The serum complement system ? a mediator of acute pancreatitis

Seelig, R; Ehemann, Volker; Tschahargane, C; Seelig, H. P.

doi:10.1007/bf00434038

Cited by 31 publications

(12 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, compression of the pancratic duct could produce an increase of duct pressure with release of pancreatic enzymes into the interstitial tissue of the pancreas. The intraductal and interstitial activation of pancreatic enzymes as well as active comple ment factors and bacteria would then result in pancreatitis [11,14,17], The assumption of an intraductal propagation of the pan creatic inflammation in acute biliary' pancre atitis [5] was not supported by our study. This kind of inflammation was absent in our patients, both in acute biliary pancreatitis and in the various subtypes of nonbiliary acute pancreatitis.…”

Section: Discussioncontrasting

confidence: 54%

Histological Alterations of the Preampullary Common Bile and Pancreatic Duct in Acute Biliary and Nonbiliary Pancreatitis

Schmitz-Moormann¹,

Schwerk²,

Sinn³

1986

Digestion

View full text Add to dashboard Cite

Histological alterations of the preampullary common bile duct and the pancreatic duct were studied in the pancreata from 16 patients with acute biliary pancreatitis and 11 patients with acute nonbiliary pancreatitis. The corresponding controls either suffered from gallstone disease without pancreatitis or had neither gallstone disease nor pancreatitis. In acute biliary pancreatitis as well as in gallstone disease, a common channel is significantly less frequent than in acute nonbiliary pancreatitis and in the normal pancreas. The inflammatory alterations of the preampullary common bile duct are increased in biliary pancreatitis compared to nonbiliary pancreatitis and to controls. The inflammatory lesions of the distal common bile duct and distal pancreatic duct are significantly correlated. These findings favor the assumption that acute biliary pancreatitis is initiated by transient obstruction of the preampullary common bile duct producing a local inflammation which encroaches upon the adjacent region of the pancreatic duct.

show abstract

Section: Discussioncontrasting

confidence: 54%

Histological Alterations of the Preampullary Common Bile and Pancreatic Duct in Acute Biliary and Nonbiliary Pancreatitis

Schmitz-Moormann¹,

Schwerk²,

Sinn³

1986

Digestion

View full text Add to dashboard Cite

show abstract

“…As the lethality rate increases at that time it is suggested that the subnormal values indicate a recovery whereas the low values represent a deterioration of the animals. Recent findings in man may support this hypothesis [24,25].…”

Section: Discussionmentioning

confidence: 88%

Complement system in sodium taurocholate pancreatitis in the rat

et al. 1978

Self Cite

View full text Add to dashboard Cite

The role of the complement system was studied in Na-taurocholate pancreatitis in rats. Complement activity (CH 50) was determined at various times in the course of pancreatitis. Immediately after induction of acute pancreatitis, serum complement activity declined and massive C 3 deposits could be detected in the vicinity of acinar necroses and necrobioses. After a phase of recovery three to six hours postoperatively a second complement consumption occurred. Lethality rate increased as serum complement activity fell below 50% of preoperative values. The degree of C 3 deposition increased up to six hours. Decline of serum complement activity and deposition within the pancreas seemed to be correlated with histologically demonstrable tissue lesion. The first decline of complement activity in serum is thought to be caused by liberation of complement activating substances within the pancreas due to the detergent action of Na-taurocholate itself. The second decline, however, may be due to the liberation of complement activating and/or destroying enzymes into the blood stream.

show abstract

“…necrotizing pancreatitis; complement activation; soluble complement receptor 1; leukocyte endothelial interaction; lung injury ACTIVATED COMPLEMENT PROTEINS have long been regarded as possible mediators of organ injury in acute pancreatitis. Evidence of complement activation has been reported by several investigators in the setting of both experimental (13,25) and human acute pancreatitis (7). Once activated, the complement cascade can initiate organ injury in a variety of ways.…”

mentioning

confidence: 96%

Interaction of complement and leukocytes in severe acute pancreatitis: potential for therapeutic intervention

Hartwig¹,

Klafs²,

Kirschfink³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

. Interaction of complement and leukocytes in severe acute pancreatitis: potential for therapeutic intervention. Am J Physiol Gastrointest Liver Physiol 291: G844 -G850, 2006; doi:10.1152/ajpgi.00016.2006.-In acute pancreatitis, local as well as systemic organ complications are mediated by the activation of various inflammatory cascades. The role of complement in this setting is unclear. The aim of the present study was to determine the level of complement activation in experimental pancreatitis, to evaluate the interaction of complement and leukocyte-endothelium activation, and to assess the effects of complement inhibition by soluble complement receptor 1 (sCR1) in this setting. Necrotizing pancreatitis was induced in Wistar rats by the combination of intravenous cerulein and retrograde infusion of glycodeoxycholic acid into the biliopancreatic duct; edematous pancreatitis was induced by intravenous cerulein only. In control animals, a sham operation (midline laparotomy) was performed. Complement activation, leukocyte sequestration, and pancreatic as well as pulmonary injury were assessed in the presence/ absence of sCR1. Increased levels of C3a were found in necrotizing but not in edematous pancreatitis. When complement activation in necrotizing pancreatitis was blocked by sCR1, levels of C3a and total hemolytic activity (CH50) were decreased. Leukocyte-endothelial interaction, as assessed by intravital microscopy, and pancreatic as well as pulmonary organ injury (wet-to-dry weight ratio, MPO activity, and histology) were ameliorated by sCR1. As a result of the present study, necrotizing but not edematous pancreatitis is characterized by significant and early complement activation. Based on the interaction of complement and leukocytes, complement inhibition by sCR1 may be a valuable option in the treatment of leukocyteassociated organ injury in severe pancreatitis. necrotizing pancreatitis; complement activation; soluble complement receptor 1; leukocyte endothelial interaction; lung injury ACTIVATED COMPLEMENT PROTEINS have long been regarded as possible mediators of organ injury in acute pancreatitis. Evidence of complement activation has been reported by several investigators in the setting of both experimental (13, 25) and human acute pancreatitis (7). Once activated, the complement cascade can initiate organ injury in a variety of ways. For example, the components C5 through C9 assemble to form the membrane attack complexes that destroy plasma cell membranes (29,30). C5a is a potent chemoattractant for neutrophils and monocytes and stimulates the release of leukocyte lysosomal enzymes, cytokines, and reactive oxygen species. The anaphylatoxins C3a and C5a induce mast cell degranulation and are thought to be involved in airway hyperresponsiveness.Complement inhibition by the C1 esterase inhibitor has been proven effective in the treatment of experimental severe pancreatitis (23, 34). Supporting these results, complement inhibition by the recombinant soluble complement receptor 1 (sCR1) attenuated leukocyt...

show abstract

The serum complement system ? a mediator of acute pancreatitis

Cited by 31 publications

References 7 publications

Histological Alterations of the Preampullary Common Bile and Pancreatic Duct in Acute Biliary and Nonbiliary Pancreatitis

Histological Alterations of the Preampullary Common Bile and Pancreatic Duct in Acute Biliary and Nonbiliary Pancreatitis

Complement system in sodium taurocholate pancreatitis in the rat

Interaction of complement and leukocytes in severe acute pancreatitis: potential for therapeutic intervention

Contact Info

Product

Resources

About