Inhibitory Effect of Lithium on the Release of Thyroid Hormones from Thyrotropin-Stimulated Mouse Thyroids in a Perifusion System*

Mori, Misuzu; Tajima, Koji; Oda, Yasuo; Matsui, Ikuko; Mashita, Kazuhiko; Tarui, Seiichiro

doi:10.1210/endo-124-3-1365

Cited by 38 publications

(18 citation statements)

References 14 publications

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“…[8][9][10] Lithium increases retention of 131 I in the thyroid. 8,11 Furthermore, because of its inhibitory effects on thyroid hormone release, 11,12 lithium may attenuate the initial rise in circulating thyroid hormones that occurs following RAI administration. [13][14][15] However, to date, it has not been clearly demonstrated that adjuvant lithium actually improves RAI efficacy.…”

Section: Introductionmentioning

confidence: 99%

Adjuvant lithium improves the efficacy of radioactive iodine treatment in Graves' and toxic nodular disease

Martin

Patel

Nijher

et al. 2012

Clinical Endocrinology

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SummaryContext Lithium increases iodine retention in the thyroid gland and inhibits thyroid hormone release. Although lithium has been reported to improve the efficacy of radioactive iodine (RAI) treatment in Graves' disease, its role as an adjunct to RAI treatment of hyperthyroidism, particularly in toxic nodular disease, remains contentious. Objective To assess whether adjuvant lithium increases the efficacy of a fixed dose RAI regimen in Graves' and toxic nodular hyperthyroid patients. Design and setting Retrospective cohort study in a tertiary referral centre. Two hundred and four hyperthyroid patients (163 Graves' disease, 26 toxic multinodular goitre and 15 solitary toxic thyroid adenoma). Intervention One hundred and three patients received RAI alone (median dose 558 MBq). One hundred and one patients received RAI (median dose 571 MBq) with adjuvant lithium (800 mg/day for 10 days). Main outcome measure Proportion of patients cured at any time over a 1-year period following RAI treatment. Cure was defined as sustained (two or more sequential time points) biochemical euthyroidism or hypothyroidism during the follow-up period.Results The likelihood of cure at any time was 60% greater in all hyperthyroid patients (Graves' plus toxic nodular disease) receiving adjuvant lithium (n = 204, P = 0·003). In patients with Graves' disease receiving RAI + lithium, there was a similar occurrence in cure (n = 163, P = 0·006). Cure was twice as likely in patients with toxic nodular (non-Graves') disease receiving RAI + lithium compared with RAI alone (n = 41, P = 0·01). Conclusions This study supports the use of adjuvant lithium to improve the efficacy of RAI in the treatment of Grave's disease and suggests a novel role in the management of toxic nodular (non-Graves') disease.

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Section: Introductionmentioning

confidence: 99%

Adjuvant lithium improves the efficacy of radioactive iodine treatment in Graves' and toxic nodular disease

Martin

Patel

Nijher

et al. 2012

Clinical Endocrinology

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“…Lazarus et al 1981). Lithium has been found to inhibit TSH-stimulated thyroid hormone release from thyroid tissue in vitro (Williams et al 1971, Mori et al 1989. Lithium-induced resistance to TSH can be demonstrated in pig thyroid cells where 1 mM inhibits TSH-stimulated cAMP accumulation within 30 min (Wragg & Mac Neil 1991).…”

Section: Introductionmentioning

confidence: 99%

Differential effect of thyroid-stimulating hormone (TSH) on intracellular free calcium and cAMP in cells transfected with the human TSH receptor

Metcalfe¹,

Findlay²,

Robertson³

et al. 1998

Journal of Endocrinology

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The thyroid-stimulating hormone (TSH) binds to a receptor which activates adenylate cyclase and elevates cAMP concentration. In addition, effects of TSH on intracellular calcium and inositol phosphate accumulation have been reported. However, the mechanism of TSH-stimulated accumulation of inositol phosphates and elevation of calcium levels is unresolved. Previous work from this laboratory has shown TSH to cause acute transient increases in intracellular calcium in pig, human and FRTL-5 rat thyroid cells as well as in cells transfected with the human TSH receptor ( JPO9 cells) in some (but not all) experiments. The aim of this study was to investigate the variability of the calcium response to TSH in JPO9 cells to learn more about the nature of this calcium signal induction. Calcium responses to TSH were determined using the fluorochrome fura-2 in both monolayers of adherent cells and adherent single cells. The responses to a single addition and to repetitive additions of TSH were compared. We also determined the cAMP response to TSH using these two protocols of TSH addition.Our data show that, whereas the cAMP response to TSH is highly predictable and consistent and does not require multiple exposures to TSH, cells were unlikely to respond to TSH with an increase in calcium unless they received multiple challenges with the hormone. A single addition of 10 mU/ml TSH failed to increase calcium in any of 40 single cells examined and in only 4 of 15 monolayers of cells (27%) examined; in contrast, 10 of 12 monolayers eventually responded with an increase in calcium after multiple exposure to TSH and 18 of 67 single cells. Similar data were obtained whether calcium was measured in single cells or in populations of cells. We also demonstrated cooperativity between an adenosine derivative, N 6 -(-2-phenylisopropyl)adenosine, and TSH such that their co-administration resulted in a consistent and marked elevation in calcium levels not achieved with either agonist alone. In summary, we suggest that the coupling between the TSH receptor and the intracellular signalling system that leads to activation of intracellular calcium in JPO9 cells requires repetitive stimulation or the influence of other agonists, in contrast with the coupling between the TSH receptor and activation of the adenylate cyclase enzyme.

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“…Valle et al (10) have also reported hypothyroidism from biochemical, haematologic, histometric and ultrastructural changes of the thyroid gland after lithium treatment in adult rats. Serum T 3 and T 4 levels are declined in rats (31,32) and in patients with unipolar depression (33). A significant decrease in FT 4 and FT 3 has also been reported after lithium treatment in male rats.…”

Section: Discussionmentioning

confidence: 99%

Inhibitions of thyroidal and extra-thyroidal T3, T4 and thyroperoxidase profiles with elevations of TSH following lithium treatment in adult and aged rats

Maiti¹

2010

Acta Endo (Buc)

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Background. Lithium, a well known antimanic drug, has adverse effects on endocrine functions; but it is unknown in aged animals.Aim. Untoward effects of lithium on thyroidal and extra-thyroidal thyroid hormones were investigated in adult and aged rats.Materials and methods. Lithium was injected intraperitoneally at a dose of 2 mEq/kg body weight daily to one group of rats for 10 days and the other for 25 days respectively. Thyroid and serum T 3 and T 4 , and extrathyroidal liver and kidney T 3 and T 4 levels were measured by ELISA. Pituitary and serum TSH-like substance was determined using a human -TSH immunoassay kit. Thyroperoxidase profile was measured spectrophotometrically.Results. Lithium decreased thyroid and serum T 3 and T 4 levels, and increased pituitary and serum TSH-like profiles after 10 and 25 days of treatments respectively in adult and aged rats. Thyroperoxidase activity was decreased in all the treatments of adult and aged rats. Liver and kidney T 3 and T 4 profiles were also decreased in lithium recipients. Lithium actions were severe after 10 days of treatment in adult rats and 25 days treatment in aged rats.Conclusion. Lithium has untoward effects on thyroid and extra-thyroidal thyroid hormone synthesis irrespective of the age of rats.

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Inhibitory Effect of Lithium on the Release of Thyroid Hormones from Thyrotropin-Stimulated Mouse Thyroids in a Perifusion System*

Cited by 38 publications

References 14 publications

Adjuvant lithium improves the efficacy of radioactive iodine treatment in Graves' and toxic nodular disease

Adjuvant lithium improves the efficacy of radioactive iodine treatment in Graves' and toxic nodular disease

Differential effect of thyroid-stimulating hormone (TSH) on intracellular free calcium and cAMP in cells transfected with the human TSH receptor

Inhibitions of thyroidal and extra-thyroidal T3, T4 and thyroperoxidase profiles with elevations of TSH following lithium treatment in adult and aged rats

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