A case of isolated ACTH deficiency who developed auto-immune-mediated hypothyroidism and impaired water diuresis during glucocorticoid replacement therapy

A case of isolated ACTH deficiency who developed autoimmune-mediated hypoth yroidism and still showed impaired water diuresis during glucocorticoid rep lacement therapy is reported. A 45-year-old woman was initially admitted fo r nausea, vomiting, and general malaise. Her serum sodium and plasma osmola lity, ACTH and cortisol values were low, but her urine osmolality was high. Other pituitary hormone levels, thyroid hormone levels, and a computed tom ogram of the pituitary gland were normal. The patient was treated with hydr ocortisone and followed in the outpatient clinic; however, she was lost to follow up 18 months after admission. Three years later she presented with h ypoglycemia and hyponatremia. Her serum or plasma ACTH, FT3, FT4, cortisol levels were low and her serum TSH level was high. Pituitary stimulation tes ts revealed a blunted response of ACTH to CRH and an exaggerated response o f TSH to TRH. Plasma ADH was inappropriately high, and a water-loading test revealed impaired water diuresis and poor suppression of ADH. Although ADH was suppressed, impaired water diuresis was observed in the water loading test after hydrocortisone supplementation. Thyroxine supplementation comple tely normalized the water diuresis. Her outpatient clinic medical records r evealed a gradual increase in TSH levels during follow up, indicating that she had developed hypothyroidism during glucocorticoid replacement therapy. The hyponatremia on the first admission was due to glucocorticoid deficien cy, whereas the hyponatremia on the second admission was due to combined de ficiencies of glucocorticoid and thyroid hormones.