Novel etiopathophysiological aspects of thyrotoxic periodic paralysis

Novel etiopathophysiological aspects of thyrotoxic periodic paralysis

Author Maciel, Rui M. B. Autor UNIFESP Google Scholar
Lindsey, Susan C. Autor UNIFESP Google Scholar
Dias da Silva, Magnus R. Autor UNIFESP Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Abstract Thyrotoxicosis can lead to thyrotoxic periodic paralysis (TPP), an endocrine channelopathy, and is the most common cause of acquired periodic paralysis. Typically, paralytic attacks cease when hyperthyroidism is abolished, and recur if hyperthyroidism returns. TPP is often underdiagnosed, as it has diverse periodicity, duration and intensity. the age at which patients develop TPP closely follows the age at which thyrotoxicosis occurs. All ethnicities can be affected, but TPP is most prevalent in people of Asian and, secondly, Latin American descent. TPP is characterized by hypokalemia, suppressed TSH levels and increased levels of thyroid hormones. Nonselective beta adrenergic blockers, such as propranolol, are an efficient adjuvant to antithyroid drugs to prevent paralysis; however, an early and definitive treatment should always be pursued. Evidence indicates that TPP results from the combination of genetic susceptibility, thyrotoxicosis and environmental factors (such as a high-carbohydrate diet). We believe that excess T-3 modifies the insulin sensitivity of skeletal muscle and pancreatic beta cells and thus alters potassium homeostasis, but only leads to a depolarization-induced acute loss of muscle excitability in patients with inherited ion channel mutations. An integrated etiopathophysiological model is proposed based on molecular findings and knowledge gained from long-term follow-up of patients with TPP.
Language English
Sponsor Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Fleury Group
Date 2011-11-01
Published in Nature Reviews Endocrinology. New York: Nature Publishing Group, v. 7, n. 11, p. 657-667, 2011.
ISSN 1759-5029 (Sherpa/Romeo, impact factor)
Publisher Nature Publishing Group
Extent 657-667
Access rights Closed access
Type Review
Web of Science ID WOS:000296565200007

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