Triiodothyronine-induced Thyrotoxicosis Increases Mononuclear Leukocyte β-Adrenergic Receptor Density in Man

Ginsberg, Ann M.; Clutter, William E.; Shah, Suresh D.; Cryer, Philip E.

doi:10.1172/jci110218

Cited by 108 publications

(44 citation statements)

References 34 publications

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“…The usual mechanism is the export of cations created by the electrogenic Na C -K C -ATPase extruding three Na C ions for every two K C ions that enter the cells (20). Hyperthyroidism can induce an increase in the number and activity of the Na C -K C pump (21) and also increase b-adrenergic sensitivity (22), further enhancing the activity of the Na C -K C pump. Thyroid hormone per se increases cardiac contractility and output, and decreases systemic Laboratory findings Serum TSH (mU/ml) !0.03 !0.03 vascular resistance, accounting for the increased systolic hypertension (23).…”

Section: Discussionmentioning

confidence: 99%

Therapeutic analysis in Chinese patients with thyrotoxic periodic paralysis over 6 years

Shiang¹,

Cheng²,

Tsai³

et al. 2009

European Journal of Endocrinology

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Objective: To characterize the course of therapy in a large cohort of Chinese patients with thyrotoxic periodic paralysis (TPP), a reversible electrolyte emergency fraught with therapeutic challenges. Design and methods: In this prospective interventional study, 78 patients with TPP (75 males and three females with an age range of 16-48 years) were consecutively enrolled over a 6-year period. Intravenous KCl at a rate of 10 mmol/h was administered until muscle strength recovered. Serum potassium (K C ) and phosphorus concentrations were measured hourly during the paralytic attack and for 6 h after recovery. Results: The serum potassium (K C ) on attack was 2.1G0.2 mmol/l. The dose of KCl administered to restore muscle strength was 63G32 mmol, and peak serum K C concentration after recovery was 5.3G0.5 mmol/l. A paradoxical fall in serum K C concentration O0.1 mmol/l difference between presentation and treatment nadir was observed in approximately one-fourth of TPP patients (nZ20). These patients had significantly higher serum-free thyroxine concentration, systolic blood pressure, and heart rate on presentation, as well as serum phosphate concentration on recovery. They not only needed much more KCl supplementation (104G34 vs 48G19 mmol, P!0.001), but also had significantly more severe rebound hyperkalemia (5.8G0.5 vs 5.1G0.4 mmol/l, P!0.001) on recovery than those who did not have paradoxical hypokalemia. There was a positive correlation between the dose of KCl administered and the difference between peak and nadir serum K C (D K C ) (rZ0.68, P!0.001). Conclusions: TPP patients who do not develop paradoxical hypokalemia need a smaller KCl dose to achieve recovery, whereas those who develop paradoxical hypokalemia have more severe hyperthyroidism and hyperadrenergic activity and may require blockage of intracellular K C shift to prevent rebound hyperkalemia. European Journal of Endocrinology 161 911-916

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Section: Discussionmentioning

confidence: 99%

Therapeutic analysis in Chinese patients with thyrotoxic periodic paralysis over 6 years

Shiang¹,

Cheng²,

Tsai³

et al. 2009

European Journal of Endocrinology

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“…Estudios han encontrado polimorfismos de un único nucleótido en genes que codifican la bomba Na/K ATPasa, haciéndola más sensible a estímulos de hormonas tiroideas. La bomba Na/K ATPasa es activada directamente por las hormonas tiroideas e indirectamente por condiciones que se presentan en estado de tirotoxicosis como el aumento del tono adrenérgico mediado por el receptor b2 (14) y el hiperinsulinismo (17). Las hormonas tiroideas por sí mismas activan e incrementan la sensibilidad de los receptores beta adrenérgicos (18).…”

Section: Discussionunclassified

Parálisis períodica hipocalcémica tirotóxica

Pinzón

Vásquez

2014

Rev. Med.

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ResumenLa parálisis hipocalémica tirotóxica se consideró una patología exclusiva de Asia, pero las migraciones han permitido la trasmisión genética de la condición a América Latina. La entidad se presenta más frecuentemente en hombres y se relaciona a alteraciones en el transporte del potasio asociadas al exceso de hormonas tiroideas circulantes. Se realiza revisión de la literatura ilustrando el caso de un hombre de 29 años con enfermedad de Graves, parálisis hipocaliémica y falla respiratoria.Palabras claves: hipertiroidismo, hipocaliemia, parálisis periódica. THYROTOXIC HYPOKALEMIC PERIODIC PARALYSIS AbstractThyrotoxic hypokalemic paralysis was considered an exclusive disease of Asia, but migration has allowed genetic transmission of the condition to Latin America. The entity appears more frequently in men and is related to alterations potassium's transport, associated with increased circulating thyroid hormones. Literature review conducted illustrating the case of 29 years old man with Graves' disease, hypokalemic paralysis and respiratory failure.Keywords: hyperthyroidism, hypokalemia, periodic paralysis. PARALISIA PERIÓDICA HIPOCALÉMICA TIROTÓXICA ResumoA paralise hipocalémica tirotóxica considerou-se uma patologia exclusiva da Ásia, mais as migrações tem permitido a transmissão genética da condição para America Latina. A entidade apresenta-se freqüentemente em homens e relaciona-se com alterações no transporte do potássio associadas ao excesso da circulação de hormônios da tireóides. Se faz uma revisão da literatura com o caso de um homem de 29 anos com doença de graves, paralise hipocalémica e insuficiência respiratória.Palavras chave: hipertireoidismo, hipocalemia, paralise periódica.

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“…Hyperthyroidism may result in a hyperadrenergic state, which may lead to the activation of the Na+/K+-ATPase pump and result in cellular uptake of potassium (1,3,4) . Thyroid hormones may also directly stimulate Na+/K+-ATPase activity and increase the number and sensitivity of beta receptors (1,5) . Patients with TPP have been found to have hyperinsulinemia during episodes of paralysis.…”

Section: Pathophysiologymentioning

confidence: 99%