In vivo and in vitro sodium pump activity in subjects with thyrotoxic periodic paralysis.

Chan, Angus C.W.; Shinde, Rituparna S.; Chow, C. C.; Cockram, Clive S.; Swaminathan, R.

doi:10.1136/bmj.303.6810.1096

Cited by 150 publications

(96 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…6 The important role of Na + -K + ATPase pumps in the pathogenesis of TPP is supported by the finding that their activity in the skeletal muscle is significantly increased. 7 Thyroid hormone can stimulate Na + -K + ATPase in skeletal muscle by genomic mechanism, acting on the thyroid hormone responsive elements to upregulate the transcription of the gene encoding Na + -K + ATPase, and through nongenomic mechanisms by enhancing the intrinsic activity or promoting membrane insertion of the pump. Hyperthyroidism may also enhance the stimulation of pump activity by b 2 -adrenergic agonists by amplifying the production of intracellular cAMP.…”

Section: Diagnosis and Management Of Tppmentioning

confidence: 99%

Mechanism of Thyrotoxic Periodic Paralysis

Lin

Huang

2012

Journal of the American Society of Nephrology

133

121

View full text Add to dashboard Cite

The pathogenesis of thyrotoxic periodic paralysis has long been thought related to increased Na + -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, associate with thyrotoxic periodic paralysis provide new insights into how reduced outward K + 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.

show abstract

Section: Diagnosis and Management Of Tppmentioning

confidence: 99%

Mechanism of Thyrotoxic Periodic Paralysis

Lin

Huang

2012

Journal of the American Society of Nephrology

133

121

View full text Add to dashboard Cite

show abstract

“…Hypokalaemia occurs due to intracellular shift of potassium rather than true potassium depletion. It is likely due to increased sodium-potassium adenosine triphosphate pump activity (Na-K ATPase), which may be upregulated due to the direct effects of thyroid hormone or indirectly due to sympathetic overactivity 5 . Patients with TPP also appear to have an exaggerated insulin response to glucose/carbohydrate ingestion.…”

Section: Discussionmentioning

confidence: 99%

Thyrotoxic periodic paralysis in a Nigerian male

Vogazianou¹,

O'Shea²,

Hyatt³

et al. 2016

EJEA

View full text Add to dashboard Cite

“…The genetic factors could include a defect in one of the ion channels involved in excitation contraction coupling (Ca2+, Na+, and K+) or a defect in one of the channel's regulatory subunits. Alterations in one of these genes would be responsible for the generation of non-functional ion channels, which would define the TPP as an endocrine channelopathy [19,20]. The environmental factors include the excessive consumption of carbohydrate-rich foods, alcohol, or resting after intense exercise.…”

Section: Discussionmentioning

confidence: 99%