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Spaulding
Lithium effects on the thyroid glandSpaulding SW in Environmental Goitrogens by E Gaitan,1989, pp 149-157.
"Lithium is concentrated by the thyroid up to five times above serum concentrations; the concentration of lithium within the follicular lumen appears to be the same as that within the follicular cell. The best recognized effect of lithium on the thyroid is to inhibit hormone release, but the precise mechanism is not understood.... Although lithium can reduce the rate of iodine uptake in rat thyroid, Li+ also blocks the release of iodide from the gland. Since elevated intrathyroidal levels of iodide inhibit hormone release, this enhanced retention of I may partially explain why lithium inhibits thyroid hormone release in the rat."
"Lithium may also affect the peripheral metabolism of thyroid hormone, and is known to prolong the half-life of thyroxine in thyrotoxic patients."
"The normal pituitary responds to a fall in thyroid hormone levels by releasing more TSH, and in fact, TSH levels have been reported to be elevated in about one third or patients following institution of lithium therapy. An exaggerated response to TRH can be demonstrated even more frequently. Interestingly, the pituitary and hypothalamus also may accumulate lithium. Because of the major inhibitory effect of lithium on the secretion of hormone from the thyroid gland, it has been difficult to assess the possibility that lithium has additional effects at the hypothalamic pituitary level. It is clear that lithium does affect the metabolism of many neurotransmitters in the brain."
"The clinical incidence of goiter in patients treated with lithium depends both upon the detection methods used and upon the underlying population, but is generally 5 to 10%. Such factors as the level of dietary iodine, the ingestion of goitrogens, as well as genetic predispositions to goiter and the prevalence of thyroiditis may all influence the susceptibility to lithium-induced goiter. When goiter does occur, it is usually observed during the first few months of lithium therapy and it then often diminishes in size, suggesting that tachyphylactic processes are occurring.... Elevations in serum TSH levels presumably cause the thyroid to hypertrophy to compensate for the initial inhibition of thyroid hormone secretion."
"As with goiter, the prevalence of clinical hypothyroidism following lithium therapy is also quite variable. A recent summary of the many collections of cases reported in the literature suggest that, on average about 5% of patients receiving lithium become chemically hypothyroid.... In most patients, such chemical evidence of hypothyroidism is only observed transiently, so it appears that most normal thyroids can adapt homeostatically. Females are affected five times more frequently than males. Hypothyroidism may develop more frequently in populations with high circulating levels of iodine or with underlying Hashimoto's disease."
"Patients on lithium have an increased prevalence of auto-antibodies, up to one third having antithyroid antibodies."
"The only treatment available for lithium overdosage is the promotion of lithium excretion. Lithium decreases renal reabsorption of sodium, and if sodium depletion is present, it will aggravate lithium toxicity, so it is important to replete sodium stores."
"Cabbage, kale, chard, spinach, onion, and radish are foodstuffs in which relatively high levels of lithium have been reported."
"Lithium, and possibly cobalt and manganese as well, are elements that can be probably regarded as minor potential environmental goitrogens by themselves, even in areas where the natural soil and/or ground water levels are elevated. Rather than considering lithium individually, however, it is probably more important to think of lithium as an agent that may potentiate the action of other goitrogenic agents, as in the reported effects of lithium in rats on a low iodine, low protein diet. Another obvious clinical example is the co-ingestion of iodide and lithium: several reports suggest that the presence of these two agents may potentiate their antithyroidal effects, particularly if thyroiditis is also present. It should be noted that several of the plants that can have high lithium content also contain other goitrogens, and such interactions should be considered in assessing a food's goitrogenic potential."
Effect of increased iodide intake on thyroid function in subjects on chronic lithium therapy.Spaulding SW, Burrow GN, Ramey JN, Donabedian RK. Acta Endocrinol (Copenh). 1977 Feb;84(2):290-6. [abstract only]
"Thyroid function tests were obtained in 10 patients on chronic lithium therapy before and after the administration of potassium iodide 250 mg q.i.d. Mean serum TSH rose by 8.9 muU/ml and mean serum T3 rose from 70 to 101 ng/dl. Two patients became hypothyroid; a third showed a rise in TSH without any change in T3 or T4. A fourth patient developed hyperthyroidism probably secondary to the Jod-Basedow phenomenon. Pharmacologic doses of iodine should be administered with caution to patients on chronic lithium therapy."
The inhibitory effect of lithium on thyroid hormone release in both euthyroid and thyrotoxic patients.Spaulding SW, Burrow GN, Bermudez F, Himmelhoch JM. J Clin Endocrinol Metab. 1972 Dec;35(6):905-11. [citation only]
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