Ateş (tıp): Revizyonlar arasındaki fark

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[[Dosya:Thermometer Fever.svg|thumb|150px|38,0 °C'den ateş var<!--Normally, a ''fever'' is when body temperature is at or over 38 °C (100.4°F).-->]]

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Temperature is regulated in the [[hypothalamus]], in response to prostaglandin E2 ([[PGE2]]). PGE2 release, in turn, comes from a trigger, a pyrogen. The hypothalamus generates a response back to the rest of the body, making it increase the temperature set-point.

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The [[cytokines]] (such as [[interleukin 1]]) are a part of the [[innate immune system]], produced by [[phagocytic cells]], and cause the increase in the thermoregulatory set-point in the hypothalamus. Other examples of endogenous pyrogens are [[interleukin 6]] (IL-6), and [[tumor necrosis factor-alpha]].

 

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One model for the mechanism of fever caused by exogenous pyrogens includes LPS, which is a cell wall component of [[Gram-negative|gram-negative bacteria]]. An immunological protein called [[lipopolysaccharide-binding protein]] (LBP) binds to LPS. The LBP–LPS complex then binds to the [[CD14]] receptor of a nearby [[macrophage]]. This binding results in the synthesis and release of various endogenous [[cytokine]] factors, such as interleukin 1 (IL-1), interleukin 6 (IL-6), and the tumor necrosis factor-alpha. In other words, exogenous factors cause release of endogenous factors, which, in turn, activate the arachidonic acid pathway.

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PGE2 release comes from the [[arachidonic acid]] pathway. This pathway (as it relates to fever), is mediated by the [[enzyme]]s [[phospholipase|phospholipase A2]] (PLA2), [[cyclooxygenase|cyclooxygenase-2]] (COX-2), and [[prostaglandin E2 synthase]]. These enzymes ultimately mediate the synthesis and release of PGE2.

 

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The brain ultimately orchestrates '''heat effector mechanisms''' via the [[autonomic nervous system]]. These may be:

* Increased heat production by increased [[muscle tone]], [[shivering]] and hormones like epinephrine.

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Fever is a common [[symptom]] of many medical conditions:

* [[Infectious disease]], e.g. [[influenza]], [[common cold]], [[HIV]], [[malaria]], [[infectious mononucleosis]], or [[gastroenteritis]]

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There are arguments for and against the usefulness of fever, and the issue is controversial.<ref name="Schaffner">Schaffner A. Fever—useful or noxious symptom that should be treated? ''Ther Umsch'' 2006; '''63''': 185-8. PMID 16613288</ref><ref name=value>Soszynski D. The pathogenesis and the adaptive value of fever. ''Postepy Hig Med Dosw'' 2003; '''57''': 531-54. PMID 14737969</ref> There are studies using [[warm-blooded]] [[vertebrates]]<ref name="VUB">Su, F.; Nguyen, N.D.; Wang, Z.; Cai, Y.; Rogiers, P.; Vincent, J.L. Fever control in septic shock: beneficial or harmful? ''Shock'' 2005; '''23''': 516-20. PMID 15897803</ref> and [[human]]s<ref name="humans">Schulman, C.I.; Namias, N.; Doherty, J., et al. The effect of antipyretic therapy upon outcomes in critically ill patients: a randomized, prospective study. ''Surg Infect (Larchmt)'' 2005; '''6''':369-75. PMID 16433601</ref> ''[[in vivo]]'', with some suggesting that they recover more rapidly from infections or critical illness due to fever.

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* Rhoades, R. and Pflanzer, R. Human physiology, third edition, chapter 27 ''Regulation of body temperature'', p. 820 ''Clinical focus: pathogenesis of fever''. ISBN 0-03-005159-2

* Kasper, D.L.; Braunwald, E.; Fauci, A.S.; Hauser, S.L.; Longo, D.L.; Jameson, J.L. ''[[Harrison's Principles of Internal Medicine]]''. New York: McGraw-Hill, 2005. ISBN 0-07-139140-1.