COMPARATIVE RADIOLOGICAL AND MORPHOLOGICAL-STUDY OF HUMAN-PANCREAS - PANCREATITIS LIKE CHANGES IN POSTMORTEM DUCTOGRAMS AND THEIR MORPHOLOGICAL PATTERN - POSSIBLE IMPLICATION FOR ERCP
COMPARATIVE RADIOLOGICAL AND MORPHOLOGICAL-STUDY OF HUMAN-PANCREAS - PANCREATITIS LIKE CHANGES IN POSTMORTEM DUCTOGRAMS AND THEIR MORPHOLOGICAL PATTERN - POSSIBLE IMPLICATION FOR ERCP
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DOI:
10.1136/gut.26.4.406
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发表时间:
1985-01-01
期刊:
影响因子:
24.5
通讯作者:
WIENBECK, M
中科院分区:
文献类型:
--
作者:
SCHMITZMOORMANN, P;HIMMELMANN, GW;WIENBECK, M
A postmortem study by ductography and histology was performed on 69 human pancreata with no clinical or histological signs of chronic pancreatitis. The ductograms, supplemented by 5 postmortem ductograms of chronic pancreatitis, were independently evaluated by 6 clinicians skilled in ERCP [endoscopic retrograde pancreatography]; the degree of alteration was estimated by simple rating, forced choice rating and by determination of the grade of chronic pancreatitis. Histologically, the amount of intraductal epithelial proliferation, periductal, intralobular and perilobular fibrosis, intraductal protein plugs and fat necrosis was determined by semiquantitative methods. The 6 ductographical evaluations significantly differed in the level of their data, but corresponded in the range of distribution. All evaluations were correct regarding judgment of ductograms from patients with chronic pancreatitis. Ductograms of patients without chronic pancreatitis, however, were also frequently classified as chronic pancreatitis; overall 81% (minimal 37%, moderate 33%, severe 11%). This high level of false positive diagnosis indicates the frequency of pancreatitis-like lesions in the main duct and its side branches in patients without chronic pancreatitis. Ductal lesions were significantly correlated with perilobular fibrosis. This finding favors the assumption that in the non-inflamed pancreas, perilobular fibrosis plays a key role in the development of ductal alterations, as in chronic pancreatitis. Perilobular fibrosis may result from intralobular inflammation caused by age-dependent intraductal epithelial hyperplasia.