[Feeding-related disorders in medicine, with special reference to cancer anorexia-cachexia syndrome].
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 results from a failure of the adaptive feeding response seen in simple starvation and includes cytokine production, release of lipid-mobilizing and proteolysis-inducing factors, and alterations in intermediary metabolism. Cytokines play a pivotal role in long-term inhibition of feeding by mimicking the hypothalamic effect of excessive negative feedback signaling from leptin, a hormone secreted by adipose tissue, which is an integral component of the homeostatic loop of body weight regulation. The two major options for pharmacological therapy have been either progestational agents or corticosteroids. However, knowledge of the mechanisms of cancer anorexia-cachexia syndrome 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. The outcomes of drug studies in cancer cachexia should focus on the symptomatic and quality-of-life advantages rather than simply on nutritional end points, since the survival of cachexia cancer patients may be limited to weeks or months due to the incurable nature of the underlying malignancy. As weight loss shortens the survival time of cancer patients and decreases their performance status, effective therapy would extend patient survival and improve quality of life.
Inui
Akio
A
Department of Behavioral Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima 890-8520.
D000273:Adipose Tissue / Q000378:metabolism; D054366:Agouti Signaling Protein; D000855:Anorexia / Q000209:etiology* / Q000523:psychology / Q000628:therapy*; D014151:Anti-Anxiety Agents / Q000627:therapeutic use; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D000928:Antidepressive Agents / Q000627:therapeutic use; D019167:Appetite Stimulants / Q000627:therapeutic use; D002100:Cachexia / Q000209:etiology* / Q000523:psychology / Q000628:therapy*; D016207:Cytokines / Q000037:antagonists & inhibitors; D004734:Energy Metabolism; D005765:Gastrointestinal Agents / Q000627:therapeutic use; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000502:physiology; D020738:Leptin / Q000502:physiology*; D009369:Neoplasms / Q000150:complications* / Q000523:psychology / Q000628:therapy; D009478:Neuropeptide Y / Q000502:physiology; D010348:Patient Care Team; D011374:Progesterone / Q000627:therapeutic use; D015398:Signal Transduction / Q000502:physiology; D013217:Starvation; D013577:Syndrome
D054366:Agouti Signaling Protein; D014151:Anti-Anxiety Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D000928:Antidepressive Agents; D019167:Appetite Stimulants; D016207:Cytokines; D005765:Gastrointestinal Agents; D005938:Glucocorticoids; D036341:Intercellular Signaling Peptides and Proteins; D020738:Leptin; D009478:Neuropeptide Y; D011374:Progesterone