Acromegaly is produced in adults by increase of GH, usually from an eosinophilic adenoma of the pituitary. About two thirds of these patients are female. Signs and symptoms include bitemporal headaches, disturbances of the visual fields, optic nerve atrophy, and physical changes in the face and hands. About 25% of patients have fasting hyperglycemia, and about 50% have decreased carbohydrate tolerance when the oral glucose tolerance test is performed. Serum prolactin is elevated in 25%-40% of patients (literature range, 0%-83%). About 65%-75% of patients with acromegaly display sella turcica enlargement on skull x-ray films. GH assay usually reveals levels above the upper limit of 5 ng/ml. The standard method of confirming the diagnosis is a suppression test using glucose. Normal persons nearly always respond to a large dose of glucose with a decrease in GH levels to less than 50% of baseline, whereas acromegalic patients in theory have autonomous tumors and should show little, if any, effect of hyperglycemia. One study, however, noted relatively normal suppression in a significant percentage of acromegalics. In acromegaly (GH excess), a high somatomedin-C result is diagnostic and is found in nearly all such patients. Other causes of elevated somatomedin-C levels include the adolescent growth spurt and the last trimester of pregnancy. Some investigators believe that somatomedin-C assay is the screening test of choice for acromegaly and that a clear-cut blood level elevation of somatomedin-C might be sufficient for the diagnosis. The major problem is the surge during adolescence.