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Brief Report
JAMA. 1975;234(2):183-185. doi: 10.1001/jama.1975.03260150053022

Hypercalcitonemia in Bronchogenic Cancer

Evidence for Thyroid Origin of the Hormone

  1. Omega L. Silva, MD;
  2. Kenneth L. Becker, MD, PhD;
  3. Aron Primack, MD;
  4. John L. Doppman, MD;
  5. Richard H. Snider, PhD
  1. From the Metabolic Research Section (Drs Silva, Becker, and Snider) and the Medical Oncology Branch (Dr Primack), Veterans Administration Hospital, Washington, DC; Department of Medicine, George Washington University, Washington, DC (Drs Silva and Becker); and the Department of Diagnostic Radiology (Dr Doppman) and the National Cancer Institute (Dr Primack), National Institutes of Health, Bethesda, Md.

Abstract

Retrograde venous catheterization in a hypercalcitonemic patient with adenocarcinoma of the lung demonstrated that the thyroid gland was secreting a very large amount of hormone (14-fold higher than the peripheral level), while the venous drainage from the tumor deposits was similar in concentration to that of the periphery. Conceivably, the calcitonin is being elaborated in response to metastatic and humoral bone resorption or both. Radiotherapy resulted in a decrease in the calcitonin level. Further studies are needed to determine the diagnostic or prognostic implications of serum calcitonin in bronchogenic cancer.

(JAMA 234:183-185, 1975)

Footnotes

  • Reprint requests to Metabolic Research (151-J), Veterans Administration Hospital, 50 Irving St, NW, Washington, DC 20422 (Dr Silva).

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