Comparison of histological features and inflammatory cell reaction in alcoholic, idiopathic and tropical chronic pancreatitis

• Published in: British journal of surgery 2003-12, Vol.90 (12), p.1565-1572
• Main Authors: Shrikhande, S. V., Martignoni, M. E., Shrikhande, M., Kappeler, A., Ramesh, H., Zimmermann, A., Büchler, M. W., Friess, H.
• Format: Article
• Language: English
• Subjects: Adult; Biological and medical sciences; Chronic Disease; Eosinophils - pathology; Female; Fibrosis - pathology; Gastroenterology. Liver. Pancreas. Abdomen; Humans; Liver. Biliary tract. Portal circulation. Exocrine pancreas; Male; Medical sciences; Other diseases. Semiology; Pancreatitis - pathology; Pancreatitis, Alcoholic - pathology; Plasma Cells - pathology
• ISSN: 0007-1323; 1365-2168
• DOI: 10.1002/bjs.4353

Background: There is increasing evidence that immune mechanisms may be crucial in the development of alcoholic chronic pancreatitis. However, it is not known whether differences in underlying aetiology influence the inflammatory reaction in patients with chronic pancreatitis. The histological features and the pattern of inflammatory cell infiltration were studied in three aetiological forms of chronic pancreatitis: alcoholic, idiopathic and tropical pancreatitis. Methods: Forty‐three patients, ten with alcoholic, 12 with idiopathic and 21 with tropical chronic pancreatitis, were evaluated for the pattern of pancreatic inflammatory cell infiltration and histological features. Ten organ donors served as controls. Haematoxylin and eosin‐stained tissue sections were used for histological evaluation. For immunohistochemical characterization of the inflammatory reaction, four antibodies—CD4, CD8, CD45 and CD68—were used. Quantitative evaluation of the various cell infiltrates was performed with computer‐assisted image analysis. The inflammatory cell infiltration pattern was also evaluated. Results: The degree of endophlebitis and the overall density of plasma cells were greater in tropical than in alcoholic chronic pancreatitis. The grade of intralobular fibrosis was significantly higher in tropical chronic pancreatitis compared with the idiopathic form. No significant quantitative differences in the specific cellular infiltrates (CD4, CD8, CD45, CD68) were observed in the three different groups. However, the perivascular inflammation number score was significantly higher in alcoholic compared with idiopathic pancreatitis (P = 0·037), and the perivascular inflammation area score was significantly lower in idiopathic than in alcoholic (P = 0·024) or tropical (P = 0·020) pancreatitis. Conclusion: Different aetiological forms of chronic pancreatitis result in similar histological features and a comparable inflammatory cell reaction, indicating that the disease, independent of the underlying aetiology, reaches a common immunological stage beyond which it appears to progress as a single distinctive entity. Copyright © 2003 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. End‐stage chronic pancreatitis looks identical, irrespective of aetiology