Ectopic secretion of chorionic gonadotropin by a lung carcinoma. Pituitary gonadotropin and subunit secretion and prolonged chemotherapeutic remission

Stewart A. Metz, Bruce Weintraub, Saul W. Rosen, Jack Singer, R. Paul Robertson

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

The ability of tumor markers to improve cancer therapy is not established. We studied a man with a human chorionic gonadotropin (HCG)-secreting large cell carcinoma of the lung and gynecomastia. Preoperatively, levels of HCG (109 ng/ml), its alpha and beta subunits (3.2 and 21 ng/ml, respectively) and plasma estradiol were elevated. Despite apparently complete tumor resection and total resolution of gynecomastia, HCG titers remained elevated (3.3 ng/ml), heralding tumor recurrence three weeks later. Because the pathophysiologic consequences of the ectopic secretion of HCG on pituitary function are not established, we administered 100 μg of gonadotropin-releasing hormone (LHRH) and observed a markedly delayed increase in pituitary gonadotropins. Early chemotherapy, guided by persistence of HCG, reduced HCG to undetectable levels, restored to normal the response to LHRH and resulted in a distinctly unusual 30-month complete remission. Use of HCG as a tumor marker levels is more sensitive than the symptom of gynecomastia and may permit detection of small, potentially curable tumor foci.

Original languageEnglish (US)
Pages (from-to)325-333
Number of pages9
JournalThe American Journal of Medicine
Volume65
Issue number2
DOIs
StatePublished - Aug 1978
Externally publishedYes

Bibliographical note

Funding Information:
From the Divisions of Endocrinology and Oncology, Seattle Veterans Administration Hospital, Department of Medicine, Universitv of Washinoton School of Medicine, Seattle, Washington; and National Institute of Arthritis, Metabolism and Digestive Diseases, National Institutes of Health, Bethesda. Marvland. This work was suo~orted in part by U.S. Veterans Administration ‘Research Education Program (MRIS Nos. 7511 and 7155), U.S. Public Health Service Research Grant AM 12829, NCI-NIH Grant CA 18029-02, and designated research funds of the Veterans Administration. Requests for reprints should be addressed to Dr. Stewart A. Metz, Veterans Administration Hospital, 4435 Beacon Avenue South, Seattle, Washington 98108. Manuscript accepted January 9, 1978. l Present address: Division of Oncology, Seattle Veterans Administration Hospital, 4435 Beacon Avenue South, Seattle, Washington 98108.

Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.

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