Background The clinical features and outcomes of mechanically ventilated patients with COVID-19 infection who develop a pneumothorax has not been rigorously described or compared to those who do not develop a pneumothorax. Purpose To determine the incidence, clinical characteristics, and outcomes of critically ill patients with COVID-19 infection who developed pneumothorax. In addition, we compared the clinical characteristics and outcomes of mechanically ventilated patients who developed a pneumothorax with those who did not develop a pneumothorax. Methods This study was a multicenter retrospective analysis of all adult critically ill patients with COVID-19 infection who were admitted to intensive care units in 4 tertiary care centers in the United States. Results A total of 842 critically ill patients with COVID-19 infection were analyzed, out of which 594 (71%) were mechanically ventilated. The overall incidence of pneumothorax was 83/842 (10%), and 80/594 (13%) in those who were mechanically ventilated. As compared to mechanically ventilated patients in the non-pneumothorax group, mechanically ventilated patients in the pneumothorax group had worse respiratory parameters at the time of intubation (mean PaO 2 :FiO 2 ratio 105 vs 150, P<0.001 and static respiratory system compliance: 30ml/cmH 2 O vs 39ml/cmH 2 O, P=0.01) and significantly higher in-hospital mortality (63% vs 49%, P=0.04). Conclusion The overall incidence of pneumothorax mechanically ventilated patients with COVID-19 infection was 13%. Mechanically ventilated patients with COVID-19 infection who developed pneumothorax had worse gas exchange and respiratory mechanics at the time of intubation and had a higher mortality compared to those who did not develop pneumothorax.

FK506 binding proteins (FKBPs), also called immunophilins, are prolyl-isomerases (PPIases) that participate in a wide variety of cellular functions including hormone signaling and protein folding. Recent studies indicate that proteins that contain PPIase activity can also alter the processing of Alzheimer's Amyloid Precursor Protein (APP). Originally identified in hematopoietic cells, FKBP52 is much more abundantly expressed in neurons, including the hippocampus, frontal cortex, and basal ganglia. Given the fact that the high molecular weight immunophilin FKBP52 is highly expressed in CNS regions susceptible to Alzheimer's, we investigated its role in Aβ toxicity. Towards this goal, we generated Aβ transgenic Drosophila that harbor gain of function or loss of function mutations of FKBP52. FKBP52 overexpression reduced the toxicity of Aβ and increased lifespan in Aβ flies, whereas loss of function of FKBP52 exacerbated these Aβ phenotypes. Interestingly, the Aβ pathology was enhanced by mutations in the copper transporters Atox1, which interacts with FKBP52, and Ctr1A and was suppressed in FKBP52 mutant flies raised on a copper chelator diet. Using mammalian cultures, we show that FKBP52 (−/−) cells have increased intracellular copper and higher levels of Aβ. This effect is reversed by reconstitution of FKBP52. Finally, we also found that FKBP52 formed stable complexes with APP through its FK506 interacting domain. Taken together, these studies identify a novel role for FKBP52 in modulating toxicity of Aβ peptides.

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Pneumocystis pneumonia is a life threatening infection that usually presents with diffuse bilateral ground-glass infiltrates in immunocompromised patients. We report a case of a single nodular granulomatous Pneumocystis pneumonia in a male with diffuse large B-cell lymphoma after R-CHOP therapy. He presented with symptoms of productive cough, dyspnea, and right-sided pleuritic chest pain that failed to resolve despite treatment with multiple antibiotics. Chest X-ray revealed right lower lobe atelectasis and CT of chest showed development of 2 cm nodular opacity with ground-glass opacities. Patient underwent bronchoscopy and biopsy that revealed granulomatous inflammation in a background of organizing pneumonia pattern with negative cultures. Respiratory symptoms resolved but the solitary nodular opacity increased in size prompting a surgical wedge resection which revealed granulomatous Pneumocystis pneumonia infection. This case is the third documented report of Pneumocystis pneumonia infection within a solitary pulmonary nodule in an individual with hematologic neoplasm. Although Pneumocystis pneumonia most commonly occurs in patients with HIV/acquired immunodeficiency syndrome and with diffuse infiltrates, the diagnosis should not be overlooked when only a solitary nodule is present.

Pulmonary necrobiotic nodules are a rare extraintestinal manifestation (EIM) of inflammatory bowel disease (IBD), which are often overlooked when diagnosing cavitary pulmonary nodules. We present this case to highlight the importance of a thorough differential diagnosis, which includes EIMs of ulcerative colitis (UC), in this case as necrobiotic nodules. Herein, we present a 25-year-old male patient with a history of poorly controlled UC who presented with fevers, left-sided abdominal pain, and bloody diarrhea. Imaging revealed cavitary pulmonary nodules without an infectious or malignant etiology. Lung biopsy and pathology confirmed a diagnosis consistent with necrobiotic nodules.

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In SSc-ILD patients, a PA:Ao ratio ≥1.1 is associated with higher risk of lung transplant or death. These data suggest that PA:Ao dimension may be used for prognostication in SSc-ILD.