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)

Recombinant activated factor VII (rFVIIa) has been successfully used ''off-label'' in patients with refractory life-threatening hemorrhage. Intravenous rFVIIa was given to 31 patients unresponsive to standard therapy with blood products and surgical reexploration, who were bleeding due to trauma, surgery, organ transplantation, liver cirrhosis, ruptured uterus. We recorded their coagulation and hematologic profiles, acid-base balance, blood loss, number of red blood cells (RBC), plasma and platelet transfusions, complications, and survival. rFVIIa (mean dose 132.2 +/- 56.3 microg/kg) effectively contained the hemorrhage in 28/31 (90.3%) cases, with a mean reduction in blood loss from 12.4 +/- 10.2 to 2.7 +/- 2.2 L (P < .0001). The need for RBC, platelet, and plasma transfusion decreased significantly after rFVIIa, with a consequent significant improvement in clotting of test hematocrit, pH, and bicarbonates. Four patients had adverse events potentially related to rFVIIa. The survival rates after 1 and 30 days were 48.4% and 29.1%, respectively.
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PMID:Effect of recombinant activated factor VII in critical bleeding: clinical experience of a single center. 1960 76

Vitamin K is frequently administered in cirrhotic patients to correct their coagulopathy, but evidence for such practice is lacking. We aimed to assess whether vitamin K administration increases the levels of the vitamin K-dependent factor VII (FVII), protein C, and protein S in patients with different stages of liver dysfunction. Eighty-nine patients were recruited into four groups: group 1 [hepatitis B virus (HBV) inactive carriers, n = 23]; group 2 [chronic HBV and hepatitis C virus (HCV) hepatitis, n = 21]; group 3 (cirrhosis, n = 24); group 4 (hepatocellular carcinoma, n = 21); and a healthy control group (n = 39). A single dose of 10 mg of vitamin K1 was administered subcutaneously to all patients. Prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen, FVII, protein C, total and free protein S, and proteins induced by vitamin K absence (PIVKA)-II (des-gamma-carboxy prothrombin) were measured at baseline and 72 h after vitamin K administration. There was progressive increment in baseline PIVKA-II, and decrements in fibrinogen, FVII, protein C, and protein S across study groups (P < 0.0001). Compared to baseline, vitamin K administration did not affect the measured parameters, whereas TT showed no reduction in any of the groups. Protein C levels declined in group 2, whereas FVII, total and free protein S did not increase in any group, for all parameters. Vitamin K therapy does not cause significant improvements in the majority of coagulation parameters and hence does not seem to be routinely indicated in patients with liver disease.
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PMID:The coagulopathy of liver disease: does vitamin K help? 2308 Mar 65

Nonalcoholic fatty liver disease (NAFLD) is increasingly being diagnosed and is considered to be the most frequent chronic liver disorder in Western countries. It represents a histopathological spectrum ranging from simple hepatic steatosis to steatohepatitis and finally cirrhosis. NAFLD is considered as the hepatic manifestation of the metabolic syndrome and is associated with increased mortality. Increasing evidence now suggests that NAFLD is also associated with higher cardiovascular disease (CVD) morbidity and mortality independent of conventional cardiometabolic risk factors (such as obesity, insulin resistance, and diabetes mellitus). The exact mechanisms linking NAFLD to increased CVD risk are still incompletely understood and likely reflect multiple coexisting pathways. Recent evidence suggests a contributive effect of an altered hemostasis in patients with NAFLD. For example, patients with NAFLD have higher levels of prothrombotic factors (e.g., von Willebrand factor, fibrinogen, factor VII activity, and plasminogen activator inhibitor-1), which correlate with underlying histological severity of the disease. The current review focuses on these hemostatic abnormalities in NAFLD and the link with increased CVD risk.
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PMID:Vascular Disease in Patients with Nonalcoholic Fatty Liver Disease. 2604 73


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