exocrine pancreatic insufficiency (EPI) in type 3c diabetes

Last edited 07/2024

Pancreatic exocrine insufficiency in diabetes

  • pancreatic exocrine insufficiency (EPI) is characterised by a deficiency of three major groups of pancreatic enzymes (amylase, protease, lipase):
    • causes an impairment in digestion and consequent nutrient malabsorption and malnutrition
  • patients with type 1 or type 2 DM have been shown to have reductions in fecal elastase levels, with some pathologic changes similar to chronic pancreatitis (CP), and this has been termed "diabetic exocrine pancreatopathy"
  • prevalence of EPI has been stated as an average of 40% in type 1 DM and 27% in type 2 DM (3)
  • co-existing EPI in people with either type 1 or type 2 diabetes is likely to be a different clinical entity to pancreatic diabetes (sometimes referred to as type 3c diabetes) (4)
    • type 3c diabetes is diabetes due to pancreatic disease or injury so both endocrine and exocrine hormone production are affected
    • most commonly identified cause of type 3c diabetes is chronic pancreatitis

Clinical features of EPI:

  • patients have varying degrees of exocrine and endocrine dysfunction
    • damage to the islet of Langerhans effects the secretion of hormones from the alpha, beta, and pancreatic polypeptide cells; the combination of low insulin, glucagon, and pancreatic polypeptide contributes to rapid fluctuations in glucose levels
      • form of "brittle diabetes" may result in the poorer glycemic control observed in patients with DEP/type 3c diabetes
      • patients are more likely to require early insulin initiation compared with those with T2DM
        • individuals should be advised about the symptoms of decompensated hyperglycemia, although they are less likely to develop ketoacidosis (5,6)
  • symptoms of EPI develop when approximately 90% of the exocrine function of the pancreas is lost
    • possible clinical features of EPI include steatorrhea (often without diarrhea), abdominal bloating, weight loss, various vitamin deficiencies, and metabolic bone disease (6)

glycaemic control following pancreatic enzyme replacement therapy (PERT)

  • pancreatic enzyme replacement therapy (PERT) can affect glycaemic control pathways via (7)
    • altered action of the hormones leptin and incretins on glucose homeostasis
      • PERT may lead to an improvement of incretin response to food and with consequent lower blood glucose levels
    • leading to improved absorption of oral diabetes medication
  • there is a need to frequently check a patient's glycaemic response and blood glucose levels during PERT as the dose of the diabetes medication may need adjustment (especially sulphonylureas and insulin)

Management

  • seek expert advice
  • is generally managed by starting with metformin, but insulin may eventually be needed
  • incretin therapy is avoided considering the risk of pancreatitis (8)
  • need consistent treatment of PEI (pancreatic exocrine insufficiency) to ensure nutrient absorption for prevention of hypoglycemia and additional vigilance to prevent hypoglycemia because of potential loss of counter-regulatory glucagon secretion (8)

Reference:

Related pages:

type 3c diabetes