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Robert S. Warren, MD; H. Fletcher Starnes, Jr, MD; Janice L. Gabrilove, MD; Herbert F. Oettgen, MD; Murray F. Brennan, MD

Arch Surg. 1987;122(12):1396-1400.

Abstract
• It has been suggested that the monokine tumor necrosis factor (TNF) (cachectin) is responsible for metabolic abnormalities frequently accompanying malignant neoplasms. The acute metabolic effects of TNF in patients with cancer were studied. Subcutaneous administration of recombinant human TNF led to a rise in the C-reactive protein level (4.4±1.2 mg/dL vs 11.6±1.8 mg/dL) and a reduction in the serum zinc level (12.9±0.8 µmol/L vs 7.3±0.8 µmol/L [79± 5 mg/dL vs 48±5 mg/dL]) (values are the mean±SEM). Forearm efflux of total amino acids more than doubled after intravenous TNF injection, principally because of increases in release of the gluconeogenic amino acids alanine and glutamine. Concomitantly, the arterial levels of alanine, glutamine, and total amino acids fell, indicating that TNF also stimulated the uptake of amino acids by other tissues. The observed amino acid pattern cannot be explained solely on the basis of measured changes in cortisol, glucagon, or insulin levels. These findings are discussed in relation to known alterations of amino acid metabolism in cancer-associated cachexia.

(Arch Surg 1987;122:1396-1400)

Author Affiliations
From the Surgical Metabolism Laboratory, the Department of Surgery (Drs Warren, Starnes, and Oettgen), and the Clinical Immunology Service (Drs Gabrilove and Brennan), Memorial Sloan-Kettering Cancer Center, New York.

Footnotes
Accepted for publication July 10, 1987.

Read before the Annual Meeting of the Society of Surgical Oncology, London, April 27, 1987.

Reprint requests to Chairman, Department of Surgery, Memorial Sloan-Kettering Cancer Center, 1275 York Ave, New York, NY 10021 (Dr Brennan).

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