Nutritional support during treatment of biliopancreatic malignancy.

Department of Surgery, University Hospital Maastricht, The Netherlands. As in many malignancies the energy balance necessary to maintain normal body composition and organ function is disturbed in biliopancreatic malignancies. Whereas the cause of the decreased nutrition intake and increased energy expenditure is in general unknown, recent data in literature suggest that pancreatic cancer is associated with increased inflammatory activity caused by elevated levels of pro-inflammatory cytokines. This leads to significant weight loss already present at the time of diagnosis in the majority of patients and progressing if the cancer remains untreated or is incurable. Similar data are unavailable in the case of biliary cancer, although biliary obstruction is also associated with increased pro-inflammatory cytokine activity precipitated by increased endotoxin levels. The clinical significance of the presence of nutritional depletion in biliopancreatic cancer has been substantiated in the distant and recent past. It's presence is associated with increased morbidity after surgery, and with increased hospital costs. In pancreatic cancer the level of inflammatory activity is the most important prognostic factor of long term survival. Nutritional intervention should aim at decreasing treatment related morbidity and mortality, at enhancing response to radiation and chemotherapy and at improving long term survival, not at improving nutritional status per se. The literature indicates that artificial nutrition support is not an effective adjuvant therapy to radiation, neither so in relation to chemotherapy. Consensus exists, however, that peri-operative artificial nutrition support is effective in reducing post-operative complications, particularly in the more severely depleted patients, but also that this effect is not cost-effective. These findings have precipitated a search to better understand the mechanisms involved in the development of nutritional depletion, and by consequently adapting the artificial nutrition support improving outcome of this treatment modality. It is still too early to make firm statements concerning clinical efficacy and cost-effectiveness of these metabolic manipulations, but glutamine and/or arginine enrichment of artificial nutrition regimens seem to improve outcome as measured by both substitute and clinical endpoints. In addition, manipulation of the inflammatory response in pancreatic cancer seems to enhance the effectiveness of artificial nutrition support in these patients. Trials are under way to support these concepts. Publication Types: Review Review, Tutoria