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These observations strengthen the evidence for a defective antioxidant system as an early pathophysiological change associated with the disease, rather than a sequela of drug effects, chronic disease and smoking (Reddy et al

Differential pathophysiological mechanisms between CHS and EHS While CHS and EHS share core pathogenic pathways (e.g., hyperthermia, inflammation, cell death), their mechanistic features differ significantly due to distinct patient demographics and triggers: Inflammatory kinetics EHS (predominant in young, active individuals) is characterized by rapid, exertion-amplified inflammatory responses

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40 C = 44.68 17.10 and 41 C = 86.57 17.10

Marchand WR, Yurgelun-Todd D