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The pathophysiology of the pancreatic defect in cystic fibrosis

P R Durie1

  • 1Department of Pediatrics, University of Toronto, Ontario, Canada.

Acta Paediatrica Scandinavica. Supplement
|January 1, 1989
PubMed

Insights

Cystic Fibrosis (CF) impairs pancreatic fluid secretion, leading to concentrated proteins that obstruct ducts. This causes pancreatic damage, suggesting bicarbonate and chloride transport defects are key in CF's exocrine dysfunction.

Area of Science:

  • Gastroenterology
  • Pediatric Pathology
  • Molecular Biology

Background:

  • Cystic Fibrosis (CF) is associated with pancreatic pathology, including acinar atrophy and duct obstruction.
  • Previous studies indicate abnormal postnatal pancreatic development in CF infants.

Purpose of the Study:

  • To investigate the functional changes in exocrine pancreatic secretions in CF patients.
  • To identify the underlying mechanisms of pancreatic dysfunction in CF.

Main Methods:

  • Comparative analysis of pancreatic secretions from CF patients and function-matched controls.
  • Evaluation of protein and fluid secretion characteristics.

Main Results:

  • CF pancreatic secretions exhibit significantly higher protein concentrations compared to controls.
  • Total protein output is not increased, indicating a primary defect in fluid secretion.
  • Impaired fluid secretion is linked to abnormal bicarbonate and chloride transport in pancreatic ducts.

Conclusions:

  • Deficient pancreatic fluid secretion is a primary phenomenon in CF.
  • Protein hyperconcentration due to impaired fluid secretion leads to duct obstruction, acinar atrophy, and fibrosis.
  • Defects in bicarbonate and chloride transport are implicated in CF pancreatic exocrine dysfunction.

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