Abstract
Background
The etiopathology of high altitude pulmonary edema (HAPE) is still not fully understood. There has been evidence of inflammation documented in cases of HAPE. If inflammation is even partially responsible for the pathophysiology of HAPE, then an understanding of its role and the type and temporal profile of the inflammatory response would be valuable in the management of HAPE and in the search for better therapies for the condition.
Objective
This study was taken up to evaluate and characterize the inflammatory response in High Altitude Pulmonary Edema (HAPE) by quantization of the cytokine/chemokines in the lung edema fluid obtained by fine needle aspiration (FNA). The temporal profile of the inflammatory response and comparison of the serum and urinary cytokine levels vis-à-vis the lung fluid cytokine levels as noninvasive surrogate markers of inflammation were also evaluated.
Methods
Inflammatory markers (C-Reactive Protein(CRP), Interleukin-1 (IL-1), Tumor Necrosis Factor α (TNF-α), Transforming Growth Factor β (TGF-β), Interferon Γ (IFN-Γ), Interleukin-2 (IL-2), Tumor Necrosis Factor β (TNF-β), Interleukin-5 (IL-5), Interleukin-10 (IL-10), Interleukin-8 (IL-8), Macrophage Chemotactic Protein 1 (MCP-1), Lymphotactin, and Granzyme-β were serially evaluated in the fine needle aspirate (FNA) of lungs, concomitant serum, and urine samples of 13 patients of HAPE. Their physiological and biochemical variables were also studied. All observations were recorded on admission to the hospital, Day 3, and Day 7.
Results
The significantly high macrophage counts in the FNA, serially high levels of MCP-1, Granzyme B, IL-8, and Gamma Interferon all support the theory of inflammation being a secondary phenomenon rather than the primary causative pathophysiology. CRP increased by Day 7, thereby indicating that inflammation may not be the cause of HAPE but a response to the presence of HAPE.
Conclusions
The role of inflammation as a cause of HAPE has not been substantiated with this study.