Pancreatic acinar atrophy in german shepherds
Academic Article
Overview
Additional Document Info
View All
Overview
abstract
Pancreatic acinar atrophy (PAA) occurs most commonly in German shepherds and has been shown to be hereditary in this breed. In this disease, pancreatic acinar cells undergo atrophy probably subsequent to immune-mediated inflammation, while islet cells are spared. The exocrine pancreas has a large secretory reserve and only when pancreatic function is decreased to less than approximately 10% do affected dogs develop signs of exocrine pancreatic insufficiency (EPI). EPI causes nutrient malabsorption, particularly of fat and fat-soluble vitamins. In most affected dogs, enzyme deficiency is complicated by concurrent small intestinal bacterial overgrowth (SIBO), which probably contributes to cobalamin malabsorption that often leads to subnormal serum concentrations of this vitamin. Signs most commonly observed in dogs with PAA are weight loss, polyphagia, soft feces, poor haircoat, borborygmus, and flatulence. Vomiting and anorexia are less common signs. Clinical signs usually resolve completely in response to pancreatic enzyme supplementation, although fat absorption does not normalize completely. Fat-soluble vitamins and cobalamin should be supplemented as required. In cases with concurrent SIBO that do not respond to therapy with replacement enzymes alone, antibiotic therapy for concurrent SIBO may be useful, as may be feeding of a highly digestible diet that is low in fiber.
