title: Cancer anorexia-cachexia syndrome: current issues in research and management.
abstract: Cachexia is among the most debilitating and life-threatening aspects of cancer. Associated with anorexia, fat and muscle tissue wasting, psychological distress, and a lower quality of life, cachexia arises from a complex interaction between the cancer and the host. This process includes cytokine production, release of lipid-mobilizing and proteolysis-inducing factors, and alterations in intermediary metabolism. Cachexia should be suspected in patients with cancer if an involuntary weight loss of greater than five percent of premorbid weight occurs within a six-month period. The two major options for pharmacological therapy have been either progestational agents, such as megestrol acetate, or corticosteroids. However, knowledge of the mechanisms of cancer anorexia-cachexia syndrome has led to, and continues to lead to, effective therapeutic interventions for several aspects of the syndrome. These include antiserotonergic drugs, gastroprokinetic agents, branched-chain amino acids, eicosapentanoic acid, cannabinoids, melatonin, and thalidomide--all of which act on the feeding-regulatory circuitry to increase appetite and inhibit tumor-derived catabolic factors to antagonize tissue wasting and/or host cytokine release. Because weight loss shortens the survival time of cancer patients and decreases performance status, effective therapy would extend patient survival and improve quality of life.
authors.affiliation: Department of Clinical Molecular Medicine, Kobe University Graduate School of Medicine, Japan.
authors.forename: Akio
authors.initials: A
authors.lastname: Inui
mesh_terms: D000855:Anorexia / Q000178:diet therapy / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism*; D002100:Cachexia / Q000178:diet therapy / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism*; D050260:Carbohydrate Metabolism; D004064:Digestive System / Q000503:physiopathology; D006801:Humans; D020738:Leptin / Q000378:metabolism; D050356:Lipid Metabolism; D009369:Neoplasms / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D009478:Neuropeptide Y / Q000378:metabolism; D011506:Proteins / Q000378:metabolism; D013577:Syndrome
chemical_list: D020738:Leptin; D009478:Neuropeptide Y; D011506:Proteins