Chest
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Recent guidelines recommend assessing medical inpatients for bleeding risk prior to providing chemical prophylaxis for VTE. The International Medical Prevention Registry on Venous Thromboembolism (IMPROVE) bleeding risk score (BRS) was derived from a well-defined population of medical inpatients but it has not been validated externally. We sought to externally validate the IMPROVE BRS. ⋯ The IMPROVE BRS calculated at admission predicts major bleeding in medical inpatients. This model may help assess the relative risks of bleeding and VTE before chemoprophylaxis is administered.
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Pathologic features of end-stage pulmonary sarcoidosis (ESPS) are not well defined; anecdotal reports have suggested that ESPS may mimic usual interstitial pneumonia (UIP). We hypothesized that ESPS has distinct histologic features. ⋯ ESPS and UIP have distinct histopathologic features in the lungs. Patients with a pretransplant diagnosis of sarcoidosis may develop other lung diseases that account for their end-stage fibrosis.
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A 49-year-old man with a history of cryptogenic cirrhosis was referred to pulmonary clinic for evaluation prior to liver transplantation. Chest imaging obtained as part of the transplant workup had shown evidence of interstitial abnormalities. The patient noted shortness of breath on moderate exertion that was worsening over the past 2 to 3 years and associated with a nonproductive cough. ⋯ He did not have a history of alcohol consumption, smoking, or occupational exposures. He noted a family history of lung disease in his father and evidence of prominent clubbing in his sister and nephew. Workup for liver failure included a liver biopsy, which showed cirrhosis without evidence of autoimmune hepatitis.
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Cigarette smoking is a major environmental contributor to COPD, but understanding its epigenetic regulation of oxidative genes involved in the pathogenesis of COPD remains elusive. ⋯ Cigarette smoke-induced hypermethylation of the GCLC promoter is related to the initiation and progression of COPD. Our finding may provide a new strategy for COPD intervention by developing demethylation agents targeting GCLC hypermethylation.