Nutritional support during treatment of biliopancreatic malignancy

As in many malignancies the energy balance necessary to maintain normal bod y composition and organ function is disturbed in biliopancreatic malignanci es. Whereas the cause of the decreased nutrition intake and increased energ y expenditure is in general unknown, recent data in literature suggest that pancreatic cancer is associated with increased inflammatory activity cause d by elevated levels of pro-inflammatory cytokines. This leads to significa nt weight loss already present at the time of diagnosis in the majority of patients and progressing if the cancer remains untreated or is incurable. S imilar data are unavailable in the case of biliary cancer, although biliary obstruction is also associated with increased pro-inflammatory cytokine ac tivity precipitated by increased endotoxin levels. The clinical significanc e of the presence of nutritional depletion in biliopancreatic cancer has be en substantiated in the distant and recent past. It's presence is associate d with increased morbidity after surgery, and with increased hospital costs . In pancreatic cancer the level of inflammatory activity is the most impor tant prognostic factor of long term survival. Nutritional intervention should aim at decreasing treatment related morbidi ty and mortality, at enhancing response to radiation and chemotherapy and a t improving long term survival, not at improving nutritional status per se. The literature indicates that artificial nutrition support is not an effec tive adjuvant therapy to radiation, neither so in relation to chemotherapy. Consensus exists, however, that peri-operative artificial nutrition suppor t is effective in reducing post-operative complications, particularly in th e more severely depleted patients, but also that this effect is not cost-ef fective. These findings have precipitated a search to better understand the mechanisms involved in the development of nutritional depletion, and by co nsequently adapting the artificial nutrition support improving outcome of t his treatment modality. It is still too early to make firm statements conce rning clinical efficacy and cost-effectiveness of these metabolic manipulat ions, but glutamine and/or arginine enrichment of artificial nutrition regi mens seem to improve outcome as measured by both substitute and clinical en dpoints. In addition, manipulation of the inflammatory response in pancreat ic cancer seems to enhance the effectiveness of artificial nutrition suppor t in these patients. Trials are under way to support these concepts.