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Medline ® Abstract for Reference 32

of 'Etiology of acute pancreatitis'

32
TI
Course of alcoholic chronic pancreatitis: a prospective clinicomorphological long-term study.
AU
Ammann RW, Heitz PU, Klöppel G
SO
Gastroenterology. 1996;111(1):224.
 
BACKGROUND& AIMS: The pathogenesis of alcoholic chronic pancreatitis and its relationship to alcoholic acute pancreatitis are debated. According to our recent clinical long-term study, alcoholic chronic pancreatitis seems to evolve from severe acute pancreatits. The aim of this study was to correlate clinical findings to the pancreatic histopathology at early and advanced stages of the disease.
METHODS: Morphological changes (pseudocysts, autodigestive necrosis, calcification, and perilobular and intralobular fibrosis) were recorded in 37 surgical and 46 postmortem pancreas specimens of 73 patients from our long-term series, who progressed from clinically acute to chronic pancreatitis (mean follow-up, 12 years). Pancreatic function was monitored at yearly intervals.
RESULTS: Surgical interventions were performed at a mean of 4.1 years from onset. Histologically, focal necrosis (49%) and mild perilobular fibrosis (54%) predominated, Pseudocysts (n = 41, mostly postnecrotic) occurred in 88% within 6 years from onset. Autopsy specimens were obtained at a mean of 12 years. These pancreata often showed severe perilobular and intralobular fibrosis (85%) and calcifications (74%), but rarely necrosis (4%). Fibrosis correlated with progressive pancreatic dysfunction (P<0.001), particularly in the 10 patients with two histological assessments (mean interval between biopsy and autopsy, 8 years).
CONCLUSIONS: The data support an evolution from severe alcoholic acute pancreatitis to chronic pancreatitis.
AD
Division of Gastroenterology, Department of Internal Medicine, University Hospital, Zurich, Switzerland.
PMID