These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Elevated plasma S100B levels in high altitude hypobaric hypoxia do not correlate with acute mountain sickness.
    Author: Winter CD, Whyte TR, Cardinal J, Rose SE, O'Rourke PK, Kenny RG.
    Journal: Neurol Res; 2014 Sep; 36(9):779-85. PubMed ID: 24620985.
    Abstract:
    OBJECTIVES: Ascent to high altitude may result in a hypobaric hypoxic brain injury. The development of acute mountain sickness (AMS) is considered a multifactorial process with hypoxia-induced blood-brain barrier (BBB) dysfunction and resultant vasogenic oedema cited as one potential mechanism. Peripheral S100B is considered a biomarker of BBB dysfunction. This study aims to investigate the S100B release profile secondary to hypoxic brain injury and comment on BBB disturbance and AMS. METHODS: A prospective field study of 12 subjects who ascended Mt Fuji (3700 m) was undertaken. RESULTS: The mean baseline plasma S100B level was 0·11 μg/l (95% CI 0·09-0·12), which increased to 0·22 μg/l (95% CI 0·17-0·27) at the average of three high altitude levels (2590, 3700, and 2590 m on descent) (P < 0·001). The mean level for the seven subjects who experienced AMS rose from 0·10 to 0·19 μg/l compared to 0·12 to 0·25 μg/l for the five subjects who did not develop AMS (P  =  0·33). CONCLUSION: Ascending to 3700 m resulted in elevated plasma S100B levels but this was not associated with AMS.
    [Abstract] [Full Text] [Related] [New Search]