TY - JOUR
T1 - Course of alcoholic chronic pancreatitis
T2 - A prospective clinicomorphological long-term study
AU - Ammann, R. W.
AU - Heitz, P. U.
AU - Kloppel, G.
PY - 1996
Y1 - 1996
N2 - Background and 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 pancreatitis. 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.
AB - Background and 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 pancreatitis. 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.
UR - http://www.scopus.com/inward/record.url?scp=0030012970&partnerID=8YFLogxK
U2 - 10.1053/gast.1996.v111.pm8698203
DO - 10.1053/gast.1996.v111.pm8698203
M3 - Article
C2 - 8698203
AN - SCOPUS:0030012970
SN - 0016-5085
VL - 111
SP - 224
EP - 231
JO - Gastroenterology
JF - Gastroenterology
IS - 1
ER -