scholarly journals MIR17HG polymorphisms contribute to High altitude pulmonary edema susceptibility in Chinese Han people

2020 ◽  
Author(s):  
Yanli Zhao ◽  
Lining Si ◽  
Qifu Long ◽  
Derui Zhu ◽  
Guoping Shen ◽  
...  

Abstract Background: High altitude pulmonary edema (HAPE) is a severe form of acute mountain sickness (AMS). The results of existing studies have shown that the onset of HAPE has obvious ethnic specificity and personal susceptibility, suggesting that the occurrence of HAPE is related to genetic factors. Therefore, six polymorphisms on MIR17HG were selected to investigate the effect of mutations on MIR17HG on HAPE in Chinese Han population.Materials and Methods: 487 healthy participants (244 participants had high altitude pulmonary edema, as the case group; and 243 participants had no symptoms of HAPE, as the control group) were genotyped via the Agena MassARRAY, and the relationship between polymorphisms on MIR17HG and HAPE risk was evaluated using a χ2 test with an odds ratio (OR) and 95% confidence intervals (CIs) in multiple genetic models.Results: In the allele model, we observed that lower risk (OR = 0.74, 95%CI: 0.56 - 0.98, p = 0.036) of the A allele for rs7318578 on the MIR17HG compared with the people with the C allele. Logistic regression analysis of four models for all selected MIR17HG SNPs between cases and controls showed significant differences for rs7318578 (OR = 0.74, 95%CI: 0.56 – 0.98, p = 0.037) and rs17735387 (OR = 1.51, 95%CI: 1.03 – 2.21, p = 0.036) in the HAPE population.Conclusion: rs7318578 and rs17735387 on MIR17HG were associated with the genetic susceptibility of HAPE in Chinese Han population.

2021 ◽  
Author(s):  
Lining Si ◽  
Haiyuan Wang ◽  
Rong Wang ◽  
Qifu Long ◽  
Yanli Zhao

Abstract Background: High-altitude pulmonary edema (HAPE) is a common acute altitude sickness. The results from existing studies have shown that the occurrence of HAPE is related to genetic factors. Therefore, six locis of MIR17HG were selected to study its effect on HAPE of Chinese population.Methods: All subjects were genotyped by the Agena MassARRAY, and the relationship between polymorphisms on MIR17HG and HAPE risk was evaluated using a χ2 test with an odds ratio (OR) and 95% confidence intervals (CIs) in multiple genetic models.Results: In the allele model, we observed that lower risk (OR = 0.74, p = 0.036) of the A allele for rs7318578 on the MIR17HG compared to the people with the C allele. Logistic regression analysis of four models for all selected MIR17HG SNPs between cases and controls showed significant differences for rs7318578 (OR = 0.74, p = 0.037) and rs17735387 (OR = 1.51, p = 0.036) in the HAPE population. Conclusion: Rs7318578 and rs17735387 on MIR17HG were associated with the genetic susceptibility of HAPE in Chinese population.


Author(s):  
Gustavo Zubieta-Calleja ◽  
Natalia Zubieta-DeUrioste

Acute high-altitude illnesses are of great concern for physicians and people traveling to high altitude. Our recent article “Acute Mountain Sickness, High-Altitude Pulmonary Edema and High-Altitude Cerebral Edema, a View from the High Andes” was questioned by some sea-level high-altitude experts. As a result of this, we answer some observations and further explain our opinion on these diseases. High-Altitude Pulmonary Edema (HAPE) can be better understood through the Oxygen Transport Triad, which involves the pneumo-dynamic pump (ventilation), the hemo-dynamic pump (heart and circulation), and hemoglobin. The two pumps are the first physiologic response upon initial exposure to hypobaric hypoxia. Hemoglobin is the balancing energy-saving time-evolving equilibrating factor. The acid-base balance must be adequately interpreted using the high-altitude Van Slyke correction factors. Pulse-oximetry measurements during breath-holding at high altitude allow for the evaluation of high altitude diseases. The Tolerance to Hypoxia Formula shows that, paradoxically, the higher the altitude, the more tolerance to hypoxia. In order to survive, all organisms adapt physiologically and optimally to the high-altitude environment, and there cannot be any “loss of adaptation”. A favorable evolution in HAPE and pulmonary hypertension can result from the oxygen treatment along with other measures.


1996 ◽  
Vol 81 (2) ◽  
pp. 922-932 ◽  
Author(s):  
A. Podolsky ◽  
M. W. Eldridge ◽  
R. S. Richardson ◽  
D. R. Knight ◽  
E. C. Johnson ◽  
...  

Ventilation-perfusion (VA/Q) mismatch has been shown to increase during exercise, especially in hypoxia. A possible explanation is subclinical interstitial edema due to high pulmonary capillary pressures. We hypothesized that this may be pathogenetically similar to high-altitude pulmonary edema (HAPE) so that HAPE-susceptible people with higher vascular pressures would develop more exercise-induced VA/Q mismatch. To examine this, seven healthy people with a history of HAPE and nine with similar altitude exposure but no HAPE history (control) were studied at rest and during exercise at 35, 65, and 85% of maximum 1) at sea level and then 2) after 2 days at altitude (3,810 m) breathing both normoxic (inspired Po2 = 148 Torr) and hypoxic (inspired Po2 = 91 Torr) gas at both locations. We measured cardiac output and respiratory and inert gas exchange. In both groups, VA/Q mismatch (assessed by log standard deviation of the perfusion distribution) increased with exercise. At sea level, log standard deviation of the perfusion distribution was slightly higher in the HAPE-susceptible group than in the control group during heavy exercise. At altitude, these differences disappeared. Because a history of HAPE was associated with greater exercise-induced VA/Q mismatch and higher pulmonary capillary pressures, our findings are consistent with the hypothesis that exercise-induced mismatch is due to a temporary extravascular fluid accumulation.


1991 ◽  
Vol 71 (3) ◽  
pp. 934-938 ◽  
Author(s):  
W. H. Reinhart ◽  
B. Kayser ◽  
A. Singh ◽  
U. Waber ◽  
O. Oelz ◽  
...  

The role of blood rheology in the pathogenesis of acute mountain sickness and high-altitude pulmonary edema was investigated. Twenty-three volunteers, 12 with a history of high-altitude pulmonary edema, were studied at low altitude (490 m) and at 2 h and 18 h after arrival at 4,559 m. Eight subjects remained healthy, seven developed acute mountain sickness, and eight developed high-altitude pulmonary edema. Hematocrit, whole blood viscosity, plasma viscosity, erythrocyte aggregation, and erythrocyte deformability (filtration) were measured. Plasma viscosity and erythrocyte deformability remained unaffected. The hematocrit level was lower 2 h after the arrival at high altitude and higher after 18 h compared with low altitude. The whole blood viscosity changed accordingly. The erythrocyte aggregation was about doubled 18 h after the arrival compared with low-altitude values, which reflects the acute phase reaction. There were, however, no significant differences in any rheological parameters between healthy individuals and subjects with acute mountain sickness or high-altitude pulmonary edema, either before or during the illness. We conclude that rheological abnormalities can be excluded as an initiating event in the development of acute mountain sickness and high-altitude pulmonary edema.


Author(s):  
Hisham Mohammed Sonbul ◽  
Abdu Saleh Alwadani ◽  
Bader Aziz Alharbi ◽  
D. Almaymuni, Saleh Mohammed ◽  
Abdulrazaq Abdulmohsen Alkhalaf ◽  
...  

High altitude pulmonary Edema (HAPE) is a severe form of high-altitude disease that, if left untreated, can result in death in up to half of those who are affected. Lowlanders who rapidly go to elevations more than 2500-3000 m are more likely to develop high altitude pulmonary Edema (HAPE). Individual sensitivity owing to a low hypoxic ventilatory response (HVR), quick pace of climb, male sex, usage of sleep medicine, high salt consumption, chilly ambient temperature, and intense physical effort are all risk factors. HAPE may be totally and quickly reversed if caught early and correctly treated. Slow climb is the most effective technique of prevention. A fall of at least 1000 meters, is the best and most certain treatment choice in HAPE. Supplemental oxygen, portable hyperbaric chambers, and pulmonary vasodilator medications (nifedipine and phosphodiesterase-5 inhibitors) may be beneficial. In this article we’ll be looking at the disease etiology, epidemiology, diagnosis and management.


2013 ◽  
Vol 690-693 ◽  
pp. 1305-1309
Author(s):  
Wen Hua Li

Objective observation of Tibetan medicine rhodiola on high altitude Pulmonary edema in rats and HIF-1a expression changes. Method Will 50 only male SD rats randomly divided into 5 group , are often oxygen control group (Xi'an , altitude 5m ), acute hypoxia control group (Xi'an , altitude 5m ), acute hypoxia Group (naqu , elevation 4500m ), rhodiola acclimatization control group ( Xi'an , altitude 5m ), rhodiola altitude acclimatization group (naqu, elevation 4500m ) , light and electron microscopic observation of lung tissue samples , immunohistochemical detection of various groups of lung tissue HIF-la expression, RT-PCR method detection altitude hypoxia group animal lungs HIF-la mRNA expression changes. Results Acute hypoxia group lung tissue microstructure and Ultrastructure of a discernible high altitude pulmonary edema, and after the Tibetan medicine rhodiola after high altitude pulmonary edema is significantly reduced, ( as in Figure 123456). Lung tissue within the immunohistochemical detection not see HIF-la protein expression, RT-PCR detection SD big rat intraperitoneal injection of rhodiola extract 40g BGE/kg, 2h open back began to rise 4h, peak, after declining 24h, basically back to their normal control group , level rhodiola medicine acclimatization group HIF a 1 am RNA expression are clearly higher than the atmospheric oxygen control group and acute hypoxia group (p < 0.01). Conclusions Tibetan medicine rhodiola on lung tissue HIF-lamRNA expression of conducive to reduce hypoxic rats high altitude pulmonary edema.


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Zi-Kai Song ◽  
Hai-Di Wu ◽  
Hong-Yan Cao ◽  
Ling Qin

Lp(a) has been well known as an independent risk factor for coronary artery disease (CAD). TheLPAgene, as it encodes apo(a) of the Lp(a) lipoprotein particle, was associated with increased risk of CAD. The purpose of this study was to analyze the relationship between the polymorphisms ofLPAgene and CAD in Chinese Han population. Five SNPs (rs1367211, rs3127596, rs6415085, rs9347438, and rs9364559) in theLPAgene were genotyped using Sequenom MassARRAY time-of-flight mass spectrometer (TOF) in 560 CAD patients as case group and 531 non-CAD subjects as control group. The numbers of these two groups were from Chinese Han ancestry. The results showed that allele (P=0.046) and genotype (P=0.026) of rs9364559 in theLPAgene was associated with CAD. The frequency of rs9364559 minor allele (G) in case group was obviously higher than that in control group. Results of haplotype analysis showed that 4 haplotypes which contained rs9364559-G were associated with increased risk of CAD in this population. This study explored rs9364559 in theLPAgene may be associated with the pathogenesis of CAD; and the risk of CAD might be higher in the population carrying 4 haplotypes of different blocks in theLPAgene.


2021 ◽  
Author(s):  
Gustavo Zubieta-Calleja ◽  
Natalia Zubieta-DeUrioste

Background: Travelling to high altitude for entertainment or work is sometimes associated with acute high altitude pathologies. In the past, scientific literature from the lowlander point of view was mostly based on mountain climbing. Nowadays, altitude descent and evacuation are not mandatory in populated highland cities. Methods: We present how to diagnose and treat acute high altitude pathologies based on 50 years of high altitude physiology and medical practice in hypobaric hypoxic diseases in La Paz, Bolivia (3,600m; 11,811ft), at the High Altitude Pulmonary and Pathology Institute (HAPPI – IPPA) altitudeclinic.com.Results: Acute Mountain Sickness, High Altitude Pulmonary Edema, and High Altitude Cerebral Edema are all medical conditions faced by some travelers. These can occasionally present after flights to high altitude cities, both in lowlanders or high-altitude residents during re-entry, particularly after spending more than 20 days at sea level.Conclusions: Acute high altitude ascent diseases can be adequately diagnosed and treated without altitude descent. Traveling to high altitude should not be feared as it has many benefits;


2021 ◽  
Author(s):  
Gustavo Zubieta-Calleja ◽  
Natalia Zubieta-DeUrioste

Healthy children and those with pre-existing conditions traveling to high altitude may experience diverse physiologic changes. Individuals who are not acclimatized and ascend rapidly are at risk of developing acute high altitude illnesses (HAI), which may occur within a few hours after arrival at high altitudes, being acute mountain sickness (AMS) the most common. In very few cases, serious complications may occur, including High Altitude Pulmonary Edema (HAPE) and very rarely High Altitude Cerebral Edema (HACE). Moreover, the number of children and adolescents traveling on commercial aircrafts is growing and this poses a need for their treating physicians to be aware of the potential risks of hypoxia while air traveling. In this article we present 50 years of medical practice at high altitude treating these pathologies succesfully with no casualties.


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