Hypercalcemia in an euthyroid patient with secondary hypoadrenalism and diabetes insipidus due to hypothalamic tumor

A 20-year-old Japanese man with a hypothalamic tumor (most likely germ-cell tumor) which caused secondary hypoadrenalism, hypogonadism and diabetes in sipidus developed hypercalcemia and acute renal failure. The serum levels o f intact PTH (iPTH), PTH-related protein (PTH-rP), 1,25-dihydroxy vitamin D (1,25-(OH)(2) D), ACTH, cortisol, gonadotropins and testosterone were decr eased, but his serum levels of triiodothyronine (T-3) and thyroxine (T-4) w ere within the normal range at admission, with depressed TSH and slightly i ncreased thyroglobulin. The hypercalcemia was refractory to extensive hydra tion and calcitonin, but was ameliorated by pamidronate. After irradiation of the hypothalamic tumor, panhypopituitarism gradually developed. The pati ent has been normocalcemic for the last 2 years and is doing well under rep lacement therapy with glucocorticoid, L-thyroxine, methyltestosterone and 1 -desamino D arginine vasopressin (dDAVP). As to the mechanism of euthyroidi sm at admission, transient destructive thyroiditis associated with hypopitu itarism or delayed development of hypothyroidism following the hypoadrenali sm was suggested. This is the first reported case of hypercalcemia in secon dary hypoadrenalism due to hypothalamic tumor. Hypercalcemia was most likel y induced by increased bone resorption, which was probably elicited by the combined effects of deficient glucocorticoid and sufficent thyroid hormones in addition to hypovolemia and reduced renal calcium excretion. Furthermor e, severe dehydration due to diabetes insipidus and disturbance of thirst s ensation caused by the hypothalamic tumor aggravated the hypercalcemia, lea ding to acute renal failure.