Mechanism of thyrotoxic periodic paralysis

Shih Hua Lin, Chou Long Huang

Research output: Contribution to journalShort surveypeer-review

85 Scopus citations


The pathogenesis of thyrotoxic periodic paralysis has long been thought related to increasedNa+-K + ATPase activity stimulated by thyroid hormone and/or hyperadrenergic activity and hyperinsulinemia. This mechanism alone, however, cannot adequately explain how hypokalemia occurs during acute attacks or the associated paradoxical depolarization of the resting membrane potential. Recent findings that loss of function mutations of the skeletal muscle-specific inward rectifying K + (Kir) channel, Kir2.6, associatewith thyrotoxicperiodicparalysisprovide newinsights intohowreduced outwardK + efflux in skeletal muscle, from either channel mutations or inhibition by hormones (adrenalin or insulin), can lead to a vicious cycle of hypokalemia and paradoxical depolarization, which in turn, inactivates Na + channels and causes muscle unexcitability and paralysis.

Original languageEnglish (US)
Pages (from-to)985-988
Number of pages4
JournalJournal of the American Society of Nephrology
Issue number6
StatePublished - Jun 2012

ASJC Scopus subject areas

  • Nephrology


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