Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

D-dimer and factor VIII levels raise in advanced cirrhosis. We investigated the behavior and the diagnostic usefulness of D-dimer and factor VIII in cirrhotic patients with asymptomatic portal venous thrombosis. Factor VIII coagulant and D-dimer values were measured in 136 consecutive outpatients with stable cirrhosis divided according to Child-Pugh (CP) classification, who underwent color/power ultrasonography to detect portal thrombosis. Portal thrombosis was found in 33 patients (24.2%). In patients without thrombosis, factor VIII was significantly higher in CP class C compared with class A and B. Conversely, class C patients with portal thrombosis had lower factor VIII levels than those without thrombosis. In both groups, D-dimer was significantly increased in class C compared with class A and B. In class C, thrombotic patients showed higher D-dimer values than did patients without thrombosis. In class C, a D-dimer value > or = 0.55 microg/mL provided a sensitivity and a negative predictive value for portal thrombosis of 100%, and a factor VIII coagulant level < or = 80% showed a specificity and a negative predictive value of 76% and 84%, respectively. In class B, a D-dimer value > or = 0.225 microg/mL had a sensitivity of 89% and a negative predictive value of 82%. In conclusion, our study shows that factor VIII values increase in severe cirrhosis but significantly decrease in the presence of concomitant portal thrombosis, likely because of consumption during thrombosis; D-dimer is enhanced by both liver failure and portal thrombosis; in severe cirrhosis, normal D-dimer and factor VIII values may safely exclude the presence of asymptomatic portal thrombosis.
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PMID:Evaluation of D-dimer and factor VIII in cirrhotic patients with asymptomatic portal venous thrombosis. 1619 85

The hallmark manifestations of Cushing's syndrome (CS) are well known, but hypercoagulability is perhaps least recognized. Patients with CS are at increased risk of both spontaneous and postoperative thromboembolism, with the significant majority of events occurring in the lower extremity and pulmonary venous circulations. We present a case of portal vein thrombosis (PVT) occurring in the setting of newly diagnosed CS due to a left adrenal adenoma. Factor VIII activity was approximately 2.5-fold elevated, a known mechanism by which hypercortisolemia predisposes to venous thrombosis. Acute abdominal pain and fever responded well to unfractionated heparin and parenteral antibiotics, and CS was eventually cured by left adrenalectomy. No thromboembolic events have occurred since surgery. PVT is uncommon and usually occurs as a complication of primary or secondary hepatobiliary malignancies and cirrhosis. To the best of our knowledge, this is just the second reported case of PVT due to CS and the first published in the English language literature.
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PMID:Portal Vein Thrombosis in the Setting of Newly Diagnosed Cushing's Syndrome. 2849 82

Essentials The role of increased factor VIII in cirrhosis-induced hypercoagulability has never been demonstrated. Factor VIII and protein C effects were characterized by thrombin generation with thrombomodulin. Factor VIII elevation plays a significant role in cirrhosis-induced plasma hypercoagulability. Only protein C and factor VIII normalization led to thrombin generation similar to controls.
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PMID:Increased factor VIII plays a significant role in plasma hypercoagulability phenotype of patients with cirrhosis. 2963 95


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