Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.5 (thrombin)
 33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acquired dysfibrinogenemia was documented in a 4-year-old child with obstructive jaundice of 1-month duration, secondary to a choledochal cyst involving the distal common bile duct. It was characterized by decreased thrombin coagulable protein with elevated immunoassayable fibrinogen resulting in abnormal thrombin and reptilase times. The liver morphology was compatible with extrahepatic obstruction, without evidence of cirrhosis or hepatocyte abnormality. All the coagulation abnormalities promptly resolved after surgical correction of the obstruction. Dysfibrinogenemia has been associated with serious liver disease in adults, including tumors, chronic active hepatitis, and cirrhosis, but never with isolated obstructive jaundice. This report documents a case of acquired dysfibrinogenemia due to extra-hepatic biliary obstruction and also emphasizes the importance of the consideration of this disorder in coagulation abnormalities associated with hepatobiliary disease.
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PMID:Dysfibrinogenemia in obstructive liver disease. 368 83

Using a new and sensitive screening method, dysfibrinogenaemia (DF) was detected in 76% of patients with cirrhosis, 78% with chronic active liver disease and 86% with acute liver failure. The incidence was much lower in obstructive jaundice (8%) and miscellaneous liver disorders (4%). It is concluded that the fibrin monomer polymerisation (FMP) ratio test is a simple and sensitive test for the detection of DF, and is useful in the differential diagnosis of hepatocellular and obstructive jaundice. Hyperfibrinogenaemia, particularly in patients with obstructive jaundice, may explain the high incidence of abnormal thrombin and Reptilase clotting times despite normal FMP ratios. Dysfibrinogenaemia dose not appear to be related to the degree of liver function impairment, but may be associated with regeneration of hepatic tissue.
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PMID:Acquired dysfibrinogenaemia in liver disease. 708 17

Hepatic artery aneurysm rupture is a rare condition that requires urgent diagnosis and treatment in order to avoid a potentially fatal outcome. The clinical presentation is often non-specific. The classic triad of abdominal pain, gastrointestinal hemorrhage, and obstructive jaundice occurs in less than one-third of cases. Physical examination is rarely helpful since bruits, masses or pulsations are infrequent. Radiologic imaging provides the best tool to early diagnosis. Angiography has historically been the gold standard of diagnosis and is needed prior to radiologic intervention. Computerized tomography, doppler ultrasound and even magnetic resonance imaging have all demonstrated visceral artery aneurysms with success. Conventional treatment has included surgical ligation and resection. More recently transcatheter embolization or even percutaneous transhepatic injection of thrombin has been successfully performed by the interventional radiologist. This article discusses the clinical presentation, imaging findings, and review of the literature of this elusive entity.
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PMID:Hepatic artery aneurysm rupture: case report, imaging findings, and literature review. 983 Mar 29

The plasma of patients with pronounced jaundice as well as that of cats with experimental obstructive jaundice inhibits the clotting of normal plasma with thrombin. The influence of different bile constituents-bilirubin, bilirubin glucuronides, sodium salts of bile acid-on the clotting of plasma or fibrinogen with thrombin was examined. Bilirubin glucuronides in concentrations above 8 mg.% showed antithrombic activity but other substances were inactive. Glucuronic acid and phenolphthalein glucuronide in concentrations up to 100 mg.% did not have any influence on the thrombin time.
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PMID:The antithrombin activity of glucuronic esters of bilirubin. 1445 19