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Urinary Leukotriene E₄ Levels Are Not Increased Prior to High-Altitude Pulmonary Edema^*

^* From the Institute of Sportsmedicine (Drs. Bärtsch and Eichenberger) and Department of General Pediatrics (Dr. Mayatepek), University Hospital, Heidelberg, Germany; the Department of Medicine (Dr. Ballmer), Kantonsspital, Winterthur, Switzerland; the Department of Clinical Cardiology (Dr. Gibbs), National Heart and Lung Institute, Imperial College of Science, Technology and Medicine, London, UK; the Institute of Physiology (Dr. Schirlo), University of Zürich, Switzerland; and the Department of Medicine (Dr. Oelz), Triemli Hospital, Zurich, Switzerland

Correspondence to: Peter Bärtsch, MD, Medizinische Klinik und Poliklinik, Abteilung für Sport und Leistungsmedizin, Hospitalstr. 3, Geb. 4100, D - 69115 Heidelberg, Germany; e-mail: peter_bartsch{at}med.uni-heidelberg.de

Study objective: To examine whether increased urinary cysteinyl-leukotriene E₄ (LTE₄) excretion, which has been found to be elevated in patients presenting with high-altitude pulmonary edema (HAPE), precedes edema formation.

Design: Prospective studies in a total of 12 subjects with susceptibility to HAPE.

Setting: In a chamber study, seven subjects susceptible to HAPE and five nonsusceptible control subjects were exposed for 24 h to an altitude of 450 m (control day), and exposed for 20 h to 4,000 m after slow decompression over 4 h. In a field study, prospective measurements at low and high altitude were performed in five subjects developing HAPE at 4,559 m.

Participants: Mountaineers with a radiographically documented history of HAPE and control subjects who did not develop HAPE with identical high-altitude exposure.

Interventions: 24-h urine collections.

Measurements and results: In the hypobaric chamber, none of the subjects developed HAPE. The 24-h urinary LTE₄ did not differ between HAPE susceptible and control subjects, nor between hypoxia and normoxic control day. In the field study, urinary LTE₄ was not increased in subjects with HAPE compared to values obtained prior to HAPE at high altitude and during 2 control days at low altitude.

Conclusions: These data do not provide evidence that cysteinyl–leukotriene-mediated inflammatory response is associated with HAPE susceptibility or the development of HAPE within the context of our studies.

Key Words: acute mountain sickness • eicosanoids • high altitude • high-altitude pulmonary edema • inflammation • leukotrienes • permeability

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