High-Altitude Pulmonary Edema Is Associated With Coagulation and Fibrinolytic Abnormalities

Ren, Yusheng; Wu, Zonggui; Cui, Fang; Lei, Yinquan; Fu, Zhongming; Cui, Bo

doi:10.1097/maj.0b013e31823e5ee4

Cited by 10 publications

(3 citation statements)

References 18 publications

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“…It has an large dynamic range with >10 orders of magnitude in concentration separating albumin and the rarest proteins, which are now measured clinically or researched in laboratories. With the availability of proteomic tools, the profiling of the human plasma proteome has become increasingly feasible; when searching for disease-related markers, the presence of a particular protein and/or its isoforms in the plasma represents the likelihood of other biologically active molecules as potential biomarkers for disease diagnosis and therapeutic monitoring (24). Cellular functions and the protein expression pattern often change during different disease states.…”

Section: Discussionmentioning

confidence: 99%

Differential plasma proteome analysis in patients with high-altitude pulmonary edema at the acute and recovery phases

Yang

Guan

et al. 2014

Experimental and Therapeutic Medicine

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This study aimed to investigate the differential expression of plasma proteins in patients suffering from high-altitude pulmonary edema (HAPE) at different phases. A complete proteomic analysis was performed using two-dimensional gel electrophoresis followed by mass spectrometry in three patients with HAPE at the acute stage and recovery phase. Comparisons between the expression patterns of the patients with HAPE at the two different phases led to the identification of eight protein spots with a >1.5-fold difference in expression between the acute and recovery phases. These differentially expressed proteins were apolipoproteins, serum amyloid P component, complement components and others. Apolipoprotein A-I (Apo A-I), serum amyloid P component and fibrinogen were overexpressed in the patients with HAPE in the acute stage compared with their expression levels in the recovery phase. However, Apo A-IV and antithrombin-III were overexpressed in the patients with HAPE in the recovery phase compared with their expression levels in the acute stage. The results indicate that the differential plasma proteome in patients with HAPE may be associated with the occurrence of HAPE, and the expression changes of Apo A-I and A-IV may offer further understanding of HAPE to aid its prognosis, diagnosis and treatment.

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Section: Discussionmentioning

confidence: 99%

Differential plasma proteome analysis in patients with high-altitude pulmonary edema at the acute and recovery phases

Yang

Guan

et al. 2014

Experimental and Therapeutic Medicine

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“…Ren, et al found that tissue plasminogen activator (tPA), D-dimers, fibrinogens, and fibrin degradation products (FDPs) levels are increased due to hypoxia at HA [32]. They suggested an important factor of HAPE to be disequilibrium between coagulation and fibrinolysis resulting in lung injury [32]. However, Swenson, et al in their study compared numerous literature and pointed out that only IL-6 to be elevated in both systemic circulation and alveolar space (elevated only after the onset of HAPE) [2].…”

Section: Clinical Relevancementioning

confidence: 99%

“…However, they concluded HAPE to be modulated but not caused by inflammatory processes [ 15 ]. Ren, et al found that tissue plasminogen activator (tPA), D- dimers, fibrinogens, and fibrin degradation products (FDPs) levels are increased due to hypoxia at HA [ 32 ]. They suggested an important factor of HAPE to be disequilibrium between coagulation and fibrinolysis resulting in lung injury [ 32 ].…”

Section: Reviewmentioning

confidence: 99%

Patchy Vasoconstriction Versus Inflammation: A Debate in the Pathogenesis of High Altitude Pulmonary Edema

Kandel

Mishra

Gautam

et al. 2020

Cureus

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High altitude pulmonary edema (HAPE) occurs in individuals rapidly ascending at altitudes greater than 2,500 m within one week of arrival. HAPE is characterized by orthopnea, breathlessness at rest, cough, and pink frothy sputum. Several mechanisms to describe the pathophysiology of HAPE have been proposed in different kinds of literature where most of the mechanisms are reported to be activated before a drop in oxygen saturation levels. The majority of the current studies favor diffuse hypoxic pulmonary vasoconstriction (HPV) as a pathophysiological basis for HAPE. However, some of the studies described inflammation in the lungs and genetic basis as the pathophysiology of HAPE. So, there is a major disagreement regarding the exact pathophysiology of HAPE in the current literature, which raises a question as to what is the exact pathophysiology of HAPE. So, we reviewed 23 different articles which include clinical trials, review articles, randomized controlled trials (RCTs), and original research published from 2010 to 2020 to find out widely accepted pathophysiology of HAPE. In our study, we found out sympathetic stimulation, reduced nitric oxide (NO) bioavailability, increased endothelin, increased pulmonary artery systolic pressure (PASP) resulting in diffuse HPV, and reduced reabsorption of interstitial fluid to be the most important determinants for the development of HAPE. Similarly, with the evaluation of the role of inflammatory mediators like C-reactive protein (CRP) and interleukin (IL-6), we found out that inflammation in the lungs seems to modulate but not cause the process of development of HAPE. Genetic basis as evidenced by increased transcription of certain gene products seems to be another promising hypoxic change leading to HAPE. However, comprehensive studies are still needed to decipher the pathophysiology of HAPE in greater detail.

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Blood and Haemostasis

Bärtsch

Milledge

2013

High Altitude

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High-Altitude Pulmonary Edema Is Associated With Coagulation and Fibrinolytic Abnormalities

Cited by 10 publications

References 18 publications

Differential plasma proteome analysis in patients with high-altitude pulmonary edema at the acute and recovery phases

Differential plasma proteome analysis in patients with high-altitude pulmonary edema at the acute and recovery phases

Patchy Vasoconstriction Versus Inflammation: A Debate in the Pathogenesis of High Altitude Pulmonary Edema

Blood and Haemostasis

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