Literature DB >> 80133

Evidence of complement catabolism in acute pancreatitis.

I M Goldstein, D Cala, A Radin, H B Kaplan, J Horn, J Ranson.   

Abstract

Active proteolytic enzymes are released into the gland parenchyma and surrounding tissues during episodes of acute pancreatitis. Since complement components are potential substrates for active proteases and may be the source of biologically active peptides capable of mediating tissue injury, we have examined sera obtained from 12 patients during 13 episodes of acute pancreatitis for evidence of complement catabolism. In 8 of 13 acute phase sera, there were decreased levels of CH50, C3, C4, or some combination thereof as well as degradation products of C3 (revealed by crossed immunoelectrophoresis). In convalescent sera, levels of complement components were normal or elevated. Measurements of alpha1-antitrypsin, alpha2-macroglobulin, and trypsin inhibitory capacity failed to reveal evidence of protease-antiprotease imbalance. These findings provide evidence of complement catabolism in acute pancreatitis and suggest the possibility that activated complement components may play a role in the pathogenesis of some systemic pathologic changes which occur in this disease.

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Year:  1978        PMID: 80133     DOI: 10.1097/00000441-197805000-00003

Source DB:  PubMed          Journal:  Am J Med Sci        ISSN: 0002-9629            Impact factor:   2.378


  11 in total

1.  Pathogenesis of Purtscher's retinopathy. An experimental study.

Authors:  W Behrens-Baumann; G Scheurer; H Schroer
Journal:  Graefes Arch Clin Exp Ophthalmol       Date:  1992       Impact factor: 3.117

Review 2.  The role of neutrophils in vascular injury: a summary of signal transduction mechanisms in cell/cell interactions.

Authors:  G Weissmann
Journal:  Springer Semin Immunopathol       Date:  1989

3.  Granulocyte elastase in assessment of severity of acute pancreatitis. Comparison with acute-phase proteins C-reactive protein, alpha 1-antitrypsin, and protease inhibitor alpha 2-macroglobulin.

Authors:  V Gross; J Schölmerich; H G Leser; R Salm; M Lausen; K Rückauer; U Schöffel; L Lay; A Heinisch; E H Farthmann
Journal:  Dig Dis Sci       Date:  1990-01       Impact factor: 3.199

4.  Role of complement activation in a model of adult respiratory distress syndrome.

Authors:  S Hosea; E Brown; C Hammer; M Frank
Journal:  J Clin Invest       Date:  1980-08       Impact factor: 14.808

5.  Pancreatic damage in fetal and newborn cystic fibrosis pigs involves the activation of inflammatory and remodeling pathways.

Authors:  Maisam Abu-El-Haija; Shyam Ramachandran; David K Meyerholz; Marwa Abu-El-Haija; Michelle Griffin; Radhamma L Giriyappa; David A Stoltz; Michael J Welsh; Paul B McCray; Aliye Uc
Journal:  Am J Pathol       Date:  2012-06-08       Impact factor: 4.307

6.  Leukocytes are required for the trypsin-induced increase in lung vascular permeability.

Authors:  R R Garcia-Szabo; A Johnson; A B Malik
Journal:  Am J Pathol       Date:  1986-09       Impact factor: 4.307

7.  Evidence of complement catabolism in experimental acute pancreatitis.

Authors:  J K Horn; J H Ranson; I M Goldstein; J Weissler; D Curatola; R Taylor; H D Perez
Journal:  Am J Pathol       Date:  1980-10       Impact factor: 4.307

8.  Endotoxaemia and complement activation in acute pancreatitis in man.

Authors:  A K Foulis; W R Murray; D Galloway; A C McCartney; E Lang; J Veitch; K Whaley
Journal:  Gut       Date:  1982-08       Impact factor: 23.059

9.  Lung injury in acute experimental pancreatitis in rats. I. Morphological studies.

Authors:  S Willemer; C O Feddersen; W Karges; G Adler
Journal:  Int J Pancreatol       Date:  1991-05

10.  Expression of C5a-like biological activities by the fifth component of human complement (C5) upon limited digestion with noncomplement enzymes without release of polypeptide fragments.

Authors:  R A Wetsel; W P Kolb
Journal:  J Exp Med       Date:  1983-06-01       Impact factor: 14.307

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