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Clinical Investigations: DIFFUSE LUNG DISEASE |

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

Peter Bärtsch, MD; Urs Eichenberger, MD; Peter E. Ballmer, MD, PD; J. Simon R. Gibbs, MD; Christian Schirlo, MD; Oswald Oelz, MD; Ertan Mayatepek, MD, PD
Author and Funding Information

*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@med.uni-heidelberg.de



Chest. 2000;117(5):1393-1398. doi:10.1378/chest.117.5.1393
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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.

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