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PubMed · 8811301

Cachexia and anorexia in malignancy.

J T Albrecht·T W Canada
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Abstract

The cancer cachexia syndrome may be present in up to 80% of patients with cancer. Malnutrition resulting from cancer cachexia is a significant cause of morbidity and mortality. Anorexia, tissue wasting, and weight loss appear to be the result of metabolic abnormalities caused by host cytokine production in response to the tumor. The host cytokines include TNF-alpha, IL-1, IL-6, IFN-gamma, and D-factor. Nutritional support in the patient with cancer has been controversial, with the belief that tumor growth may be augmented; however, human studies fail to confirm that tumor growth occurs in excess of normal tissue growth. The efficacy of nutritional support in the cancer has not been adequately studied. Considerable interest exists in providing nutritional support pharmacologically to modify the response to malignancy.

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AnorexiaCachexiaHumansParaneoplastic SyndromesJournal ArticleReview

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BibTeXRIS

J T Albrecht, T W Canada. 1996. Cachexia and anorexia in malignancy.. https://doi.org/10.1016/s0889-8588(05)70368-3

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Wasting in cancer.

Progressive weight loss is a common feature of many types of cancer and is responsible not only for a poor quality of life and poor response to chemotherapy, but also a shorter survival time than is found in patients with comparable tumors without weight loss. Although anorexia is common, a decreased food intake alone is unable to account for the changes in body composition seen in cancer patients, and increasing nutrient intake is unable to reverse the wasting syndrome. Although energy expenditure is increased in some patients, cachexia can occur even with a normal energy expenditure. Various factors have been investigated as mediators of tissue wasting in cachexia. These include cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interferon-gamma (IFN-gamma) and leukemia inhibitory factor (LIF), as well as tumor-derived factors such as lipid mobilizing factor (LMF) and protein mobilizing factor (PMF), which can directly mobilize fatty acids and amino acids from adipose tissue and skeletal muscle respectively. Induction of lipolysis by the cytokines is thought to result from an inhibition of lipoprotein lipase (LPL), although clinical studies provide no evidence for an inhibition of LPL in the adipose tissue of cancer patients. Instead there is an increased expression of hormone sensitive lipase, the enzyme activated by LMF. Protein degradation in cachexia is associated with an increased activity of the ATP-ubiquitin-proteasome pathway. The biological activity of both the LMF and PMF was shown to be attenuated by eicosapentaenoic acid (EPA). Clinical studies show that this polyunsaturated fatty acid is able to stabilize the rate of weight loss and adipose tissue and muscle mass in cachectic patients with unresectable pancreatic cancer. Knowledge of the mechanism of cancer cachexia should lead to the development of new therapeutic agents.

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