Use of Massive Doses of Vitamin a in the Treatment of Hyperthyroidism

Simkins, Samuel

doi:10.1210/jcem-7-8-574

Cited by 44 publications

(4 citation statements)

References 23 publications

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“…In non-transformed rat FRTL-5 cells, 1 mM all-trans retinoic acid (RA) down-regulated NIS mRNA and protein levels, inhibited the TSH-or forskolintriggered induction of NIS message after TSHdepletion, and reduced iodide uptake to 38% after 5 days. This observation may explain the early observation that high doses of vitamin A, the biologically active metabolite of which is RA, can reduce thyroid hormone levels in experimental animals or even relieve symptoms of hyperthyroidism in patients (Garcin et al, 1984;Simkins, 1947). Recently, also central inhibitory effects of retinoids on the hypophyseal-thyroidal axis have been described.…”

Section: Thyroid Cell Linesmentioning

confidence: 91%

Regulation of the sodium/iodide symporter by retinoids - a review

Schmutzler¹

2001

Exp Clin Endocrinol Diabetes

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Decrease or loss of iodide uptake, due to impaired expression and/or function of the sodium/iodide-symporter (NIS), is a major obstacle to the treatment of advanced thyroid carcinomas by radioiodide therapy. Several approaches are being evaluated to optimise or restore sufficient iodide transport in those cases, among them retinoid therapy. Retinoids with their growth-inhibiting and differentiation-inducing properties have been repeatedly used for treatment and chemoprevention of various cancers. In thyroid carcinoma cell lines they trigger changes in gene expression that may be interpreted as partial redifferentiation. Especially, they stimulate NIS mRNA expression and iodide uptake in human follicular thyroid carcinoma cells. Moreover, they also increase NIS expression and function in human mammary tumour cells. In a clinical pilot study to evaluate the feasibility of retinoid redifferentiation in the case of otherwise untreatable thyroid cancers, 21 of 50 patients showed an increase of radioiodide uptake after 5 weeks. This indicates that increasing NIS activity and radioiodide uptake by retinoic acid redifferentiation may be a therapeutic alternative for thyroid cancers refractory to other therapeutic modalities and probably also for mammary cancer.

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Section: Thyroid Cell Linesmentioning

confidence: 91%

Regulation of the sodium/iodide symporter by retinoids - a review

Schmutzler¹

2001

Exp Clin Endocrinol Diabetes

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“…In 1947, Simkins described the use of high doses of vitamin A (retinol) for the treatment of hyperthyroidism [56]. Through extensive conversion in vivo, retinol is modified to retinaldehyde, all-trans retinoic acid, and finally 13-cis and 9-cis retinoic acid, which are known to activate genes through the RAR and RXR pathways.…”

Section: Safety Of Rexinoids As Therapeutic Agentsmentioning

confidence: 99%

Therapeutic Potential of Retinoid X Receptor Modulators for the Treatment of the Metabolic Syndrome

Pinaire

Reifel‐Miller

2007

PPAR Research

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The increasing prevalence of obesity is a fundamental contributor to the growing prevalence of the metabolic syndrome. Rexinoids, a class of compounds that selectively bind and activate RXR, are being studied as a potential option for the treatment of metabolic syndrome. These compounds have glucose-lowering, insulin-sensitizing, and antiobesity effects in animal models of insulin resistance and type 2 diabetes. However, undesirable side effects such as hypertriglyceridemia and suppression of the thyroid hormone axis also occur. This review examines and compares the effects of four RXR-selective ligands: LGD1069, LG100268, AGN194204, and LG101506, a selective RXR modulator. Similar to selective modulators of other nuclear receptors such as the estrogen receptor (SERMs), LG101506 binding to RXR selectively maintains the desirable characteristic effects of rexinoids while minimizing the undesirable effects. These recent findings suggest that, with continued research efforts, RXR-specific ligands with improved pharmacological profiles may eventually be available as additional treatment options for the current epidemic of obesity, insulin resistance, type 2 diabetes, and all of the associated metabolic sequelae.

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“…An association between vitamin A and thyroid hormones has been known since the 1940s. 1 Investigators observed an increase in thyroid hormones in the serum of vitamin A-depleted rats 2 and, conversely, a signi cant decrease in the serum thyroid hormones triiodothyronine (T 3 ) and tetraiodothyronine (T 4 ) in rats fed excess vitamin A. 3 The anterior pituitary gland was implicated because vitamin A-de cient rats also showed increased serum levels of the anterior pituitary thyroid-stimulating hormone (TSH).…”

Section: The Regulation Of the Thyroid-stimulating Hormone Of The Antmentioning

confidence: 99%