in the event of further deterioration. The family was hopeful for his full recovery. On day 36 of illness, he developed atrial flutter with a pulse rate of 160bpm on 12-lead electrocardiography (ECG) with a blood pressure of 109/79mmHg. He received rate control measures, including intravenous amiodarone, oral bisoprolol, and digoxin, and his heart rate improved to sinus rhythm at 76bpm on 12-lead ECG.

On day 40 of illness, the patient was found unresponsive with pulseless electrical activity on the cardiac monitor. Cardiopulmonary resuscitation (CPR) was initiated and he was intubated by the on-call airway team. Despite the resuscitation team’s best efforts, no return of spontaneous circulation was achieved, and the patient was pronounced demised.

There are a number of mechanisms that lead to the development of spontaneous pneumomediastinum. First is the alveolar rupture secondary to inflammation and diffuse alveolar pressures due to coughing. The escaping air from the ruptured alveoli tracks along the bronchovascular sheaths, dissecting into the pulmonary hila and escaping into the mediastinal space. This is seen on thoracic computed tomography scans demonstrating the Macklin effect, described as linear collections of air continuous to the bronchovascular sheaths dissecting into the pulmonary hilum [6]. Second is the direct viral invasion of the lung parenchyma, visceral and parietal pleura causing disruption of the parenchymal and pleural integrity or ruptured alveoli leading to subsequent air leak [7]. Third is the prothrombotic effect of COVID-19 infection-causing pulmonary vascular thrombosis and subsequent necrosis in the alveolar membranes. Fourth is cytokine storm-induced diffuse alveolar injury or direct viral infection of type 1 and type 2 pneumocytes increasing the risk of alveolar rupture [3].

COVID-19 related SPM affects an older population aged 38-72 years of age versus 5-34 years for non-COVID SPM [8]. COVID-19 related SPM has been associated with a more severe course of the disease and a mortality rate of 28.5% versus non-COVID SPM, which has an estimated mortality rate of 5.6% [1].

We highlight the risk of SPM, PP, and subcutaneous emphysema developing in COVID-19 patients without the usually associated conditions who did not receive invasive positive pressure ventilation at the post-acute phase of the disease. We also hope this launches further investigations comparing the non-invasive and invasive modalities of oxygen supplementation and the respective settings for severe COVID-19 to achieve the optimal oxygenation profile while minimizing the risk of barotrauma and PP and PM. We also anticipate more studies that look into developing multidisciplinary treatment protocols for patients who develop COVID-19 related PP and PM. The question is: which modality achieves optimal oxygenation while minimizing the risk of barotrauma and SPM? 



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What Is Lynparza?

Lynparza (olaparib) is an oral medication used to treat certain types of cancer in the ovaries, breast, prostate, or pancreas. It is in a class of medications called poly (ADP-ribose) polymerase inhibitors, also known as PARP inhibitors.

PARP is an enzyme that repairs DNA damage in cells. Blocking PARP from working in cancer cells prevents the enzymes from repairing the DNA, which causes the cancer cells to die. Lynparza comes in tablet form.

Drug Facts

Generic Name: Olaparib

Brand Name: Lynparza

Drug Availability: Prescription

Administration Route: Oral

Therapeutic Classification: Antineoplastic agent

Available Generically: No

Controlled Substance: N/A

Active Ingredient: Olaparib

Dosage Form: Tablet

What Is Lynparza Used For?

The Food and Drug Administration (FDA) approved Lynparza to treat multiple cancers, including certain types of:

  • Ovarian cancer
  • Breast cancer
  • Prostate cancer
  • Pancreatic cancer 

Ovarian Cancer

Lynparza can be used to treat advanced ovarian cancer with a germline or somatic BRCA mutation that has responded well to treatment with certain chemotherapy medications, called platinum drugs. A germline BRCA mutation means a person has been born with that mutation, passed down from one of their parents. A somatic BRCA mutation means that cancer has developed that genetic mutation, and the person was not born with it. 

Lynparza can also be combined with another medication called bevacizumab to treat advanced ovarian cancer.


Breast Cancer

Lynparza can be used to treat breast cancer that has become metastatic (spread to other areas of the body outside of the breast) in someone with a germline BRCA mutation and HER2 negative breast cancer. After hormonal therapy, it should be used if breast cancer is estrogen receptor-positive.

Prostate Cancer

Lynparza can help treat metastatic prostate cancer if the person has a germline or somatic homologous recombination repair (HRC) gene mutation. It is used after previous treatment with either of the medications, enzalutamide or abiraterone.  

Pancreatic Cancer

Lynparza is used to treat metastatic pancreatic cancer with a germline BRCA mutation. It can be used after the person has not progressed on at least four months of chemotherapy, which contains a platinum-based medication.

How to Take Lynparza

You can take Lynparza without regard to food. Doses are usually taken two times a day, about 12 hours apart. Swallow the tablets whole; do not break or crush them before taking them.

Avoid grapefruit products and products containing Seville oranges (such as orange marmalade), as they can interfere with how much of the medication is absorbed in the body.

Storage 

Store Lynparza tablets at room temperature (between 68 degrees and 77 degrees Fahrenheit). Keep the medication in its original packaging; do not move the tablets to a pillbox or separate container.

How Long Does Lynparza Take to Work?

After a few months of taking Lynparza, your oncologist will order imaging studies to see how well the medication is working.

What Are the Side Effects of Lynparza?

This is not a complete list of side effects and others may occur. A healthcare provider can advise you on side effects. If you experience other effects, contact your pharmacist or a healthcare provider. You may report side effects to the FDA at fda.gov/medwatch or 1-800-FDA-1088.

Common Side Effects 

The most common side effects associated with Lynparza include:

Severe Side Effects 

Call your healthcare provider right away if you have serious side effects. Call 911 if you think your symptoms are life-threatening or think you’re having a medical emergency. Serious side effects and their symptoms can include the following:

  • Pneumonitis: Severe cough, shortness of breath, fever
  • Blood clots: Chest pain, shortness of breath, redness, or swelling to an extremity

Long-Term Side Effects 

Rarely, Lynparza use can cause myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML). The risk was higher in people who had previously received chemotherapy or radiation for their ovarian or breast cancers. 

The symptoms of MDS or AML can include:

  • Weight loss
  • Fever
  • Frequent infections
  • Extreme fatigue
  • Easy bleeding or bruising
  • Shortness of breath

Report Side Effects

Lynparza may cause other side effects. Call your healthcare provider if you have any unusual problems while taking this medication.

If you experience a serious side effect, you or your healthcare provider may send a report to the FDA's MedWatch Adverse Event Reporting Program or by phone (800-332-1088).

Dosage: How Much Lynparza Should I Take?


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The dose of this medicine will be different for different patients. Follow your doctor's orders or the directions on the label. The following information includes only the average doses of this medicine. If your dose is different, do not change it unless your doctor tells you to do so.

The amount of medicine that you take depends on the strength of the medicine. Also, the number of doses you take each day, the time allowed between doses, and the length of time you take the medicine depend on the medical problem for which you are using the medicine.

  • For oral dosage form (capsules):

    • For advanced ovarian cancer:

      • Adults—400 milligrams (mg) (eight 50 mg capsules) 2 times a day. Each dose should be taken 12 hours apart. Your doctor may adjust your dose as needed.
      • Children—Use and dose must be determined by your doctor.
  • For oral dosage form (tablets):

    • For breast cancer, ovarian cancer, fallopian tube cancer, pancreas cancer, primary peritoneal cancer, or prostate cancer:

      • Adults—300 milligrams (mg) (two 150 mg tablets) 2 times a day. Each dose should be taken 12 hours apart. Your doctor may adjust your dose as needed or tolerated. However, dose is usually not more than 600 mg (four 150 mg tablets) per day.
      • Children—Use and dose must be determined by your doctor.
    • For maintenance treatment of advanced ovarian cancer:

      • Adults—300 milligrams (mg) (two 150 mg tablets) 2 times a day for up to 2 years. Each dose should be taken 12 hours apart. Your doctor may adjust your dose as needed or tolerated. However, dose is usually not more than 600 mg (four 150 mg tablets) per day.
      • Children—Use and dose must be determined by your doctor.

Modifications 

A dose reduction may be required if significant side effects occur while taking Lynparza. 

Additionally, you may need a lower dose if you have kidney disease.

Missed Dose 

If you miss a dose of Lynparza, you should take it at the next scheduled time. Never take a double dose to make up for the missed dose.

Overdose: What Happens If I Take Too Much Lynparza?

If you take too much Lynparza, call your cancer care team right away or go to an emergency room.  

What Happens If I Overdose on Lynparza?

If you think you or someone else may have overdosed on Lynparza, call a healthcare provider or the Poison Control Center (800-222-1222).

If someone collapses, has a seizure, has trouble breathing, or can’t wake up after taking too much Lynparza, call 911 immediately.

Precautions


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It is very important that your doctor check your progress at regular visits. This will allow your doctor to see if the medicine is working properly and to decide if you should continue to take it. Blood tests may be needed to check for unwanted effects.

Using this medicine while you are pregnant can harm your unborn baby. The tablet form may also cause birth defects if the father is using it when his sexual partner becomes pregnant. Female patients should use an effective form of birth control to keep from getting pregnant during treatment with this medicine and for at least 6 months after the last dose. Male patients who have female partners should use effective birth control during treatment with this medicine and for at least 3 months after the last dose. If you think you have become pregnant while using this medicine, tell your doctor right away.

Do not donate sperm while you are using the tablet form of this medicine and for 3 months after your last dose.

This medicine may cause bone marrow problems, such as myelodysplastic syndrome or acute myeloid leukemia. Check with your doctor right away if you have a fever, blood in the urine or stool, chills, unusual bleeding, bruising, tiredness, or weakness, or weight loss.

Tell your doctor right away if you have a chest pain, cough, or any type of breathing problem with this medicine. These could be symptoms of a serious lung problem.

This medicine may increase your risk for having blood clots (eg, venous thrombosis, pulmonary embolism). Call your doctor right away if you have chest pain, fast, pounding, or irregular heartbeat or pulse, pain or swelling in the arms or legs, or rapid shallow or trouble breathing.

Do not take other medicines unless they have been discussed with your doctor. This includes prescription or nonprescription (over-the-counter [OTC]) medicines and herbal (eg, St. John's wort) or vitamin supplements.

What Are Reasons I Shouldn’t Take Lynparza? 

People who are pregnant or breastfeeding should not take Lynparza. This medication can potentially cause harm to the fetus, although there are currently only animal studies of its use during pregnancy. 

What Other Medications Interact With Lynparza?

Avoid medications in the class of CYP3A inhibitors and inducers while taking Lynparza.

These medications can include:

  • Tegretol (carbamazepine)
  • Rifadin, Rimactane (rifampin)
  • St. John’s Wort
  • Diflucan (fluconazole)
  • Nizoral (ketoconazole)
  • Cordarone, Pacerone (amiodarone)
  • Diltiazem
  • Phenobarbital

What Medications Are Similar?

Other PARP inhibitors include:

  • Rubraca (rucaparib), which is used for ovarian and prostate cancers
  • Talzenna (talazoparib), which is used to treat breast cancer

These medications should not be taken along with Lynparza.

Frequently Asked Questions

  • What is Lynparza used for?

    Lynparza is used to treat certain types of ovarian cancer, breast cancer, prostate cancer, and pancreatic cancer.

  • How does Lynparza work?

    Lynparza is a PARP inhibitor. It blocks the action of the PARP enzyme in cancer cells. The PARP enzyme repairs the DNA in a cell, and by blocking it, the cancer cell dies.

  • Is Lynparza expensive?


  • How do I stop taking Lynparza?

    Lynparza should not be stopped unless instructed by the oncologist.

How Can I Stay Healthy While Taking Lynparza?

Anytime a new medication is prescribed, there can be hesitation and nervousness about the potential side effects. 

Lynparza offers a new treatment option for people with these types of cancers. Unfortunately, like many medications, it can also bring side effects. Understanding which side effects are normal and which ones are not is important for managing your therapy. Be sure to talk to your cancer care team about any concerns you may have. They can be a great resource to help you manage any side effects you may experience.

If you are having difficulty affording your cancer medication, you can take steps to find help. Lynparza’s manufacturer, AstraZeneca, offers financial assistance programs. You can also talk to a social worker or pharmacist at your cancer care center for advice. They can help you look for financial assistance opportunities.

Medical Disclaimer

Verywell Health's drug information is meant for educational purposes only and not intended as a replacement for medical advice, diagnosis, or treatment from a healthcare provider. Consult your healthcare provider before taking any new medication(s). IBM Watson Micromedex provides some of the drug content, as indicated on the page.

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