Hepato-gastroenterology · 1996
Damage to duct epithelium is necessary to develop progressing lesions of chronic pancreatitis in the cat.
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Zhao P, Tu J, van den Oord J J, Fevery J
Аннотация
BACKGROUND: The pathogenesis of chronic pancreatitis remains unclear. This investigation aimed to evaluate the relative importance of acinar or ductal lesions or of ductal subobstruction in the development of chronic pancreatitis in cats.
MATERIALS AND METHODS: Ethanol was injected either interstitially in the parenchyma or in the main pancreatic duct, whereas in other animals the main duct was partially obstructed to 70% of its original diameter or totally obstructed.
RESULTS: Total obstruction led to well known chronic obstructive pancreatitis and atrophy. Chronic progressive fibrosing pancreatitis developed only when the ductal epithelium was injured by intraductal injection of ethanol. It differed from the obstructive lesions, as demonstrated by biopsies taken over a one year period. Temporary, acute, or chronic-like lesions developed after intraparenchymal injection or in sub obstruction. Minor lesions were obtained in cats fed alcohol or submitted to ethanol feeding combined with partial duct obstruction. None of the laboratory tests used were very useful to detect mild chronic damage at an early stage but fecal fat and the plasma pancreolauryl test seemed the most sensitive.
CONCLUSION: Damage of the ductal epithelium represents the most important pathogenetic factor to induce chronic pancreatitis. Further refinements, and investigations with more pathophysiologic agents are necessary to ultimately lead to a reproducible model resembling the human disease.
MATERIALS AND METHODS: Ethanol was injected either interstitially in the parenchyma or in the main pancreatic duct, whereas in other animals the main duct was partially obstructed to 70% of its original diameter or totally obstructed.
RESULTS: Total obstruction led to well known chronic obstructive pancreatitis and atrophy. Chronic progressive fibrosing pancreatitis developed only when the ductal epithelium was injured by intraductal injection of ethanol. It differed from the obstructive lesions, as demonstrated by biopsies taken over a one year period. Temporary, acute, or chronic-like lesions developed after intraparenchymal injection or in sub obstruction. Minor lesions were obtained in cats fed alcohol or submitted to ethanol feeding combined with partial duct obstruction. None of the laboratory tests used were very useful to detect mild chronic damage at an early stage but fecal fat and the plasma pancreolauryl test seemed the most sensitive.
CONCLUSION: Damage of the ductal epithelium represents the most important pathogenetic factor to induce chronic pancreatitis. Further refinements, and investigations with more pathophysiologic agents are necessary to ultimately lead to a reproducible model resembling the human disease.