Improving food intake in anorectic cancer patients.
OBJECTIVE
Anorexia and reduced food intake are important issues in the management of cancer patients. This article discusses the currently proposed hypothesis of its pathogenesis, and reviews the available and future therapeutic options as they relate to the pathogenic mechanisms.


RESULTS
Currently available data suggest that the pathogenesis of cancer anorexia is multifactorial, and involves most of the hypothalamic neuronal signaling pathways modulating energy intake. Thus, a number of factors have been proposed as putative mediators of cancer anorexia, including hormones (e.g. leptin), neuropeptides (e.g. neuropeptide Y), cytokines (e.g. IL-1, IL-6, tumor necrosis factor) and neurotransmitters (e.g. serotonin and dopamine). It is unlikely, however, that they represent separate and distinct pathogenic mechanisms, rather it appears that close interrelationships may exist among them. In line with this reasoning, consistent experimental and human data suggest that hypothalamic monoaminergic neurotransmission may represent a major target on which different anorexia-related factors converge.


CONCLUSIONS
In the pathogenesis of cancer anorexia, cytokines appear to play a key role. Their increased expression during tumor growth inhibits the hypothalamus to appropriately respond to peripheral signals, by persistently activating the melanocortin system and inhibiting the neuropeptide Y neuronal pathway. Hypothalamic monoaminergic neurotransmission may significantly contribute to these effects. Thus, interfering pharmacologically with cytokine expression or hypothalamic monoaminergic neurotransmissions is an effective therapeutic strategy in anorectic cancer patients.
Laviano
Alessandro
A
Department of Clinical Medicine, University 'La Sapienza', Rome, Italy. alessandro.laviano@unirima1.it
Meguid
Michael M
MM
Rossi-Fanelli
Filippo
F
D000855:Anorexia / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D016207:Cytokines / Q000378:metabolism / Q000502:physiology*; D002149:Energy Intake / Q000502:physiology*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D009369:Neoplasms / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D009434:Neural Pathways / Q000502:physiology*; D015398:Signal Transduction
D016207:Cytokines