Fever

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(Redirected from Ague)

See Fever (album) for the Kylie Minogue album, "Fever (Kylie Minogue song)" for the album's title track; "Fever" is also a song by Otis Blackwell, Fever*Fever Puffy AmiYumi album.

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Fever (also known as pyrexia, or a febrile response, and archaically known as ague) is a medical symptom that describes an increase in internal body temperature to levels that are above normal (37°C, 98.6°F). Fever should not be confused with hyperthermia, which is an increase in body temperature over the body’s thermoregulatory set-point (normally approximately 37°C, but increased during a fever). A fever is most accurately characterized as a temporary elevation in the body’s thermoregulatory set-point, which is usually by about 1-2°C. This elevation in thermoregulatory set-point means that the previous "normal body temperature" would be considered hypothermic. Effector mechanisms, such as increased blood pressure, increased heart rate, activation of brown adipose tissue, and muscular shivering attempt to counteract the perceived hypothermia, thereby reaching the new thermoregulatory set-point. It is the most common symptom of many diseases.

1 Mechanism
2 Types
3 References
4 See also
5 External links

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Mechanism

Fever is a positive feedback mechanism that acts toward the direction of change (as opposed to negative feedback, which acts opposite to change to maintain homeostasis). Therefore, fever is the opposite of thermoregulation. Substances that induce fever are called pyrogens. Although external pathogens may be the ultimate reason for a fever, it is the internal or endogenous pyrogens that directly cause the increase in the thermoregulatory set-point. An adaptive mechanism, fever is the body's reaction to pathogens; it attempts to raise core body temperature to levels that will speed up the actions of the immune system, and may also directly denature, debilitate, or kill the pathogen. Most fevers are caused by infections, and almost all infectious diseases can cause fever. When a patient has or is suspected of having a fever, that person's body temperature is measured using a thermometer. If successful in ridding the body of an invasive pathogen, fever is an important protective immune mechanism and should generally not be suppressed. However, there are instances when fever escalates to temperatures where the body is at risk of destroying its own cells and must be brought under control with suppressive medication. Image:Fever-conceptual.jpg

By using a reliable thermometer, you can tell if a fever is present if temperature is at or higher than one of the following levels:

38 degrees Celsius (100.4 degrees Fahrenheit ) measured rectally (in the anus)
37.5 degrees Celsius (99.5 degrees Fahrenheit ) measured orally (in the mouth)
37.2 degrees Celsius (99 degrees Fahrenheit ) measured in an axillary position (under the arm)

One model for the mechanism of fever is the detection of lipopolysaccharide (LPS), which is a cell wall component of 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 cytokine factors, such as interleukin 1, interleukin-6, and the tumor necrosis factor-alpha. These cytokine factors are released into general circulation where they migrate to the circumventricular organs of the brain, where the blood-brain barrier is reduced. The cytokine factors bind with endothelial receptors on vessel walls, or interact with local microglial cells. When these cytokine factors bind, they activate the arachidonic acid pathway. This pathway (as it relates to fever), is mediated by the enzymes phospholipase A2 (PLA2), cyclooxygenase-2 (COX-2), and PGE2 synthase (membrane-associated protein involved in eicosanoid and glutathione metabolism, also known as mPEGS-1). These enzymes ultimately mediate the synthesis and release of prostaglandin E2 (PGE2).

PGE2 is the ultimate mediator of the febrile response. It acts near the ventromedial preoptic area (VMPO) of the anterior hypothalamus and the parvocellular portion of the periventricular nucleus (PVH), where the thermal properties of fever emerge. It is presumed that the elevation in thermoregulatory set-point is mediated by the VMPO, whereas the neuroendocrine effects of fever are mediated by the PVH, pituitary gland, and various endocrine organs. Other heat effector mechanisms are mediated by the brain stem/medullary premotor sympathetic activation to the autonomic nervous system, which ultimately leads to the activation of brown adipose tissue. The body can also induce shivering, or raise blood pressure through a mechanism of vasoconstriction.

The set-point temperature of the body will remain elevated until PGE2 is no longer present (something that is likely to follow the disappearance of the foreign pathogen).

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Types

Pyrexia can be classed as low-grade, 38 - 39 °C (99.5 - 102.2 °F), moderate, 39 - 40 °C (102.2 - 104 °F), or high-grade (more than 40 °C or 104 °F) depending on how much the body temperature has deviated from normal.

Fever may be of benefit and is part of the body's response to a disease; however, if the fever goes above 42 °C (107.6 °F), then it may cause significant tissue damage. This is termed hyperpyrexia. 43.3^oC (110^oF) is considered the upper limit compatible with life.

Temperature normally fluctuates over the day, and the same applies to fever. If this characteristic pattern is lost, the raised body temperature may be due to hyperthermia, a more dangerous disorder. Hyperthermia is commonly caused by overheating or sunstroke, which elevates the body's temperature above the thermoregulatory set-point.

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References

Primary Sources

Cao, C., Matsumura, K., Yamagata, K., and Watanabe, Y., (1996) Endothelial cells of the rat brain vasculature express cyclooxygenase-2 mRNA in response to systemic interleukin-1B: a possible site of prostaglandin synthesis responsible for fever. Brain Res 733, 263-272.
Castellani JW, Young AJ, Sawka MN, Pandolf KB.(1998) Human thermoregulatory responses during serial cold-water immersions. J Appl Physiol, 85(1), 204-209.
Feng, JD, Price M, Cohen J, and Satinoff E. (1989) Prostaglandin fevers in rats: regulated change in body temperature or change in regulated body temperature? Am J Physiol Regulatory Integrative Comp Physiol 257: R695-R699.
Jakobsson, P. J., Thoren, S, Morgenstern, R., and Samuelsson B. (1999) Identification of human prostaglandin E synthase: A microsomal, glutathione-dependent, inducible enzyme, constituting a potential novel drug target. Proc Natl Acad Sci U S A. 96, 7220-7225
Milton, A. S. & Wendlandt, S. (1970). A possible role for prostaglandin E1 as a modulator for temperature regulation in the central nervous system. J Physiol, 207(2), 76P-77P.
Milton, A. S. & Wendlandt, S. (1971) Effects on body temperature of prostaglandins of the A, E and F series on injection into the third ventricle of unanaesthetized cats and rabbits. J Physiol, 218, 325-336.
Opp M. R. & Krueger J. M. (1991) Interleukin 1-receptor antagonist blocks interleukin 1-induced sleep and fever. Am J Physiol, 260(2), R453-R457.
Scammell, T. E., Elmquist, J. K., Griffin, J. D., & Saper, C. B., (1996) <i>Ventromedial preoptic prostaglandin E2 activates fever-producing autonomic pathways. J Neurosci, 16(19), 6246-6254.
Scammel., T. E., Griffin, J. D., Elquist, J. K. and Saper C. B. (1998) Microinjection of a cyclooxygenase inhibitor into the anteroventral preoptic region attenuates LPS fever. Am J Physiol Regulatory Integrative Comp Physiol. 274 (3), R783-R789.
Vane, J. R. & Flower, R. J. (1972) Inhibition of prostaglandin synthetase in brain explains the anti-pyretic activity of paracetamol (4-Acetamidophenol).</i> Nature, 240, 410-411.

Secondary Sources

Engblom, D., Ek, M., Saha, Sipra, S., Ericsson-Dahistrand, A., Jakobsson P.J., Blomqvist, A (2002) Prostaglandins as inflammatory messengers across the blood-brain barrier. J Mol Med, 80, 5-15.
Moltz, H. (1993). Fever: causes and consequences. Neurosci Biobehav Rev. 17(3), 237-69
Waag T, Hesselberg O, Reinertsen RE. (1995) <i>Heat production during cold water immersion: the role of shivering and exercise in the development of hypothermia. Arctic Med Res. 54(2), 60-64.

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