Exocrine pancreatic atrophy in German Shepherd Dogs and Rough-coated Collies: an end result of lymphocytic...

Previously published studies of the pathology of canine exocrine pancreatic insufficiency (EPI) have been based on morphological findings during the clinical phase of the disease, when atrophy of acinar parenchyma occurs. Recently, low serum trypsinlike immunoreactivity (TLI) concentration has been shown to precede clinical signs, making it possible to diagnose EPI prior to onset of the clinical disease. This study presents histological and ultrastructural findings of pancreatic biopsies from 11 German Shepherd Dogs and 2 Rough-coated Collies with subclinical EPI (SEPI). These findings were compared with those from dogs with clinical EPI (n = 11) and healthy control dogs (n = 5). Biopsied tissue from dogs with SEPI typically contained both normal and atrophied acinar parenchyma. The most significant finding was the marked lymphocytic infiltration, which was most prevalent at the border zone of affected and nonaffected parenchyma but had spread into the normal acinar tissue. Numerous intraacinar lymphocytes were found. Most of the lymphocytes were positive by immunostaining for CD3. In more advanced stages of destruction, the findings were characteristic of pancreatic acinar atrophy. In the atrophied parenchyma, the inflammatory reaction, if present, was less prominent. Ultrastructural changes were in accordance with those of the histological study showing infiltration of lymphocytes both in affected acini and in acini that revealed no obvious ultrastructural changes. Progressive degenerative changes of acinar cells were considered a nonspecific finding. Apoptotic death of acinar cells was occasionally found. The inflammatory reaction was clearly shown to precede the pancreatic acinar atrophy, and the findings suggested that lymphocytic pancreatitis leads to atrophy of the pancreas. The possibility that EPI is an immune-mediated disease in German Shepherd Dogs and Rough-coated Collies is discussed.