© 1997 by Oxford University Press
Journal Of The National Cancer Institute, Vol 89, 1763-1773, Copyright © 1997 by Oxford University Press
MJ Tisdale
About half of all cancer patients show a syndrome of cachexia,
characterized by loss of adipose tissue and skeletal muscle mass. Such
patients have a decreased survival time, compared with the survival time
among patients without weight loss, and loss of total body protein leads to
substantial impairment of respiratory muscle function. These changes cannot
be fully explained by the accompanying anorexia, and nutritional
supplementation alone is unable to reverse the wasting process. Despite a
falling caloric intake, patients with cachexia frequently show an elevated
resting energy expenditure as a result of increases in Cori cycle (i.e.,
catalytic conversion of lactic acid to glucose) activity, glucose and
triglyceride-fatty acid cycling, and gluconeogenesis. A number of
cytokines, including tumor necrosis factor- apha, interleukins 1 and 6,
interferon gamma, and leukemia-inhibitory factor, have been proposed as
mediators of the cachectic process. However, the results of a number of
clinical and laboratory studies suggest that the action of the cytokines
alone is unable to explain the complex mechanism of wasting in cancer
cachexia. In addition, cachexia has been observed in some xenograft models
even without a cytokine involvement, suggesting that other factors may be
involved. These probably include catabolic factors, which act directly on
skeletal muscle and adipose tissue and the presence of which has been
associated with the clinical development of cachexia. A polyunsaturated
fatty acid, eicosapentaenoic acid, attenuates the action of such catabolic
factors and has been shown to stabilize the process of wasting and resting
energy expenditure in patients with pancreatic cancer. Such a pharmacologic
approach may provide new insights into the treatment of cachexia.
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Biology of cachexia
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