Abstract
Background: Lithium is frequently used in the treatment of bipolar affective disorder, and is widely known to affect thyroid function, most commonly resulting in hypothyroidism and goiter. Less well-known is the association between lithium therapy and hyperthyroidism and the potential for lithium to moderate the effects of thyroxine at a cellular level. Lithium excretion relates principally to glomerular filtration rate and proximal tubule function. Thyroxine, through its effects on tubular function, alters lithium clearance such that thyroid disease may cause retention of lithium and subsequent toxicity. Case Reports: We report 2 cases with lithium toxicity, both of whom were later found to be hyperthyroid. One patient developed thyroid storm following dialysis to remove lithium. The other received antithyroid medication early. Both suffered a protracted multifactorial delirium requiring intensive inpatient care. Conclusion: In addition to altering thyroid function, lithium therapy may mask the signs of hyperthyroidism by inducing cellular unresponsiveness. In some lithium-treated patients with biochemical hyperthyroidism, early antithyroid treatment may be appropriate. Altered renal tubular function induced by hyperthyroidism may result in retention of lithium and systemic toxicity. We propose induction of the proximal tubule sodium hydrogen antiporter as the relevant mechanism.