Comment on “Soluble Urokinase-Type Plasminogen Activator Receptor Plasma Concentration May Predict Susceptibility to High Altitude Pulmonary Edema”

Abstract EN

We read with profound interest the article titled “Soluble Urokinase-Type Plasminogen Activator Receptor Plasma Concentration May Predict Susceptibility to High Altitude Pulmonary Edema” by Hilty et al.

[1].

The authors have concluded that soluble urokinase-type plasminogen activator receptor (suPAR) plasma concentration measured before hypoxic exposure may predict susceptibility of a lowlander to high altitude pulmonary edema (HAPE).

Despite the fact that inflammation is associated with acute hypoxia exposure in both HAPE and acute mountain sickness (AMS), studying these two high altitude illnesses together in the same cohort in this study seems to be convoluted.

AMS and HAPE are known to have pathophysiological processes involving central nervous system and cardiopulmonary systems, respectively, with hypoxia being the common triggering factor [2].

This has also been indirectly acknowledged by the authors, while suggesting that cellular based inflammation does not play a role in the central form of high altitude disease, comprising AMS and high altitude cerebral edema.

Moreover, occurrence of HAPE may not always be associated with AMS [3].

Though the role of inflammation in priming pulmonary endothelium towards hypoxia-related pulmonary edema is well established, the study of the biomarker with respect to AMS is intriguing.