scholarly journals Identifying risk factors that contribute to acute mountain sickness

2015 ◽  
Vol 27 (3) ◽  
pp. 82-86
Author(s):  
Z Mahomed ◽  
D Martin ◽  
E Gilbert ◽  
CC Grant ◽  
J Patricios ◽  
...  

Background. Acute mountain sickness (AMS) is an ever-increasing burden on the health sector. With reported incidences of greater than 50%, coupled with the fact that recreational activities at high altitude are gaining increasing popularity, more persons are developing AMS. Physicians are therefore increasingly faced with the task of managing and preventing AMS.Objectives. The pathophysiology of AMS is poorly understood, with little understanding of risk factors for the development of AMS. This research aimed to identify epidemiological and physiological risk factors for development of AMS.Methods. This study is a questionnaire-based study conducted in London and at Everest Base Camp, in which 116 lowlanders were invited to participate and fill in a questionnaire to identify potential risk factors in their history that may have contributed to development of or protection against AMS.Results. A total of 89 lowlanders enrolled in the study. Thirty-seven of the participants had AMS at  Everest Base Camp, giving a prevalence of 42%. Of the demographic variables, only weight and body  mass index (BMI) were statistically significantly associated with AMS, with those who weighed less or had a lower BMI more likely to get AMS. Previous high-altitude experience was also associated with AMS, with those who had such experience less likely to get AMS.Conclusion. Predicting AMS and furthering our understanding of the pathophysiology of AMS will be of tremendous benefit. Further research is needed in this regard.

2020 ◽  
Vol 16 (3) ◽  
pp. 275-279
Author(s):  
Grzegorz Zieliński ◽  
◽  
Aleksandra Byś ◽  

High-altitude tourism is gaining popularity. Mountains are also becoming an increasingly popular destination for school or family trips. This suggests that the number of children with high-altitude diseases, including acute mountain sickness (AMS), will also rise. The aim of this literature review was to determine the epidemiology of acute mountain sickness, its most common manifestations and risk factors in children. We analysed papers from the last 5 years, which were found by two independent authors using PubMed, ResearchGate and Google Scholar. The following keywords were used to identify relevant studies: acute mountain sickness, altitude sickness, children (by Medical Subject Headings). After screening with the exclusion criteria, the final analysis included 5 papers, which were assessed for the quality of evidence. The incidence of acute mountain sickness in children is 30–45% at elevations below 4,000 m. There were no differences compared to an adult population. Headache, sleep disorders and dizziness are the most common symptoms of acute mountain sickness in children. Further research is needed to identify factors that predispose children to this disease. In the light of the increasingly intensive alpine tourism among children, research on the sequelae of acute mountain sickness is recommended.


2014 ◽  
Vol 12 (5) ◽  
pp. 534-540 ◽  
Author(s):  
Maud Santantonio ◽  
Jean-Marc Chapplain ◽  
Pierre Tattevin ◽  
Hélène Leroy ◽  
Eric Mener ◽  
...  

2020 ◽  
pp. bjophthalmol-2020-317717
Author(s):  
Tou-Yuan Tsai ◽  
George Gozari ◽  
Yung-Cheng Su ◽  
Yi-Kung Lee ◽  
Yu-Kang Tu

Background/aimsTo assess changes in optic nerve sheath diameter (ONSD) at high altitude and in acute mountain sickness (AMS).MethodsCochrane Library, EMBASE, Google Scholar and PubMed were searched for articles published from their inception to 31st of July 2020. Outcome measures were mean changes of ONSD at high altitude and difference in ONSD change between subjects with and without AMS. Meta-regressions were conducted to investigate the relation of ONSD change to altitude and time spent at that altitude.ResultsEight studies with 248 participants comparing ONSD from sea level to high altitude, and five studies with 454 participants comparing subjects with or without AMS, were included. ONSD increased by 0.14 mm per 1000 m after adjustment for time (95% CI: 0.10 to 0.18; p<0.01). Restricted cubic spline regression revealed an almost linear relation between ONSD change and time within 2 days. ONSD was greater in subjects with AMS (mean difference=0.47; 95% CI: 0.14 to 0.80; p=0.01; I2=89.4%).ConclusionOur analysis shows that ONSD changes correlate with altitude and tend to increase in subjects with AMS. Small study number and high heterogeneity are the limitations of our study. Further large prospective studies are required to verify our findings.


PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e75644 ◽  
Author(s):  
Martin J. MacInnis ◽  
Eric A. Carter ◽  
Michael G. Freeman ◽  
Bidur Prasad Pandit ◽  
Ashmita Siwakoti ◽  
...  

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Juliane Hannemann ◽  
Julia Zummack ◽  
PATRICIA SIQUES ◽  
JULIO BRITO ◽  
Rainer Boeger

Introduction: Chronic (CH) and chronic-intermittent (CIH) exposure to hypoxia at high altitude causes acute or chronic mountain sickness and elevation of mean pulmonary arterial pressure (mPAP). This is paralleled by increased plasma levels of ADMA, an endogenous inhibitor of NO synthesis. ADMA is cleaved by dimethylarginine dimethylaminohydrolase (DDAH1 and DDAH2), whilst symmetric dimethylarginine (SDMA) is cleaved by AGXT2. Arginase (ARG1 and ARG2) competes with endothelial NO synthase (NOS3) for L-arginine as substrate. We have shown previously that baseline ADMA (at sea level) determines mPAP after six months of CIH; cut-off values of 25 mm Hg and 30 mm Hg are being used to diagnose high altitude pulmonary hypertension. Hypothesis: We hypothesized that genetic variability in genes coding for core enzymes of ADMA, SDMA, and L-arginine metabolism may predispose individuals for high altitude disease and pulmonary hypertension. Methods: We genotyped 16 common single nucleotide polymorphisms in the NOS3, DDAH1, DDAH2, AGXT2, ARG1 and ARG2 genes of 69 healthy male Chilean subjects. Study participants adhered to a CIH regimen (5d at 3,550m, 2d at sea level) for six months. Metabolites were measured by LC-MS/MS; mPAP was estimated by echocardiography at six months, and altitude acclimatization was assessed by Lake Louise Score and arterial oxygen saturation. Results: Carriers of the minor allele of DDAH1 rs233112 had a higher mean baseline ADMA level (0.76±0.03 vs. 0.67±0.02 μmol/l; p<0.05), whilst the major allele of DDAH2 rs805304 was linked to an exacerbated increase of ADMA in hypoxia (0.10±0.03 vs. 0.04±0.04 μmol/l; p<0.02). Study participants carrying the minor allele of ARG1 rs2781667 had a relative risk of elevated mPAP (>25 mm Hg) of 1.70 (1.56-1.85; p<0.0001), and carriers of the minor allele of NOS3 rs2070744 had a relative risk of elevated mPAP (>30 mm Hg) of 1.58 (1.47-1.69; p<0.0001). The NOS3 and DDAH2 genes were associated with the incidence of acute mountain sickness. Conclusions: We conclude that genetic variability in the L-arginine / ADMA / NO pathway is an important determinant of high altitude pulmonary hypertension and acute mountain sickness. DDAH1 is linked to baseline ADMA, whilst DDAH2 determines the response of ADMA to hypoxia.


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