Lithium hypothyroidism from

In a review of lithium-induced subclinical hypothyroidism (TSH over 5 mU/1, free thyroxine normal), a prevalence of up to 23% in lithium patients was contrasted with up to 10% in the general population. It was stressed that subclinical hypothyroidism from any cause can be associated with subtle neuropsychiatric symptoms, such as depression, impaired memory and concentration, and mental slowing and lethargy, as well as with other somatic symptoms. Management guidelines were discussed (628). 

Lithium carbonate, administered for affective and bipolar disorders, may enhance the effects of antithyroid drugs. Potassium iodide, used as an expectorant, is a major ingredient in many cough medications. Iodide derived from this source may enhance the effects of antithyroid drugs and lead to iodine-induced hypothyroidism. Iodine in topical antiseptics and radiological contrast agents may act in a similar manner. 

Lithium Plus Thyroid Supplementation. Treatment-resistant and rapid-cycling bipolar patients may have an increased frequency of thyroid dysfunction. Further, some patients suffer from subclinical hypothyroidism and improve with the addition of thyroid supplementation. In this context, several case reports involving this population found that high doses of the thyroid hormone levothyroxine sodium (T ) were clinically beneficial (122,123 and 124). Kusalic (1.25) found that 6 of 10 rapid cyclers had hypothyroidism, based on their thyrotropin-releasing hormone stimulation tests. Further, the average number of mood episodes per year decreased by more than 75% (i.e., from 9.7 to 2.2) after thyroxine was added to the treatment regimen. 

Because lithium affects second-messenger systems involving both activation of adenylyl cyclase and phosphoinositol turnover, it is not surprising that G proteins are also found to be affected. Several studies suggest that lithium may uncouple receptors from their G proteins indeed, two of lithium s most common side effects, polyuria and subclinical hypothyroidism, may be due to uncoupling of the vasopressin and thyroid-stimulating hormone (TSH) receptors from their G proteins. 

In 1989, in 150 patients at different stages of lithium therapy, thyroid function was assessed and subsequently 118 were reassessed at least once and 54 completed a 10-year follow-up (625). The annual rates of new cases of thyroid dysfunction were subclinical hypothyroidism 1.7%, goiter 2.1%, and autoimmunity 1.4%. While these figures were little different from those found in the general population, the authors acknowledged that lithium was a potential cause of thyroid dysfunction. 

In 1705 patients, aged 65 years or over, who had recently started to take lithium, identified from the 1.3 million adults in Ontario receiving universal health care coverage, the rate of treatment with thyroxine was 5.65 per 100 person-years, significantly higher that the rate of 2.70/100 person-years found in 2406 new users of valproate (629). Of 46 adults taking lithium in a psychiatric clinic, 17% developed overt hypothyroidism while 35% had subclinical hypothyroidism (raised concentrations of thyroid stimulating hormone, TSH) (630). 

When 22 men and 38 women who had taken lithium for at least a year (mean 6.9 years) for bipolar disorder were evaluated for adverse effects, hypothyroidism requiring thyroid supplementation was found in 16 (14 women and 2 men) 9 had a goiter (637). The area from which some of the patients came was known to have a high background incidence of thyroid dysfunction. 

As discussed above, hthium inhibits the synthesis of thyroid hormone and its release from the thyroid, and stimulates the formahon of antithyroid anhbodies in susceptible subjects [122]. Lithium-induced hypothyroidism responds to thyroxine therapy. Lithium... 

Thyroid hormones are frequently affected by lithium, but rarely in a clinically significant way. Changes in certain laboratory tests of thyroid function are common but seldom require discontinuation of treatment. However, approximately 5 percent of patients develop hypothyroidism, which some clinicians elect to treat with thyroid supplementation while continuing lithium (Weber, Saklad, and Kastenhol 1992). Periodic thyroid function monitoring is important, not only from a safety standpoint but to rule out (in the bipolar individual with depressed or mixed-state features), that hypothyroidism is not the cause of symptoms. 

Lithium carbonate is used in the treatment of manic depressive illnesses. The exact mechanism of its action is not known but it may interfere with cyclic-AMP mediated processes. The level of the drug in the blood must be monitored periodically as toxic reactions (tremors, diarrhoea, vomitting and drowsiness) can result from overdosage. Recently it has been found that lithium inhibits thyroxine biosynthesis and this may lead to hypothyroidism. 

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