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

Citation
Me. Wiberg et al., Exocrine pancreatic atrophy in German Shepherd Dogs and Rough-coated Collies: An end result of lymphocytic pancreatitis, VET PATH, 36(6), 1999, pp. 530-541
Citations number
45
Categorie Soggetti
Veterinary Medicine/Animal Health","Medical Research Diagnosis & Treatment
Journal title
VETERINARY PATHOLOGY
ISSN journal
03009858 → ACNP
Volume
36
Issue
6
Year of publication
1999
Pages
530 - 541
Database
ISI
SICI code
0300-9858(199911)36:6<530:EPAIGS>2.0.ZU;2-C
Abstract
Previously published studies of the pathology of canine exocrine pancreatic insufficiency (EPI) have been based on morphological findings during the c linical phase of the disease, when atrophy of acinar parenchyma occurs. Rec ently, low serum trypsinlike immunoreactivity (TLI) concentration has been shown to precede clinical signs, making it possible to diagnose EPI prior t o onset of the clinical disease. This study presents histological and ultra structural findings of pancreatic biopsies from 11 German Shepherd Dogs and 2 Rough-coated Collies with subclinical EPI (SEPI). These findings were co mpared 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 th e marked lymphocytic infiltration, which was most prevalent at the border z one of affected and nonaffected parenchyma but had spread into the normal a cinar tissue. Numerous intraacinar lymphocytes were found. Most of the lymp hocytes 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 l ess prominent. Ultrastructural changes were in accordance with those of the histological study showing infiltration of lymphocytes both in affected ac ini and in acini that revealed no obvious ultrastructural changes. Progress ive degenerative changes of acinar cells were considered a nonspecific find ing. Apoptotic death of acinar cells was occasionally found. The inflammato ry reaction was clearly shown to precede the pancreatic acinar atrophy, and the findings suggested that lymphocytic pancreatitis leads to atrophy of t he pancreas. The possibility that EPI is an immune-mediated disease in Germ an Shepherd Dogs and Rough-coated Collies is discussed.