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Urinary leukotriene E4 levels in high-altitude pulmonary edema. A possible role for inflammation
D A Kaminsky1, K Jones, R B Schoene
1Pulmonary Disease and Critical Care Medicine Unit, University of Vermont College of Medicine, Burlington 05405, USA.
Study Objectives:
Inflammation may contribute to the pathogenesis of high-altitude pulmonary edema (HAPE). This study was designed to determine whether a marker of inflammation, urinary leukotriene E4 (LTE4), is elevated in patients with HAPE.
Design:
We conducted a case-control study to collect clinical data and urine samples from HAPE patients and healthy control subjects at moderate altitude (> or = 2727 m), and follow-up urine samples from HAPE patients following their return to low altitude (< or = 1,600 m).
Setting:
Five medical clinics in Summit County, Colorado.
Patients:
Questionnaire data were evaluated in 71 HAPE patients and 36 control subjects. Urinary LTE4 levels were determined from a random subset of 38 HAPE patients and 10 control subjects presenting at moderate altitude, and on 5 HAPE patients who had returned to low altitude.
Measurements And Results:
Using an enzyme immunoassay technique, urinary LTE4 levels were found to be significantly higher in HAPE patients (123 [16 to 468] pg/mg creatinine, geometric mean [range]) than in control subjects (69 [38 to 135]), p = 0.02. Following return to low altitude, urinary LTE4 levels fell significantly from 122 (41.8 to 309) to 53.6 (27.6 to 104) pg/mg creatinine (p = 0.05). Urinary LTE4 levels were not related to age, sex, time at altitude, physical condition or habitual exercise, recent use of alcohol or nonsteroidal anti-inflammatory drugs (NSAIDs), or oxygen saturation. Clinical factors associated with HAPE included male sex, regular exercise, and recent use of NSAIDs.
Conclusions:
We conclude that urinary LTE4 levels are elevated in patients with HAPE, supporting the view that HAPE involves inflammatory mechanisms.