Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antithrombin III (AT III) levels in 37 healthy people and in 103 patients diagnosed of hepatic cirrhosis (75 due to ethylism, 26 cryptogenic and 7 post-hepatitis) have been studied. Forty seven patients presented a compensation in their cirrhosis and 56 an unbalance. AT III concentration was decreased in cirrhotic patients (14.9 + 1.09 mg/dl), being p less than 0.0005 in relation to healthy patients (24.3 + 0.87 mg/dl). Concentration resulted lesser in patients with unbalance (13.9 + 1.8 mg/dl) than in patients with compensation (18.1 + 1.6 mg/dl). Moreover, statistical study between them showed significant results. AT III, though is a protein whose hepatic synthesis is not clear, decreases in diffuse hepatic disease and so much as more severe is the hepatic damage. Cirrhotic patients did not present thromboembolic phenomena, perhaps because of depression of coagulation factors.
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PMID:[Antithrombin III and liver cirrhosis]. 203 69

Antithrombin III is of potential value for replacement therapy in patients with acquired or congenital deficiencies. Pasteurization of the purified inhibitor for 10 h at 60 degrees C can reduce the risk of transfusion hepatitis. Addition of appropriate stabilizers can largely prevent the loss of antithrombin activity which otherwise occurs during pasteurization. Studies of the mechanism of denaturation and stabilization have been facilitated by the use of 8-anilino-1-naphthalene sulfonate which binds weakly to the inhibitor and whose fluorescence undergoes a sigmoidal response to increasing temperature. The extent of the increase in 8-anilino-1-naphthalene sulfonate fluorescence correlates roughly with the loss of antithrombin activity and with the extent of protein aggregation as determined by high pressure liquid chromatography. The midpoint, Td, of the thermal denaturation curve increases by 13 degrees C and 19 degrees C in the presence of 0.5 M and 1.0 M sodium citrate, respectively. Phosphate, sulfate, and EDTA are also strong stabilizers while the chaotropic anions, iodide and thiocyanate are potent destabilizers. Heparin at 10 mg/ml increases Td by 7 degrees C, presumably through a direct binding mechanism; chondroitin sulfate and hyaluronic acid have no effect. Samples pasteurized for 10 h at 60 degrees C in the presence of 0.5 M and 1.0 M citrate retain essentially full activity but exhibit evidence of minor alterations in their interaction with heparin.
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PMID:Thermal denaturation of antithrombin III. Stabilization by heparin and lyotropic anions. 729 49

Fresh frozen plasma (FFP) contains higher levels of intact coagulation factors and coagulation and fibrinolysis inhibitors than solvent/detergent-treated plasma (SD plasma), and also greater residual cell contamination. SD plasma is a particle-free plasma of uniform quality. SD treatment, however, has the specific result of reducing the activities of some inhibitors. Both plasma types carry a minimal residual risk of transmitting human immunodeficiency virus (HIV)-1/2, hepatitis virus B (HBV), and hepatitis virus C (HCV), but SDP is, in addition, also safe with respect to other lipid-enveloped viruses and perhaps with respect to hepatitis virus A (HAV), also due to its antibody (Ab) content. Future revisions of therapeutic plasma safety and quality standards should consider the following points:For FFP:reduce residual cell count in all FFP units to values below 5 x 10(6) leukocytes/l;screen donors for Parvovirus B19 genome and antibodies in order to establish a sufficiently large collection of genome-negative and antibody-positive donors whose FFP can be used for selected patients;For SDP:introduce pool testing for Parvovirus B19 genome; fix an upper limit for genome and a lower limit for antibody content;in addition to the standard quality control methods for therapeutic plasma, focus on assays to test for functionally intact proteinase inhibitors such as alpha(2)antiplasmin (alpha(2)AP) and alpha(1)proteinase inhibitor (alpha(1)PI) that are important for plasma indications. Commercially available kits may not be sufficient to show changes in inhibition kinetics. For both types:introduce an activation marker such as thrombin-antithrombin complex (TAT) as a random test to monitor activation processes during withdrawal, separation, manufacturing, and storage;abolish inappropriate parameters like Antithrombin III (AT III) and coagulation factor XI that are not relevant for changes in plasma quality;finally, support every effort towards establishing an efficient documentation and reporting system on efficacy and side effects of plasma transfusions. Effective reporting alone might help to reveal deficiencies of specific plasma quality and to overcome them through modifications to manufacturing processes and testing, or by defining its indications more precisely.
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PMID:Quality of therapeutic plasma-requirements for marketing authorization. 1237 93

Acute fatty liver of pregnancy is a rare complication of pregnancy that may result in fulminant hepatic failure. We present a review of all patients presenting to a quaternary obstetric hospital over a 15-year period, with particular regard to biochemical changes, results of gene testing, and pre-existing conditions. Seventeen patients with acute fatty liver of pregnancy were identified. Six patients were documented to have pre-existing gastrointestinal disease; five with inflammatory bowel disease, and one with influenza A hepatitis. Antithrombin III levels were low in this study, consistent with previously published data. There were no recurrences of acute fatty liver of pregnancy in nine subsequent pregnancies to seven mothers. The authors are not aware of any literature addressing pre-existing medical conditions which may predispose to acute fatty liver of pregnancy.
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PMID:Acute fatty liver of pregnancy and concomitant medical conditions: A review of cases at a quaternary obstetric hospital. 3057 79