ESPE Abstracts

Cholestatic hepatitis and hypercalcemia are rare features of hypopituitarism in the newborn. So diagnosis of hypopituitarism is frequently delayed. Herein, we report a newborn that was investigated for cortisol deficiency and other pituitary hormone deficiencies and diagnosed with panhypopituitarism upon detection of cholestasis after referral to the endocrinology department for hypercalcemia, a very rare sign of cortisol deficiency. It is unclear which hormone causes cholestasis in patients with congenital panhypopituitarism. Some authors suggested that growth hormone deficiency is the major cause of cholestasis. But there is now good evidence that central adrenal insufficiency is the main cause of cholestatic hepatitis in hypopituitarism. Glucocorticoids were shown to augment bile flow in vitro as well as in rats and dogs. Hypercalcemia was reported in 5.5% of primary adrenocortical insufficiency in adults. The proportion of hypercalcemia is unknown in secondary adrenocortical insufficiency. Although the mechanism of hypercalcemia in adrenocortical insufficiency is unknown, lack of serum cortisol is considered to be related increased calcium reabsorbtion from renal tubules and release from bone. Herein, we report a newborn that was investigated for cortisol deficiency and other pituitary hormone deficiencies and diagnosed with panhypopituitarism upon detection of cholestasis after referral to the endocrinology department for hypercalcemia, a very rare sign of cortisol deficiency. Diagnosed with panhypopituitarism clinically and biochemically, the patient’s cholestasis recovered at 45th day. A hypophysis MRI revealed a hypophyseal height of 1.5 mm and an ectopic neurohypophysis. This case repot was reported to stress that newborns with cholestasis and hypercalcemia should definitely be investigated for cortisol deficiency and panhypopituitarism.