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'''Hypokalemic periodic paralysis''' ('''hypoKPP'''), also known as '''familial hypokalemic periodic paralysis''' ('''FHPP'''),<ref>{{Cite book|title=Harrison's principles of internal medicine|publisher=|others=Jameson, J. Larry; Kasper, Dennis L.; Longo, Dan L. (Dan Louis), 1949-; Fauci, Anthony S., 1940-; Hauser, Stephen L.; Loscalzo, Joseph|date=13 August 2018|isbn=978-1-259-64403-0|edition=20th|location=New York|pages=307|oclc=1029074059}}</ref> is a rare, [[autosomal dominant]] [[channelopathy]] characterized by muscle weakness or paralysis when there is a fall in [[potassium]] levels in the [[blood]]. In individuals with this mutation, attacks sometimes begin in [[adolescence]] and most commonly occur with individual triggers such as rest after strenuous exercise (attacks during exercise are rare), high [[carbohydrate]] meals, meals with high [[sodium]] content, sudden changes in temperature, and even excitement, noise, flashing lights, cold temperatures and stress. Weakness may be mild and limited to certain muscle groups, or more severe full-body paralysis. During an attack, reflexes may be decreased or absent. Attacks may last for a few hours or persist for several days. Recovery is usually sudden when it occurs, due to release of potassium from swollen muscles as they recover. Some patients may fall into an abortive attack or develop chronic muscle weakness later in life.
Some people only develop symptoms of periodic paralysis due to [[hyperthyroidism]] (overactive [[thyroid]]). This entity is distinguished with [[thyroid function test]]s, and the diagnosis is instead called [[thyrotoxic periodic paralysis]].<ref>{{cite journal |author=Kung AW |title=Clinical review: Thyrotoxic periodic paralysis: a diagnostic challenge |journal=J. Clin. Endocrinol. Metab. |volume=91 |issue=7 |pages=2490–5 |date=July 2006 |pmid=16608889 |doi=10.1210/jc.2006-0356 |url=http://jcem.endojournals.org/cgi/content/full/91/7/2490|doi-access=free }}</ref>
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