The etiology of capillary leak leading to peripheral edema and proteinuria associated with acute mountain sickness is elusive. Although some inflammatory mediators (e.g. plasma eicosanoids, serum phospholipid bound arachidonic acid, urinary leukotriene E4 levels) are found to be elevated in patients with acute mountain sickness but without high-altitude pulmonary edema, others (e.g. IL-1-b, IL-2 and its soluble receptors, IL-6, IL-8, tumor necrosis factor-a and its soluble receptor) are not. Thus overall endothelial cell activation seems to be minor, although regional differences cannot be excluded.
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