[Hyperparathyroidism induced by lithium. A new case].

INTRODUCTION

Lithium salts, used for the first time in 1949, had proved to be a highly effective preventive measure in bipolar illness. The first report of lithium-induced hyperparathyroidism was suggested by Garfinkel et al. in 1973. About 40 cases have been reported since, suggesting an enhancement of occurrence of hyperparathyroidism in patients cured by lithium carbonate. We report here a new case discovered by a systematic measurement of calcemia after a surgical intervention for a hip joint prosthesis.

EXEGESIS

Unusual metabolic features associated with this case of hyperparathyroidism include low urinary calcium excretion, normal cyclic AMP excretion and lack of calcic nephrolithiasis. The mechanism probably results from lithium linking with the calcium receptor on the parathyroid and then stimulating PTH secretion. In the same way it could enhance the tubular reabsorption of urinary calcium. Lithium withdrawal is often inefficient in clinical and laboratory test abnormalities and surgery is usually required.

CONCLUSION

It is very important to recognise this particular secondary effect of lithium therapy because clinical symptoms of hypercalcemia can simulate a worsening of the bipolar illness.