The clinical spectrum of primary hyperparathyroidism has been greatly broadened in recent years. Initially this disease was recognized only by the presence of osteitis fibrosa cystica generalisata.1 In 1925 Mandl was the first to excise a parathyroid tumor in a patient with classical skeletal changes.2 Albright and his associates subsequently showed that hyperparathyroidism was more commonly associated with kidney stones.1 More recent studies have shown an association of hyperparathyroidism with peptic ulcers,3-8 pancreatitis,9-11 steatorrhea,12 multiple endocrine adenomas,13-15 and a multitude of clinical signs and symptoms secondary to the hyperparathyroid state.4,7 An accurate diagnosis of primary hyperparathyroidism can be made only by correlation of the clinical findings and laboratory studies. Unfortunately, there is no direct test for parathyroid gland activity, and laboratory studies depend upon indirect procedures such as the determination of serum calcium and inorganic phosphorus and the various tests of phosphate