The authors presented and discussed the pathophysiology and the inhibitor of coagulofibrinolytic system based upon 172 clinical materials and the experimental acute pancreatitis. Quantitative determination of α
2-M, α
1-AT, and AT-III was carried out by SRID.
Result and conclusion.
1) In fulminant hepatitis, the mean values of α
2-M, α
1-AT, and AT-III was markedly decreased. In liver cirrhosis, AT-III was decreased following the degree of hepatic injury and correlation was recognized between AT-III and Normotest, ch-E. AT-III is an excellent index to evaluate the total functioning hepatic cell mass.
2) Increased AT-III, decreased plasminogen activator activity, and increased α
1-AT level were observed in PBC (2 cases). Analysis Normotest, AT-III was specially helpful in the differential between PBC and liver cirrhosis.
3) Coagulation abnormalities in early stage of acute pancreatitis revealed the hypercoagulable state such as an increased fibrinogen, positive SDPS test and decreased AT-III, plasminogen. Fibrinolytic inhibitor (mostly α
1-AT) will increase during acute pancreatitis. It is suggested that the hypercoagulable state in experimental acute pancreatitis has a tendency to become DIC and pancreatic enzyme (such as trypsin) or toxic substances from the inflammed pancreas may have an important role to induce DIC. The role of α
1-AT and α
1-typsin or elastase complex are unknown, and might have some important role as fibrinolytic inhibitors.
View full abstract