Asymptomatic Graves' disease during lithium

The incidence of biochemical hypothyroidism has been estimated to be as high as 30% in patients taking lithium (Lazarus et al., 1981). There are several different mechanisms involved. Lithium has been shown to block release of thyroxine from the thyroid gland (Spaulding et al., 1972) and probably also directly inhibits thyrotrophin-stimulated adenyl cyclase in the thyroid gland. Lazarus et al. (1981) showed that 24% of patients on lithium had thyroid antibodies compared with 10%-14% of a normal population studied by Tunbridge et al. (1977). Weetman et al. (1981) demonstrated a rise in thyroid antibodies in patients treated with lithium and showed that lithium increased immunoglobulin synthesis. Furthermore, Hassman & Lazarus (1984) showed that lithium increased the severity of autoimmune thyroid disease by modification of the autoimmune process. Lithium thus not only inhibits the action of thyrotrophin and the release of thyroxine, but also interferes with the autoimmune process. Rosser (1976) and Rons et al. (1979) have reported cases of thyrotoxicosis occurring during lithium therapy though none showed convincing evidence of autoimmune disease as the aetiological factor. Schoenberg et al. (1979) reported Graves' disease manifesting after cessation of maintenance lithium. We report a case of a patient with Graves' disease occurring during lithium therapy but who remained free from symptoms until lithium was withdrawn. We would suggest that the antithyroid actions of lithium caused suppression ofthe symptoms ofthyrotoxicosis, and propose that lithium might have initiated the autoimmune disease in our patient. Case report