AIMS: To assess retrospectively pancreatic changes in non-alcoholic duct-destructive chronic pancreatitis and to investigate the role of apoptosis in duct destruction. METHODS AND RESULTS: Eighteen patients (mean age 46 years, nine women and nine men) underwent pancreatic resection for suspected pancreatic tumour and were diagnosed as having non-alcoholic duct-destructive chronic pancreatitis. We performed a morphological study either semiquantitatively (fibrosis and inflammation) or quantitatively (CD3+ intraepithelial lymphocytes, M30 and TUNEL+ apoptotic cells). The results were compared with those obtained in 10 cases of chronic alcoholic pancreatitis and nine cases of chronic obstructive pancreatitis. Pancreatic changes were diffuse and heterogeneous in 14 cases, but segmental in four cases. The main pancreatic lesions were ductal epithelial alteration, periductal inflammation and fibrosis. There were no cysts or calcifications. We found a marked increase in mast cells in the infiltrate, a slight increase in TiA1+ lymphocytes and in intraepithelial lymphocytes compared with other types of chronic pancreatitis. No significant increase in ductal apoptosis was observed. CONCLUSION: Non-alcoholic duct-destructive chronic pancreatitis is a well-defined pathological entity, distinct from alcoholic and obstructive chronic pancreatitis. Our results indicate that apoptosis probably does not play a major role in ductal alterations.
AIMS: To assess retrospectively pancreatic changes in non-alcoholic duct-destructive chronic pancreatitis and to investigate the role of apoptosis in duct destruction. METHODS AND RESULTS: Eighteen patients (mean age 46 years, nine women and nine men) underwent pancreatic resection for suspected pancreatic tumour and were diagnosed as having non-alcoholic duct-destructive chronic pancreatitis. We performed a morphological study either semiquantitatively (fibrosis and inflammation) or quantitatively (CD3+ intraepithelial lymphocytes, M30 and TUNEL+ apoptotic cells). The results were compared with those obtained in 10 cases of chronic alcoholic pancreatitis and nine cases of chronic obstructive pancreatitis. Pancreatic changes were diffuse and heterogeneous in 14 cases, but segmental in four cases. The main pancreatic lesions were ductal epithelial alteration, periductal inflammation and fibrosis. There were no cysts or calcifications. We found a marked increase in mast cells in the infiltrate, a slight increase in TiA1+ lymphocytes and in intraepithelial lymphocytes compared with other types of chronic pancreatitis. No significant increase in ductal apoptosis was observed. CONCLUSION: Non-alcoholic duct-destructive chronic pancreatitis is a well-defined pathological entity, distinct from alcoholic and obstructive chronic pancreatitis. Our results indicate that apoptosis probably does not play a major role in ductal alterations.