Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous reports have indicated that patients with severe acute respiratory syndrome (SARS)-associated coronavirus infection could develop atypical pneumonia with fulminant pulmonary edema. However, the target cells of SARS viral infection have not been characterized in detail. We report the pathologic findings of the lung in 3 cases of SARS. Chest radiographs at 2 to 3 weeks of infection revealed an atypical pneumonia with pulmonary consolidation, a clinical characteristic of SARS infection. The presence of the SARS virus was determined by nested reverse transcription-polymerase chain reaction (RT-PCR), and the infected cells were identified by in situ hybridization in open-lung biopsy and postmortem necropsy specimens. Expression of SARS virus-encoded RNA was detected in all 3 cases by RT-PCR, and the SARS viral signal was localized in pneumocytes by using in situ hybridization.
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PMID:Detection of severe acute respiratory syndrome-associated coronavirus in pneumocytes of the lung. 1536 78

Among the multiple organ disorders caused by the severe acute respiratory syndrome coronavirus (SARS-CoV), acute lung failure following atypical pneumonia is the most serious and often fatal event. We hypothesized that two of the hydrophilic structural coronoviral proteins (S and E) would regulate alveolar fluid clearance by decreasing the cell surface expression and activity of amiloride-sensitive epithelial sodium (Na(+)) channels (ENaC), the rate-limiting protein in transepithelial Na(+) vectorial transport across distal lung epithelial cells. Coexpression of either S or E protein with human alpha-, beta-, and gamma-ENaC in Xenopus oocytes led to significant decreases of both amiloride-sensitive Na(+) currents and gamma-ENaC protein levels at their plasma membranes. S and E proteins decreased the rate of ENaC exocytosis and either had no effect (S) or decreased (E) rates of endocytosis. No direct interactions among SARS-CoV E protein with either alpha- or gamma-ENaC were indentified. Instead, the downregulation of ENaC activity by SARS proteins was partially or completely restored by administration of inhibitors of PKCalpha/beta1 and PKCzeta. Consistent with the whole cell data, expression of S and E proteins decreased ENaC single-channel activity in oocytes, and these effects were partially abrogated by PKCalpha/beta1 inhibitors. Finally, transfection of human airway epithelial (H441) cells with SARS E protein decreased whole cell amiloride-sensitive currents. These findings indicate that lung edema in SARS infection may be due at least in part to activation of PKC by SARS proteins, leading to decreasing levels and activity of ENaC at the apical surfaces of lung epithelial cells.
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PMID:SARS-CoV proteins decrease levels and activity of human ENaC via activation of distinct PKC isoforms. 1911

Torsades de pointes (TdP) is a rapid, polymorphic and usually self-terminating ventricular tachycardia associated with the long QT syndrome. Many drugs may cause prolongation of QT interval and be the trigger for TdP occurrence. We present the case of 52-year-old male who was treated with clarithromycin due to bilateral atypical pneumonia. However, on the fourth day of hospitalization he deteriorated, developed pulmonary edema and short cardiac arrest. After successful resuscitation, unfortunately amiodarone and co-trimoxazole were given causing the arrhythmic storm which required many defibrillations. The case highlights the importance of careful QT measurement, appropriate TdP treatment and difficulties resulting from the patient's disagreement for invasive treatment. We think, that knowledge of drug-induced long QT syndrome and its consequences should be widely spread not only in cardiologists, but also in others doctors.
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PMID:Cardiac arrest and electrical storm due to recurrent torsades de pointes caused by concomitant clarithromycin, cotrimoxazole and amiodarone treatment. 2554 90