GOLDMAN (1) in 1949 reported a patient with the combination of bronchial endocrine tumor, pituitary adenoma composed of three cell types, and bilateral adrenal adenomas; clinical features included coarse skin, a large tongue, hypertrichosis, and hypertension. He suggested that the bronchial tumor produced a factor which stimulated adenomatous growth in other organs. The role of a pulmonary endocrine tumor as a cause of typical acromegaly was first demonstrated in 1959 by Altmann and Schiitz (2), who observed regression of acromegalic features after removal of the pulmonary tumor. Subsequently, several cases of acromegaly associated with extrapituitary endocrine tumors were reported and the presence of GH-releasing activity in extrapituitary tumors was suggested by several investigators (3–6).

In 1979, two groups successfully demonstrated for the first time GH-releasing activity in bronchial endocrine tumors derived from acromegalic patients (7,8), and the next year Frohman et al. (9) reported that extracts of a pancreatic endocrine tumor removed from a patient with acromegaly had considerable bioactivity in inducing GH release.