Although a number of pathological studies using various names/synonyms for autoimmune pancreatitis (AIP) have been reported, they do not mention the pathological staging related to origin/pathogenesis. Here, we propose a pathological staging for AIP lesions.
We histopathologically examined pancreatic tissue specimens of 31 AIP patients (14 pancreatectomized and 17 needle-biopsied materials) provided by 15 hospitals in Japan and studied the relevance of clinical manifestations to the pathological stage of AIP.
Based on the presence or absence of acinar cells in AIP lesions, pancreatic tissue specimens were successfully divided into 20 cases in the early stage and 11 cases in the advanced stage, respectively. In the early stage, fibrosis was distributed in the interlobular and intralobular areas, admixed with acinar atrophy. Lymphoplasmacytic infiltration caused the narrowing of the ductal lumen and obliterative phlebitis. The common bile duct wall was also involved. In the advanced stage, the lesion was replaced by massive/extensive interlobular fibrosis with lymphoplasmacytic infiltrates to various degrees. Phlebitis was mild. Comparative analysis of clinical parameters between the early and advanced stages showed a significantly higher prevalence of jaundice and positive antinuclear antibodies in the early stage, and decreased serum lipase levels in the advanced stage.
Autoimmune pancreatitis can be divided into early and advanced stages according to the presence or absence of acinar cells. Our pathological staging will facilitate understanding and evaluation of the clinical course in AIP.
Abbreviations: AIP = autoimmune pancreatitis, ANA = antinuclear antibody, CAP = chronic alcoholic pancreatitis, COP = chronic obstructive pancreatitis
From the *Department of Pathology, Juntendo University School of Medicine, Tokyo; †Department of Gastroenterology and Hepatology, Kochi Medical School, Kochi; ‡Department of Internal Medicine, Tokyo Woman's Medical University, Tokyo; and §Department of Surgery, Kumamoto University School of Medicine, Kumamoto, Japan.
Received for publication April 11, 2006; accepted July 6, 2006.
This work was supported in part by Health and Labor Sciences Research Grants, Research on Specific Diseases (Intractable Diseases of the Pancreas).
Reprints: Koichi Suda, MD, PhD, Department of Pathology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan (e-mail: email@example.com).