Chest
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A 49-year-old man was sent by his primary care physician to the rheumatology clinic with complaints of several months of bilateral lower extremity swelling. The swelling migrated from both ankles up to his knees. Presenting symptoms consisted of bilateral knee pain as well as bilateral wrist and hand pain with swelling. ⋯ The examination was notable for bilateral knee effusions. Radiographs of his wrists, hands, and knee were obtained, along with a chest radiograph. He was then referred to a pulmonologist for further workup.
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A 24-year-old man was admitted for a new episode of hemoptysis. He reported 3 episodes of hemoptysis in the past 2 years. He had no other medical history and was a nonsmoker. ⋯ He never experienced pneumonia. He coughed up a small amount of fresh with air red blood (around 5 mL each time) several time for 3 days. He had no dyspnea, no chest pain, no fever, no asthenia, and no anorexia.
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Classically, mitochondria have largely been believed to influence the development of illness by modulating cell metabolism and determining the rate of production of high-energy phosphate compounds (eg, adenosine triphosphate). It is now recognized that this view is simplistic and that mitochondria play key roles in many other processes, including cell signaling, regulating gene expression, modulating cellular calcium levels, and influencing the activation of cell death pathways (eg, caspase activation). ⋯ This article reviews these evolving concepts relating mitochondrial function and acute illness. The discussion is organized into four sections: (1) basics of mitochondrial physiology; (2) cellular mechanisms of mitochondrial pathophysiology; (3) critical care disease processes whose initiation and evolution are shaped by mitochondrial pathophysiology; and (4) emerging treatments for mitochondrial dysfunction in critical illness.
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We report a case of a man in his 60s who developed pulmonary arterial hypertension (PAH) in association with profound vitamin C deficiency. Decreased availability of endothelial nitric oxide and activation of the hypoxia-inducible family of transcription factors, both consequences of vitamin C deficiency, are believed to be mechanisms contributing to the pathogenesis of the pulmonary hypertension. The PAH resolved following vitamin C supplementation. The current case highlights the importance of testing for vitamin C deficiency in patients with PAH in the proper clinical setting.
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The development of combination antiretroviral therapies (cARTs) in the mid-1990s has dramatically modified the clinical presentation of critically ill, HIV-infected patients. Most cART-treated patients aging with controlled HIV replication are currently admitted to the ICU for non-AIDS-related events, mostly bacterial pneumonia and exacerbation of comorbidities, variably affected by chronic HIV infection (COPD, cardiovascular diseases, or solid neoplasms). Today, Pneumocystis jirovecii pneumonia, cerebral toxoplasmosis, TB, and other severe opportunistic infections only occur in patients with unknown viral status, limited access to cART, viral resistance, or compliance issues. ⋯ Case fatality dropped substantially over the past decades, reaching figures of HIV-uninfected critically ill patients with similar demographic characteristics, comorbidities, and level of organ dysfunctions. Several other facets of critical care management have evolved in this population, including diagnostic procedures, cART management at the acute phase of critical illness, and ethical considerations. The goal of this narrative review was to depict the current evidence and emerging challenges for the management of critically ill, HIV-infected patients, almost 40 years following the onset of the AIDS epidemic.