c-peptide and Hyponatremia

As a rare condition characterized by inflammation of the pituitary gland, hypophysitis usually results in hypopituitarism and pituitary enlargement. The most critical outcome of hypopituitarism is caused by secondary adrenal insufficiency. Glucocorticoid deficiency is a life-threatening condition, and patients who develop this deficiency require prompt diagnosis and treatment. However, a delayed diagnosis of hypopituitarism may occur due to its non-specific clinical manifestations. A common presenting sign of glucocorticoid deficiency is hypoglycemia. The amelioration of hyperglycemia has been observed in diabetic patients with adrenal insufficiency. We report the case of a 70-year-old Japanese woman who had suffered from fatigue and anorexia for several months; she was admitted based on refractory hyponatremia (sodium 125-128 mEq/L) and hypoglycemia (glucose 58-75 mg/dL). Laboratory findings and magnetic resonance imaging findings led to the diagnosis of panhypopituitarism caused by autoimmune hypophysitis. After receiving 10 mg/day of hydrocortisone, the patient developed severe hyperglycemia (glucose >500 mg/dL). Undetectable C-peptide levels and positive results of both insulinoma-associated antigen-2 antibodies and insulin autoantibodies indicated that she had experienced a recent onset of type 1 diabetes. The pathophysiological process indicated that overt hyperglycemia could be masked by the deficient action of glucocorticoids even in a diabetic patient with endogenous insulin deficiency. This uncommon case reinforces the importance of the prompt diagnosis and treatment of hypopituitarism. Clinicians should remain aware of the possibility of hidden diabetes when treating hypoglycemia in patients with adrenal insufficiency.

Topics: Adrenal Insufficiency; Aged; Autoantibodies; Autoimmune Hypophysitis; Blood Glucose; C-Peptide; Diabetes Mellitus, Type 1; Female; Glucocorticoids; Glycated Hemoglobin; Humans; Hydrocortisone; Hypoglycemic Agents; Hyponatremia; Hypopituitarism; Hypothyroidism; Insulin; Thyroxine

We report a patient with Addison's disease whose clinical features became worse during interferon therapy for chronically active hepatitis C. A 47-year-old male was admitted because somnolence developed during a 4 week treatment with interferon-alpha-2a (IFN: 900 x 104U/day). Serum Na level was 113mEq/l and plasma osmolarity was lowered to 238mOsm/kg on admission. Plasma ACTH level was high, while serum cortisol, urinary 17-OHCS and 17-KS excretion were far below the normal levels. On admission, serum prolactin, insulin levels and urinary CPR excretion increased. Normalization of serum Na level by NaCl administration attenuated hyperinsulinemia associated with the reduction of increased CPR excretion. It was supposed that IFN administration might increase cortisol consumption and worsen hypoadrenocortinism in a patient with Addison's disease. In addition, the present case raised the possibility that hyposmolarity may induce a hyperinsulinemic state in humans.

Topics: Addison Disease; C-Peptide; Hepatitis C; Hepatitis, Chronic; Humans; Hyponatremia; Insulin; Insulin Secretion; Interferon alpha-2; Interferon-alpha; Male; Middle Aged; Osmolar Concentration; Recombinant Proteins; Water-Electrolyte Imbalance