A Armond | PubMed Health

PubMed1985

A prospective study of the effects of lithium on thyroid function and on the prevalence of antithyroid antibodies.

Tests of thyroid function and pathology were carried out on 133 patients before they were treated with lithium (Li+). Of the 12 patients who subsequently became hypothyroid during treatment with lithium 9 had, before the commencement of treatment, thyroid autoantibodies and/or an exaggerated thyroid stimulating hormone (TSH) response to thyrotropin releasing hormone (TRH), whereas 3 patients had neither of these indicators. Lithium administration was accompanied by a rise in thyroid antibody titre in 20 patients but a fall in only 5, a statistically significant difference. Evidence that it may be an immunostimulant is discussed. Li+-induced thyroid failure cannot be accurately predicted, and may occur suddenly. The best minimum safeguard, therefore, is serial thyroxine (T4) (or free T4) estimation, supplemented if equivocal by a free thyroxine index (FTI), a basal TSH and, if doubt remains, by a TRH test.

Antibodies, Antinuclear↗

PubMed1981

Lithium continuation therapy following electroconvulsive therapy.

Thirty-eight depressed patients who were treated with ECT were randomly assigned to receive lithium therapy or identical-looking placebo tablets for one year after clinical recovery in a double-blind trial. The patients who received placebo tablets spent an average of 7.8 weeks with an episode of depression (either as in-patients or day-patients) during the year. In comparison, patients who received lithium spent on average 1.7 weeks with an episode (P less than 0.02). The trial confirms the high rate of relapses after ECT and suggests that lithium considerably reduces this morbidity. It is suggested that ECT without continuation therapy is not a satisfactory treatment of depressive illness.

Adult↗