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A Unique Growth Factor in Patients with Acromegaloidism^*

MICHAEL W. ASHCRAFT, PAMELA I. HARTZBAND, ANDRE J. VAN HERLE, NOELLE BERSCH and DAVID W. GOLDE

Divisions of Endocrinology and Hematology-Oncology, Department of Medicine, UCLA School of Medicine Los Angeles, California 90024

Address requests for reprints to: A. J. Van Herle, M.D., Department of Medicine, Division of Endocrinology, UCLA School of Medicine, Los Angeles, California 90024.

Acromegaloidism is a syndrome characterized by features of acromegaly without biochemical evidence of excessive GH or somatomedin production. We searched for a growth factor in the serum of patients with this syndrome. Growth-promoting activity was measured by determining the stimulatory effect of whole and fractionated serum on colony formation by human erythroid progenitors in vitro. Sera from five subjects with acromegaloidism gave a mean (±SEM) stimulated colony growth of 211 ± 4.0 colonies, in contrast to normal sera which yielded a mean colony growth of 100 ± 11.0 (n = 9; P < 0.001). When serum was chromatographed on a Sephadex G-200 column, the maximal stimulation of colony growth was found in the fractions coinciding with the descending slope of the second protein peak. Based on gel filtration chromatography, the estimated molecular weight was 70,000 daltons. Epidermal growth factor, nerve growth factor, fibroblast growth factor, and platelet-derived growth factor resulted in no substantial stimulation of colony growth under the conditions used. Although the erythroid progenitor cells of a Laron dwarf were unresponsive to 200 ng/ml human GH, they were clearly stimulated by serum from a patient with acromegaloidism. The present study describes the presence of a heretofore unidentified growth factor in the serum of subjects with acromegaloidism. This factor also stimulated the erythroid precursor cells of a Laron dwarf whose cells were unresponsive to GH. The physiological role of this growth factor in normal man as well as its pathogenic role in subjects with acromegaloidism remain to be established.

^* This work was supported in part by USPHS Training Grant AM-07049, USPHS Grants CA-32737 and CA-30388 awarded by the NCI, DHHS, and Grant RR-00865. Presented in part at the 63rd Annual Meeting of The Endocrine Society, Cincinnati, OH, June 1981.

Recipient of a Bio-Science Laboratories Fellowship.

Received July 31, 1982.

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