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The Inhibitory Effect of Lithium on Thyroid Hormone Release in Both Euthyroid and Thyrotoxic Patients
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1972
Year
T4 ReleaseMedicinePhysiologyLithium TherapyThyroid DiseaseParathyroid HormoneThyrotoxic PatientsThyroid Hormone ReleaseThyroid DisordersParathyroid GlandThyroid HormoneBoth EuthyroidEndocrinologyPharmacologyHormone Release
Previous studies suggesting that lithium inhibits thyroid hormone release in thyrotoxic patients have been based on epithyroid counting or single isotope studies, both of which have technical limitations. To obviate these difficulties, we injected patients with 125Iā to prelabel the thyroid, and then injected 131I-T4 to account for T4 degradation. The rate of T4 release was determined by the semilog plot of both the PB125I/131I ratio and the PB127I/131I ratio vs time in five euthyroid and six thyrotoxic patients. Lithium carbonate therapy (900 mg q.i.d.) was given for five days following a five-day control period. Peak serum lithium concentration ranged from 0.39ā1.45 mEq/1. At the end of lithium treatment, the mean serum PBI had dropped 18% (p = .05) from the mean pre-treatment value in the thyrotoxic patients and was unchanged in the controls. There was a significant decrease in the mean rate of disappearance of exogenous 131I-T4 during lithium treatment, both in the hyperthyroid 36% (p < .005) and euthyroid subjects, 31% (p < .01). The mean regression coefficient for PB125I/131I fell by 60% (p < .005) during lithium therapy in thyrotoxic patients and by 43% (p < .01) in control patients, indicating an inhibition of thyroidal hormone release. Similarly, the PB127I/131I slope fell by 54% (p < .01) in the hyperthyroid patients and 357% (p < .02) in the controls. The findings presumably reflect the fact that lithium blocks the release of hormone from the thyroid gland in both normal and hyperthyroid patients, although the latter seem more sensitive to this effect.