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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The morphologic characteristics of ductlike tubular complexes were studied in human acute pancreatitis. Pancreatic specimens were obtained from 10 patients who were operated on for acute pancreatitis. Immunocytochemistry for pancreatic enzymes, keratin, actin, and carcinoembryonic antigen were combined with lectin-binding studies and ultrastructural investigations. Irrespective of clinical onset and duration of pancreatitis, tubular complexes situated in the vicinity of fat necrosis were observed in all patients. Intermediate forms of ductlike structures were characterized by widening of acinar lumina, decreased height of acinar cells, and large autophagic vacuoles. These structures bound all of the lectins employed and retained their immunoreactivity to secretory proteins. Typical tubular complexes were composed of low cuboidal or flattened cells surrounding a large acinar lumen. They revealed a loss for pancreatic enzymes, a reduced lectin-binding for L-fucose and N-acetylgalactosamine, and an increase for cytoskeletal proteins (keratin, actin). It is concluded that tubular complexes in human acute pancreatitis represent degenerating acinar cells which lost their secretory and membrane characteristics.
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PMID:Histochemical and ultrastructural characteristics of tubular complexes in human acute pancreatitis. 253 80

Ductlike tubular complexes in cerulein-induced pancreatitis and oleic acid-induced pancreatic insufficiency were studied to analyze further their origin and development. Immunocytochemistry for pancreatic enzymes, lectin-binding studies, and ultrastructural investigations were combined with autoradiographic quantitation of labeling indices of ductlike cells in tubular complexes. In one group of rats, pancreatitis was induced by infusion of cerulein (10 micrograms kg-1 h-1). In a second group, pancreatic insufficiency was induced by intraductal injection of oleic acid (50 microliters). The investigations were carried out at distinct intervals following induction of pancreatic injury. In both groups of animals, after 3 days, a significant widening of acinar lumina was paralleled by a decreasing height of acinar cells, which showed pronounced retrogressive changes. At this time, acinar cells bound all of the lectins used and retained their immunoreactivity for amylase, trypsinogen, chymotrypsinogen, and lipase. At further intervals, acinar structures formed typical ductlike complexes, with a progressive loss of immunoreactivity for pancreatic enzymes and a reduced lectin-binding for L-fucose and N-acetylgalactosamine. Autoradiographic quantitation demonstrated no significant labeling of acinar cells undergoing tubular dedifferentiation. In both models, tubular complexes were removed by macrophages. It is concluded that lining cells in tubular complexes represent degenerating acinar cells that have no regenerative potency and have lost their secretory and membrane characteristics.
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PMID:Tubular complexes in cerulein- and oleic acid-induced pancreatitis in rats: glycoconjugate pattern, immunocytochemical, and ultrastructural findings. 343 4