Pancreatic acinar atrophy in german shepherds

Citation
Gm. Rutz et al., Pancreatic acinar atrophy in german shepherds, COMP CONT E, 23(4), 2001, pp. 347
Citations number
63
Categorie Soggetti
Veterinary Medicine/Animal Health
Journal title
COMPENDIUM ON CONTINUING EDUCATION FOR THE PRACTICING VETERINARIAN
ISSN journal
01931903 → ACNP
Volume
23
Issue
4
Year of publication
2001
Database
ISI
SICI code
0193-1903(200104)23:4<347:PAAIGS>2.0.ZU;2-H
Abstract
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.