Search Results

You are looking at 1 - 10 of 10 items for :

  • "pancreatic acinar atrophy" x
  • Refine by Access: All Content x
Clear All

Abstract

Objective—To assess the heritability of pancreatic acinar atrophy (PAA) in German Shepherd Dogs (GSDs) in the United States.

Animals—135 GSDs belonging to 2 multigenerational pedigrees.

Procedure—Two multigenerational pedigrees of GSDs with family members with PAA were identified. The clinical history of each GSD enrolled in the study was recorded, and serum samples for canine trypsinlike immunoreactivity (cTLI) analysis were collected from 102 dogs. Dogs with a serum cTLI concentration ≤ 2.0 µg/L were considered to have exocrine pancreatic insufficiency (EPI) and were assumed to have PAA.

Results—Pedigree I consisted of 59 dogs and pedigree II of 76 dogs. Serum cTLI concentrations were measured in 48 dogs from pedigree I and 54 dogs from pedigree II. A total of 19 dogs (14.1%) were determined to have EPI, 9 in pedigree I (15.3%) and 10 in pedigree II (13.6%). Of the 19 dogs with EPI, 8 were male and 11 were female.

Conclusion and Clinical Relevance—Evaluation of data by complex segregation analysis is strongly suggestive of an autosomal recessive mode of inheritance for EPI in GSDs in the United States. (Am J Vet Res 2002;63:1429–1434)

Full access
in American Journal of Veterinary Research

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.

Free access
in American Journal of Veterinary Research

and cats can develop EPI at any age, but the underlying etiology may affect the age of onset of clinical signs. Breeds affected by pancreatic acinar atrophy (PAA) are often affected at a younger age than those affected by EPI secondary to chronic

Open access

hepatitis, biliary hyperplasia and cholangitis; diffuse, moderate pancreatic acinar atrophy; and mild interstitial fibrosis and ductular hyperplasia. Necropsy specimens of the semimembranosus muscle were sent to the University of Minnesota Neuromuscular

Full access
in Journal of the American Veterinary Medical Association

pancreatic acinar atrophy, a disorder most often diagnosed in German Shepherd Dogs and Collies. 11,12 In contrast, EPI in humans and cats is most commonly caused by chronic pancreatitis, which can also cause EPI in dogs. 11,13–15 Whatever the cause, it has

Full access
in American Journal of Veterinary Research

. Pancreatic acinar atrophy in German Shepherd Dogs and Rough-coated Collies. Etiopathogenesis, diagnosis and treatment. A review . Vet Q 2004 ; 26 : 61 – 75 . 4 Westermarck E , Wiberg M . Exocrine pancreatic

Full access
in Journal of the American Veterinary Medical Association

their absorption of fat-soluble vitamins. 8,9 However, the pathogenesis of EPI from cystic fibrosis in people is different from that of EPI in dogs, which includes pancreatic acinar atrophy and chronic pancreatitis. 2 Also, conjugation of bile acids

Full access
in American Journal of Veterinary Research

real-time RT-PCR—how well do they correlate? BMC Genomics 2005 ; 6 : 59 . 10.1186/1471-2164-6-59 34. Clark LA Wahl JM Steiner JM , et al Linkage analysis and gene expression profile of pancreatic acinar atrophy in the German Shepherd Dog

Full access
in American Journal of Veterinary Research

limit and diagnosis of clinical EPI is complicated by the potential spectrum of pancreatic acinar atrophy in EPI. 5 A serum cTLI concentration < 2.5 μg/L is considered diagnostic for EPI, whereas concentrations between 2.5 and 5.7 μg/L may be associated

Full access
in American Journal of Veterinary Research

. Tsai KL , Starr-Moss AN , Venkataraman GM , et al. Alleles of the major histocompatibility complex play a role in the pathogenesis of pancreatic acinar atrophy in dogs . Immunogenetics 2013 ; 65 : 501 – 509 . 10.1007/s00251-013-0704-y 73

Full access
in American Journal of Veterinary Research