Pancreatic acinar atrophy (PAA) occurs most commonly in German shepherds an
d has been shown to be hereditary in this breed. In this disease, pancreati
c acinar cells undergo atrophy probably subsequent to immune-mediated infla
mmation, while islet cells are spared. The exocrine pancreas has a large se
cretory reserve and only when pancreatic function is decreased to less than
approximately 10% do affected dogs develop signs of exocrine pancreatic in
sufficiency (EPI). EPI causes nutrient malabsorption, particularly of fat a
nd fat-soluble vitamins. In most affected dogs, enzyme deficiency is compli
cated by concurrent small intestinal bacterial overgrowth (SIBO), which pro
bably 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, borborygmu
s, and flatulence. Vomiting and anorexia are less common signs. clinical si
gns usually resolve completely in response to pancreatic enzyme supplementa
tion although fat absorption does not normalize completely. Fat-soluble vit
amins and cobalamin should be supplemented as required. In cases with concu
rrent SIBO that do not respond to therapy with replacement enzymes alone, a
ntibiotic therapy for concurrent SIBO may be useful, as may be feeding of a
highly digestible diet that is low in fiber.