TY - JOUR
T1 - The role of platelets in heat-related illness and heat-induced coagulopathy
AU - Iba, Toshiaki
AU - Helms, Julie
AU - Levi, Marcel
AU - Levy, Jerrold H.
N1 - Funding Information: TI has received a research grant from Japan Blood Products Organization and JIMRO. JH has received grants from Diagnostica Stago, Pfizer PFE France and Sanofi Aventis France. ML has received grants and has participated in advisory boards of NovoNordisk, Eli Lilly, Asahi Kasei Pharmaceuticals America, and Johnson & Johnson. JHL serves on the Steering Committees for Instrumentation Laboratories, Merck, and Octapharma. Publisher Copyright: © 2022 Elsevier Ltd
PY - 2022
Y1 - 2022
N2 - Heat-related illness is becoming more problematic due to ongoing global warming. Heat-related injury causes systemic inflammation and coagulopathy, due to leukocyte, platelet, and vascular endothelial cell activation and injury. Hyperthermia directly modulates platelet function and can induce cellular damage. Meanwhile, heat also affects platelet function via activated coagulation, excess inflammation, production of cytokines, and heat shock proteins. Aberrant hyperthermia-induced interactions between leukocytes and endothelial cells are also involved in platelet regulation. Heat-induced coagulopathy commonly progresses to disseminated intravascular coagulation (DIC), leading to multiple organ failure and in some cases enhanced bleeding. Consequently, platelet count, prothrombin time, and DIC score are useful for evaluating the severity of heat-related illness in addition to other organ damage markers such as Glasgow Coma Scale, creatinine, and bilirubin. Despite the increasing risk, therapeutic modalities targeting platelets are limited and no established therapy exists. In this review, we summarize the current knowledge about the role of platelets in the pathogenesis, diagnosis, and management of heat-related illness.
AB - Heat-related illness is becoming more problematic due to ongoing global warming. Heat-related injury causes systemic inflammation and coagulopathy, due to leukocyte, platelet, and vascular endothelial cell activation and injury. Hyperthermia directly modulates platelet function and can induce cellular damage. Meanwhile, heat also affects platelet function via activated coagulation, excess inflammation, production of cytokines, and heat shock proteins. Aberrant hyperthermia-induced interactions between leukocytes and endothelial cells are also involved in platelet regulation. Heat-induced coagulopathy commonly progresses to disseminated intravascular coagulation (DIC), leading to multiple organ failure and in some cases enhanced bleeding. Consequently, platelet count, prothrombin time, and DIC score are useful for evaluating the severity of heat-related illness in addition to other organ damage markers such as Glasgow Coma Scale, creatinine, and bilirubin. Despite the increasing risk, therapeutic modalities targeting platelets are limited and no established therapy exists. In this review, we summarize the current knowledge about the role of platelets in the pathogenesis, diagnosis, and management of heat-related illness.
KW - Coagulopathy
KW - Disseminated intravascular coagulation
KW - Heat shock protein
KW - Heatstroke
KW - Hyperthermia
KW - Platelet
UR - http://www.scopus.com/inward/record.url?scp=85136261524&partnerID=8YFLogxK
U2 - https://doi.org/10.1016/j.thromres.2022.08.009
DO - https://doi.org/10.1016/j.thromres.2022.08.009
M3 - Article
C2 - 35989192
SN - 0049-3848
JO - Thrombosis research
JF - Thrombosis research
ER -