Chest
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Heparin-induced thrombocytopenia (HIT) is associated with clinically significant morbidity and mortality. Patients who are critically ill are commonly thrombocytopenic and exposed to heparin. ⋯ If the patient is deemed as being at intermediate or high risk for HIT or if HIT is confirmed by means of the serotonin-release assay, heparin should be stopped, heparin-bonded catheters should be removed, and a direct antithrombin or fondaparinux should be initiated to reduce the risk of thrombosis. Warfarin is absolutely contraindicated in the acute phase of HIT; if administered, its effects must be reversed by using vitamin K.
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A drug-induced sarcoidosis-like reaction (DISR) is a systemic granulomatous reaction that is indistinguishable from sarcoidosis and occurs in a temporal relationship with initiation of an offending drug. DISRs typically improve or resolve after withdrawal of the offending drug. Four common categories of drugs that have been associated with the development of a DISR are immune checkpoint inhibitors, highly active antiretroviral therapy, interferons, and tumor necrosis factor-α antagonists. ⋯ However, the offending drug need not be discontinued if it is useful, and antigranulomatous therapy can be added. In some situations, the development of a DISR may suggest a beneficial effect of the inducing drug. Understanding the mechanisms leading to DISRs may yield important insights into the immunopathogenesis of sarcoidosis.
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As marijuana smoking prevalence increases in the United States, concern regarding its potential risks to lung health has also risen, given the general similarity in the smoke contents between marijuana and tobacco. Most studies have found a significant association between marijuana smoking and chronic bronchitis symptoms after adjustment for tobacco. Although reports are mixed regarding associations between marijuana smoking and lung function, none have shown a relationship to decrements in FEV1 and few have found a relationship to a decreased ratio of FEV1/FVC, possibly related to an association between marijuana and an increased FVC. ⋯ Although bronchial biopsies from habitual marijuana smokers have shown precancerous histopathologic changes, a large cohort study and a pooled analysis of six well-designed case-control studies have not found evidence of a link between marijuana smoking and lung cancer. The immunosuppressive effects of delta-9 tetrahydrocannabinol raise the possibility of an increased risk of pneumonia, but further studies are needed to evaluate this potential risk. Several cases series have demonstrated pneumothoraces/pneumomediastinum and bullous lung disease in marijuana smokers, but these associations require epidemiologic studies for firmer evidence of possible causality.
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How Fragile Are Clinical Trial Outcomes That Support the CHEST Clinical Practice Guidelines for VTE?
VTE remains a health concern for global populations. Clinical practice guidelines are necessary to guide physicians in the prophylaxis and treatment of VTE. ⋯ Our conclusions parallel those of previous investigations of the fragility of RCT outcomes; we found that some outcomes used to support recommendations in AT10 are fragile. We recommend that the fragility index and fragility quotient be adopted as measures of robustness of clinical trial outcomes.
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The deficiency of α1-antitrypsin (AAT) is secondary to misfolding and polymerization of the abnormal Z-AAT in liver cells and is associated with lung emphysema. Alveolar macrophages (AMs) produce AAT; however, it is not known whether Z-AAT can polymerize in AMs, further decreasing lung AAT and promoting lung inflammation. Our intention was to investigate whether AAT polymerizes in human AMs and to study the possible relation between polymerization and degree of lung inflammation. ⋯ Polymerization of AAT in alveolar macrophages occurs in the lungs of individuals with AATD but also in smokers with normal AAT levels with or without COPD. Our findings highlight the similarities in the pathophysiology of COPD in individuals with and without AATD, adding a potentially important step to the mechanism of COPD.