High-altitude pulmonary edema: an immunogenetically mediated disease?

High-altitude pulmonary edema (HAPE), a potentially life-threatening complication of acute mountain sickness, is postulated to be a noncardiogenic permeability edema caused by acute pulmonary arteriolar vasoconstriction and resultant pulmonary hypertension in response to the hypoxia of rapid ascent to high altitudes. HAPE typically occurs unexpectedly in young, otherwise healthy mountaineers. A constitutional susceptibility has been noted for some time; the disease tends to recur in the same individuals on reexposure to high altitude, whereas others appear not to be susceptible at all. The basis for this predisposition to HAPE, whether genetic or environmental, and its underlying pathophysiology remain poorly understood.