Chest
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Return of spontaneous circulation after cardiac arrest results in a systemic inflammatory state called the post-cardiac arrest syndrome, which is characterized by oxidative stress, coagulopathy, neuronal injury, and organ dysfunction. Perturbations in oxygenation and ventilation may exacerbate secondary injury after cardiac arrest and have been shown to be associated with poor outcome. Further, patients who experience cardiac arrest are at risk for a number of other pulmonary complications. ⋯ Risk factors include aspiration, pulmonary contusions (from chest compressions), systemic inflammation, and reperfusion injury. Early evidence suggests that they may benefit from ventilation with low tidal volumes. Meticulous attention to mechanical ventilation, early assessment and optimization of respiratory gas exchange, and therapies targeted at potential pulmonary complications may improve outcomes after cardiac arrest.
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Lung cancer is a leading cause of death and hospitalization for patients with COPD. A detailed understanding of which clinical features of COPD increase risk is needed. ⋯ The degree of COPD severity, including airflow obstruction, visual emphysema, and respiratory exacerbations, was independently predictive of lung cancer. These risk factors should be further studied as inclusion and exclusion criteria for the survival benefit of lung cancer screening. Studies are needed to determine if reduction in respiratory exacerbations among smokers can reduce the risk of lung cancer.
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Thoracic sarcoidosis is the most common form of sarcoidosis, encompassing a heterogeneous group of patients with a wide range of clinical features and associated outcomes. The distinction between isolated thoracic lymphadenopathy and pulmonary involvement matters. Morbidity is often higher, and long-term outcomes are worse for the latter. ⋯ This review highlights recent advances in the pathogenesis of pulmonary sarcoidosis, including the nature of the sarcoidosis antigen, the role of serum amyloid A and other host factors that contribute to alterations in innate immunity, factors that shape adaptive T-cell profiles in the lung, and how these mechanisms influence the maintenance of granulomatous inflammation in sarcoidosis. We discuss questions raised by recent findings, including the role of innate immunity in the pathogenesis, the meaning of immune cell exhaustion, and mechanisms that may contribute to lung fibrosis in sarcoidosis. We conclude with a reflection on when and how immunosuppressive therapies may be helpful for pulmonary sarcoidosis, a consideration of nonpharmacologic management strategies, and a survey of potential novel therapeutic targets for this vexing disease.
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Rare diseases pose particular challenges to patients who are affected, to the clinicians who care for them, and to the investigators who study their conditions. Although individually uncommon, rare diseases are common in the aggregate, with approximately 7,000 described rare diseases affecting 25 to 30 million US adults. Challenges posed to affected individuals and their families largely regard being diagnosed, receiving optimal care, and affording disease-specific medications. ⋯ Fortunately, in the face of these challenges, the steadfast resolve of patient and clinical/scientific communities to enhance care and generate new knowledge has fostered a large inventory of countermeasures to offset these challenges. Although further progress is surely needed, successes to date include the formation of powerful patient advocacy groups which have brokered collaborations between the patient, scientific communities, the government, and pharma/device communities in service of detection, optimal care, and research; procurement of funds to support research; formation of consortia of clinicians and scientists to collaborate; and general activation of the respective patient communities to perpetuate these successes. Persisting needs include enhanced detection strategies, dissemination of knowledge regarding optimal care, and research to prevent, treat, and cure disease.
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Heparin-induced thrombocytopenia (HIT) is a prothrombotic drug reaction caused by platelet-activating antibodies that recognize platelet factor 4 (PF4)/heparin complexes. It is unknown whether platelet-activating antibodies are detectable at the onset of the HIT-related platelet count fall. ⋯ Platelet-activating HIT antibodies are detectable at the onset of the HIT-related platelet count fall. The SRA has high sensitivity and specificity for HIT, and indicates that presence of HIT antibodies can blunt postoperative platelet count recovery.