TPN-related digestive alterations. Animal and human data in the non-critical setting

In TPN-fed animals the lack of enteral nutrition (EN) induces significant and early alterations in gut mucosal morphology, crypt cell proliferation, and sugar and amino acid absorption. Both changes in gut mucosal immunity (reduction of total lymphocytes and bile secretory IgA, impairment of mitogenic response of gut lymphoid populations) and loss of respiratory immunity have been documented. In addition, an imbalance between Th2 IgA stimulating cytokines and Th1 IgA inhibiting cytokines has been observed; this imbalance upregulates the inflammatory response in the intestine and other organs. Intestinal motility, bacterialecosystemandbloodflowarealsoaffectedbyTPN:thedurationofMMCisprolonged; cecal and ileal bacterial content is greatly increased and both portal and superior mesenteric artery blood flows are decreased by 30% after 8 h of TPN. In humans the available data are remarkably less. Fourteen days of TPN in healthy volunteers induce a significant decrease in mucosal thickness and in the number of villous cells, while crypt cells are unaffected. No remarkable alterations in cell proliferative activities have been reported, except in subjects affected by inflammatory bowel diseases.Alterations in immunity (decrease of IgA immunocytes) have been clearly demonstrated only in infants and children on TPN, while in adults the TPN- induced changes in intestinal immunity may only be suggested on the basis of speculative considerations.Theminimumenteralfeedingthatcanprotectthegutintegrityhasbeenindicated in rats (20-25% of the caloric requirement to reduce bacterial translocation) and in piglets (40- 80% to maintain proliferative and functional gut activities). (Nutritional Therapy & Metabolism 2006;24:120-6)