Fever. What to do and what not to do.
Body temperature is monitored and regulated by the anterior hypothalamus, which acts as a thermostat by altering the balance of heat production and loss via the sympathetic nervous system. Fever results when the thermoregulatory set point in the hypothalamus is shifted upward. Fever is a part of the acute phase response, a generalized reaction to infection or inflammation initiated by interleukin-1 (IL-1). Prostaglandin E2 is the neural mediator of fever induced by IL-1, so fever can be suppressed by drugs that interfere with prostaglandin synthesis. Fever can be reduced by peripheral cooling, but the preferred method is treatment with antipyretic drugs. Although the host's response to infection is enhanced by small increases in body temperature, antipyretic treatment does not appear to interfere with recovery in humans.
D000082:Acetaminophen / Q000627:therapeutic use; D000210:Acute-Phase Reaction / Q000503:physiopathology; D001241:Aspirin / Q000627:therapeutic use; D001833:Body Temperature Regulation; D003080:Cold Temperature; D005334:Fever / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D007032:Hypothalamus, Anterior / Q000503:physiopathology; D007052:Ibuprofen / Q000627:therapeutic use; D007375:Interleukin-1 / Q000502:physiology
D007375:Interleukin-1; D000082:Acetaminophen; D001241:Aspirin; D007052:Ibuprofen