Summary
Sequential assessments of pancreatic structure and function were performed on a female German Shepherd Dog bred from parents with exocrine pancreatic insufficiency (epi), to monitor development of pancreatic acinar atrophy in this breed. Determinations of serum trypsin-like immunoreactivity (tli), results of N-benzoyl-l-tyrosyl-p-aminobenzoic acid test, fecal soy bean stimulation test (sst), and gross and histologic examinations of the pancreas did not provide evidence of exocrine pancreatic disease up to 13 months of age. However, electron microscopy revealed degenerative abnormalities of acinar cells that were already apparent at 6 weeks and became more extensive with age. Examination of the pancreas at 22 months of age also indicated no gross or histologic abnormalities, but electron microscopy revealed widespread degenerative changes, including dilatation of the rough endoplasmic reticulum and extensive fusion of zymogen granules affecting most of the acinar cells. Serum tli concentration was markedly reduced at that time, indicative of epi, but the dog remained healthy and results of the sst were normal. Within 1 month, the dog had developed clinical signs of epi, and not only serum tli concentration, but also results of the N-benzoyl-l-tyrosyl-p-aminobenzoic acid test and sst were compatible with severe loss of exocrine pancreatic tissue. This loss was confirmed by gross and histologic examination of the pancreas at 25 months, which revealed typical features of pancreatic acinar atrophy, including scattered and disorganized exocrine cells in the small remnants of pancreatic tissue. These findings indicate that in German Shepherd Dogs, pancreatic acinar atrophy may involve interference with normal intracellular processing of zymogen granules, which precedes progressive and eventual rapid loss of exocrine pancreatic tissue.
