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Thromboinflammation and microcirculation damage in heatstroke.

Publication ,  Journal Article
Iba, T; Maier, CL; Levi, M; Levy, JH
Published in: Minerva Med
April 2024

Rising temperatures associated with climate change have significantly increased the risk of heatstroke. Unfortunately, the trend is anticipated to persist and increasingly threaten vulnerable populations, particularly older adults. According to Japan's environment ministry, over 1000 people died from heatstroke in 2021, and 86% of deaths occurred in those above 65. Since the precise mechanism of heatstroke is not fully understood, we examined the pathophysiology by focusing on the microcirculatory derangement. Online search of published medical literature through MEDLINE and Web of Science using the term "heatstroke," "heat-related illness," "inflammation," "thrombosis," "coagulation," "fibrinolysis," "endothelial cell," and "circulation." Articles were chosen for inclusion based on their relevance to heatstroke, inflammation, and thrombosis. Reference lists were reviewed to identify additional relevant articles. Other than preexisting conditions (genetic background, age, etc.), factors such as hydration status, acclimatization, dysregulated coagulation, and inflammation are the additional major factors that promote tissue malcirculation in heatstroke. The fundamental pathophysiologic mechanisms significantly overlap with those seen in the systemic inflammatory response to sepsis, and as a result, coagulation-predominant coagulopathy develops during heat stress. Although a bleeding tendency is not common, bleeding frequently occurs in the microcirculation, causing additional injury. Sterile inflammation is mediated by proinflammatory cytokines, chemokines, and other humoral mediators in concert with cellular factors, including monocytes, neutrophils, platelets, and endothelial cells. Excess inflammation results in inflammatory cell death, including pyroptosis and necroptosis, and the release of danger signals that further propagate systemic inflammation and coagulopathy. Consequently, thromboinflammation is the critical factor that induces microcirculatory disturbance in heatstroke.

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Published In

Minerva Med

DOI

EISSN

1827-1669

Publication Date

April 2024

Volume

115

Issue

2

Start / End Page

191 / 202

Location

Italy

Related Subject Headings

  • Thrombosis
  • Microcirculation
  • Inflammation
  • Humans
  • Heat Stroke
  • General & Internal Medicine
 

Citation

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Iba, T., Maier, C. L., Levi, M., & Levy, J. H. (2024). Thromboinflammation and microcirculation damage in heatstroke. Minerva Med, 115(2), 191–202. https://doi.org/10.23736/S0026-4806.23.08919-X
Iba, Toshiaki, Cheryl L. Maier, Marcel Levi, and Jerrold H. Levy. “Thromboinflammation and microcirculation damage in heatstroke.Minerva Med 115, no. 2 (April 2024): 191–202. https://doi.org/10.23736/S0026-4806.23.08919-X.
Iba T, Maier CL, Levi M, Levy JH. Thromboinflammation and microcirculation damage in heatstroke. Minerva Med. 2024 Apr;115(2):191–202.
Iba, Toshiaki, et al. “Thromboinflammation and microcirculation damage in heatstroke.Minerva Med, vol. 115, no. 2, Apr. 2024, pp. 191–202. Pubmed, doi:10.23736/S0026-4806.23.08919-X.
Iba T, Maier CL, Levi M, Levy JH. Thromboinflammation and microcirculation damage in heatstroke. Minerva Med. 2024 Apr;115(2):191–202.

Published In

Minerva Med

DOI

EISSN

1827-1669

Publication Date

April 2024

Volume

115

Issue

2

Start / End Page

191 / 202

Location

Italy

Related Subject Headings

  • Thrombosis
  • Microcirculation
  • Inflammation
  • Humans
  • Heat Stroke
  • General & Internal Medicine