Novel etiopathophysiological aspects of thyrotoxic periodic paralysis

dc.contributor.authorMaciel, Rui M. B. [UNIFESP]
dc.contributor.authorLindsey, Susan C. [UNIFESP]
dc.contributor.authorDias da Silva, Magnus R. [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T14:17:25Z
dc.date.available2016-01-24T14:17:25Z
dc.date.issued2011-11-01
dc.description.abstractThyrotoxicosis 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.en
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Dept Biochem, BR-04039032 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Dept Med, Lab Mol & Translat Endocrinol, BR-04039032 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Dept Biochem, BR-04039032 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Dept Med, Lab Mol & Translat Endocrinol, BR-04039032 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipFleury Group
dc.format.extent657-667
dc.identifierhttp://dx.doi.org/10.1038/nrendo.2011.58
dc.identifier.citationNature Reviews Endocrinology. New York: Nature Publishing Group, v. 7, n. 11, p. 657-667, 2011.
dc.identifier.doi10.1038/nrendo.2011.58
dc.identifier.issn1759-5029
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/34205
dc.identifier.wosWOS:000296565200007
dc.language.isoeng
dc.publisherNature Publishing Group
dc.relation.ispartofNature Reviews Endocrinology
dc.rightsAcesso restrito
dc.titleNovel etiopathophysiological aspects of thyrotoxic periodic paralysisen
dc.typeResenha
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