Acute Pancreatitis in Man and Blood Coagulation Disturbances

The pathogenesis of blood coagulation-disturbances in patients with acute pancreatitis in man is still unknown. Therefore we studied repeatedly the blood coagulation system of all patients with acute pancreatitis, who were admitted to our clinic or were transferred from other hospitals after complications occurred. 19 patients with a severe pancreatitia were studied. Most of them showed oliguria, pancreatic lungs, thrombosis or haemorrhage. Only 9 determinations (in 5 patients) resulted an enhancement of thrombin generation in the Thrombin-Generation-Test (TGT). All the other patients showed already hypocoagulsbility in the TGT and severe signs of DIC and consumption coagulopathy with a loss of platelets, fibrinogen and prothrombin complex. In 9 patients, who died, we found histomorphologicaliy fibrin deposites and hyaline thrombi. In comparison to 58 patients with elevated amylases but no severe pancreatitiS we found, that the initial alteration of blood coagulation system in pancreatitis is a hypercoagulaoility, possibly caused by trypsin, phospholipase A or elastase.

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Investigation for role of tissue factor and blood coagulation system in severe acute pancreatitis and associated liver injury

Biomedicine & Pharmacotherapy ◽

10.1016/j.biopha.2016.11.039 ◽

2017 ◽

Vol 85 ◽

pp. 380-388 ◽

Cited By ~ 10

Author(s):

Zhi-Bing Ou ◽

Chun-Mu Miao ◽

Ming-Xin Ye ◽

Ding-Pei Xing ◽

Kun He ◽

...

Keyword(s):

Acute Pancreatitis ◽

Liver Injury ◽

Tissue Factor ◽

Blood Coagulation ◽

Severe Acute Pancreatitis ◽

Coagulation System ◽

Blood Coagulation System

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The Ability of Thrombin Inhibitors to Reduce the Thrombin Activity Generated in Plasma on Extrinsic and Intrinsic Activation

Thrombosis and Haemostasis ◽

10.1055/s-0038-1655996 ◽

1997 ◽

Vol 77 (03) ◽

pp. 498-503 ◽

Cited By ~ 26

Author(s):

D Prasa ◽

L Svendsen ◽

J Stürzebecher

Keyword(s):

Active Site ◽

Thrombin Generation ◽

Anion Binding ◽

Thrombin Inhibitors ◽

Coagulation System ◽

Thrombin Activity ◽

Continuous Registration ◽

High Concentrations ◽

20 Nm ◽

Generation Test

SummaryIn a thrombin generation test with continuous registration of thrombin activity in plasma we studied the ability of a variety of thrombin inhibitors of different type and mechanism of action to influence the activity of thrombin after activation of the coagulation system. Depending on the inhibitor, the peak of thrombin activity is delayed and/or reduced.By blocking the active site of generated thrombin inhibitors cause a concentration dependent reduction of the thrombin peak and inhibit feed-back reactions of thrombin resulting in a delay of thrombin generation. Highly potent synthetic active-site directed inhibitors (Ki ≤ 20 nM) reduce the thrombin activity formed in plasma after extrinsic or intrinsic activation with the same efficiency (IC50 0.1 - 0.6 μM) as hirudin. The delay and reduction of thrombin generation by inhibitors of the anion-binding exosite 1 of thrombin is only attributed to an inhibition of feed-back reactions of thrombin. For a 50% reduction of thrombin activity in plasma by this type of inhibitors relatively high concentrations were determined.

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Thrombotic complications and changes in the hemocoagulation system in acute myocardial infarction

Kazan medical journal ◽

10.17816/kazmj64469 ◽

1982 ◽

Vol 63 (5) ◽

pp. 7-9

Author(s):

L. A. Shcherbatenko ◽

S. Z. Gabitov ◽

I. E. Voronina ◽

R. I. Litvinov

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Blood Coagulation ◽

Disseminated Intravascular Coagulation ◽

Coagulation System ◽

Blood Coagulation System ◽

Maximum Activation ◽

Great Vessels ◽

Anticoagulant System ◽

Thrombotic Complications

A natural relationship was revealed between the incidence of thrombotic complications and changes in the indicators of the blood coagulation system in patients with acute myocardial infarction. The totality of tests revealed two periods of maximum activation of the blood coagulation system, combined with inhibition of the anticoagulant system, on the 3-5th and 9-17th days of illness. These periods coincide with the time of the maximum incidence of thrombosis of the great vessels, disseminated intravascular coagulation and recurrence of myocardial infarction.

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