Zinc toxicity with pancreatic acinar necrosis in piglets receiving total patenteral nutrition

Two Hampshire-Duroc cross piglets maintained on 100% total patenterai nutrition (TPN) for 3 weeks developed pancreatic epithelial cell necrosis, diffuse acinar atrophy, and marked interstitial fibrosis. In addition, the piglets had severe villus atrophy in the small intestine as a result of TPN. Atomic absorption spectrophotometric analysis of liver samples revealed toxic hepatic zinc levels (513.5 and 491.2 ppm) in the TPN piglets (40-90 ppm in control piglets). Administering TPN bypasses homeostatic control mechanisms regulating zinc absorption at the gastrointestinal level and may reduce pancreatic secretion contributing to the accumulation of zinc in tissues. Intestinal villus atrophy, a sequela to TPN, may have also affected zinc excretion by impairing intestinal flux and desquamation. These factors should be considered in formulating TPN solutions and zinc levels administered must be reduced accordingly to avoid toxicity. Furthermore, sources and tissue levels of zinc should be investigated when necrosis, acinar atrophy, and fibrosis of the pancreas are encountered in young pigs.