Pancreatic Atrophy, Exocrine

AKA Pancreatic Acinar Athropy (PAA)

Pancreatic atrophy (Image sourced from Bristol Biomed Image Archive with permission)

• Degeneration of acinar cells ccurs as a sequel to
  • Starvation - loss of zymogen granules
  • Maldigestion
  • Obstruction of the pancreatic ducts by
    • Neoplasm
    • Chronic inflammation and associated fibrosis
    • Foreign bodies (parasites, pancreoliths
  • Specific nutritional deficiencies include: essential amino acids, zinc, copper, selenium

Clinical signs

• By the time clinical signs of exocrine pancreatic insufficiency (EPI) appear, the pancreas is usually almost totally destroyed
• Chronic diarrhoea with steatorrhoea and undigested muscle fibres. Large quantities of pale faeces are passed (due to dilution of bile pigment and the presence of undigested fats). The faeces have a characteristic rancid or cheesy odour.
• Loss of condition despite marked increase in appetite

Macroscopic appearance

• The pancreas is extremely thin and almost lace-like
• Primarily acinar tissue affected; the ducts and Islets of Langerhans are relatively normal

Microscopic appearance

• In these cases the parenchyma is replaced by atypical parenchyma and adipose tissue
• Irregular, shrunken acini composed of cells with little cytoplasm
• Some cases show a few areas of apparently normal glandular tissue or foci of cellular infiltraton which have been interpreted as suggesting degenerative changes

Aetiology

• The underlying cause is not known, possibly due to nutritional imbalances
• Chronic pancreatitis is a rare cause of EPI
• Possible hereditary EPI in GSDs and rough coated collies

Diagnosis

• Low serum trypsin-like immunoreactivity is an early, preclinical diagnostic test for EPI

Extra information for Exocrine Pancreatic Atrophy

Exocrine pancreatic atrophy in GSDs and rough coated collies: an end result of lymphocytic pancreatitis. Wiberg ME et al. Vet Path (1999) 36 530-41

• Histological changes in EPI dogs
• Histological changes in the subclinical pancreas (ie; just TLI):
• Patchy areas of normal and abnormal exocrine parenchyma
• Consistently a marked lymphoid infiltrate (lesser numbers of plasma cells seen, occasional eosinophils), starting in the border zone with gradual loss of the pancreatic parenchyma
• Mainly CD3+ T cells, with fewer CD3+ lymphocytes.
• Some lymphoid follicles (mainly B cells) scattered throughout.
• No associated increase in fibrous connective tissue
• Some intra-acinar lymphocytes seen
• As tissue destruction continued, ductal structures became more obvious
• Apoptosis seen in the acini often in normal looking acini.
• Ultrastructure
  • Degenerative changes in acinar cells – dilation of rER, swelling of mitochondria, nuclear pyknosis, aptotitic bodies
• Histology of clinical EPI:
  • Totally atrophied exocrine pancreas
  • Some dogs had areas of normal acinar structures
  • Little inflammation in the border zone
  • Most of the remaining exocrine pancreas was disorganized, prominent ducts, increased amounts of adipose tissue.
  • Slight increase in fibrous tissue compared to subclinical phase, but replacement with fat was more prominent than fibrosis.
  • No ductular epithelial hyperplasia evident
• Ultrastructure
  • Often no remaining acinar cells
• Suggests and immune-mediated destruction - ?hereditary
• Islet cells usually well preserved in the atrophied pancreas.