Ablation of abnormal energy expenditure by curative tumor resection
J. D. Luketich, J. L. Mullen, I. D. Feurer, J. Sternlieb and R. C. Fried
Department of Surgery, University of Pennsylvania School of Medicine, Philadelphia.
Resting energy expenditure is abnormal in most patients with cancer and may
contribute to cancer cachexia. These metabolic abnormalities may be a
direct measure of tumor metabolism, or represent alterations in the size or
activity of the body cell mass, or both. To unravel this pathogenesis, we
prospectively studied 68 preoperative patients with cancer about to undergo
curative resection by measuring resting energy expenditure before and after
tumor resection. The preoperative measured resting energy expenditure was
compared with expected resting energy expenditure based on Harris-Benedict
resting energy expenditure predictions: 10 patients were hypometabolic
(less than 90% Harris-Benedict); 35 were normometabolic (90% to 110%
Harris-Benedict); and 23 were hypermetabolic (greater than 110%
Harris-Benedict). Using each patient as his or her own control, resting
energy expenditure normalized or remained normal following curative
resection. In contrast, after palliative resection, resting energy
expenditure remained hypermetabolic or significantly increased toward
hypermetabolism. Tumor induces an abnormal metabolic rate, since tumor
removal results in prompt normalization of resting energy expenditure. The
abnormal energy expenditure of patients with cancer cannot be solely
attributed to abnormal host body composition.