PERIACINAR COLLAGENIZATION IN PATIENTS WITH CHRONIC-ALCOHOLISM

Citation
J. Kuroda et al., PERIACINAR COLLAGENIZATION IN PATIENTS WITH CHRONIC-ALCOHOLISM, Pathology international, 48(11), 1998, pp. 857-868
Citations number
43
Categorie Soggetti
Pathology
Journal title
ISSN journal
13205463
Volume
48
Issue
11
Year of publication
1998
Pages
857 - 868
Database
ISI
SICI code
1320-5463(1998)48:11<857:PCIPWC>2.0.ZU;2-N
Abstract
To examine the development of pancreatic fibrosis in alcoholics, the f ibrosis types grouped according to Martin's classification were examin ed by immunohistochemistry using an antibody against alpha-smooth musc le actin (alpha-SMA). The initial stage of periacinar collagenization was also investigated by electron microscopy. The total incidence of p ancreatic fibrosis at autopsy of the 29 alcoholics was significantly h igher than that of the 40 non-alcoholics. Intralobular sclerosis was o bserved to be the most frequent type of fibrosis regardless of alcohol intake. No differences in the enhancement of alpha-SMA expression in each type of fibrosis were found between the alcoholics and nonalcohol ics. Electron microscopically, myofibroblasts were found around acini in the early stage of periacinar collagenization, and were accompanied by numerous fine filaments (8-15 nm in diameter). The various changes in zymogen granules (ZG), lysosomes and lipid droplets were augmented in the acinar cells of alcoholics. Medium-density materials were also found in dilated rough endoplasmic reticulum (RER). The contents of Z G and RER occasionally leaked out. In conclusion, pancreatic fibrosis was increased in alcoholics; myofibroblasts may play an important role in the initial stage of periacinar collagenization; and the intracell ular transport blockage of protein as represented by abnormalities of ZG, ER and lysosomes may contribute to the development of periacinar c ollagenization.