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)

Determination of the complement titer in the serum and plasm of 120 patients with chronic liver diseases showed that in eight (7%) patients with cirrhosis of the liver, chronic active or chronic inactive hepatitis complement in the serum was less than half in the plasma. The dissociation of complement serum and plasma was due to cold activation of the classical pathway of complement in vitro since serum drawn from these patients at 37 degrees C lost hemolytic activity in 4 hours when transferred to a cold environment. Neither HB antigen nor cryoglobulin participated in this phenomenon. The activation of complement in the cold could be prevented by increasing the ionic strength, or by adding vitamin E or, to a lesser extent its vehicle HCO-60, while heparin, Trasylol, soybean trypsin inhibitor, or hirudin had no effect. Trans-AMCHA prevented activation in one case. It is speculated that a factor appearing as a result of blood clotting is able to activate the classical pathway of complement in the cold; it is probably not related to Hageman factor (factor XII), factor VII, thrombin, kallikrein.
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PMID:Cold activation of complement i. presence of coagulation-related activator. 5 81

A case is described in which a patient developed TT prolongation and bleeding during CMV hepatitis following successful renal transplantation. Bence-Jones proteinuria was noted, but there was no other evidence of myeloma. Bence-Jones proteinuria, TT prolongation, and bleeding abated as hepatitis resolved. In vitro, a protein isolated from the patient's urine was capable of prolonging the TT markedly, but it did not impair thrombin esterase activity. The effect of the protein seemed to be inhibition of fibrin polymerization. Sephadex gel filtration revealed a single TT-prolonging peak at 11,000 daltons, containing kappa, lambda, and delta antigens. By radioimmunoassay, virtually all the protein present reacted as beta2-microglobulin. Incubation with anti-beta2-microglobulin antiserum markedly attenuated anticoagulant activity. The paraprotein observed transiently in this patient's urine during hepatitis had potent anticoagulant activity and may well have accounted for his abnormal TT and bleeding diathesis; this paraprotein was not distinguishable from beta2-microglobulin.
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PMID:Impaired fibrin polymerization in viral hepatitis. Report of a case: probable identity of the inhibitor with beta2-microglobulin. 21 57

Normal platelets incubated with anti-actin autoantibodies (AAA) (from the serum of patients with chronic aggressive hepatitis) do not show binding of these antibodies as seen by indirect immunofluorescence. AAA serum does not inhibit thrombin-induced clot retraction, despite the binding of the antibodies to platelets in the clot. Similarly, AAA serum does not affect "reversible" or "irreversible" aggregation (induced by ADP, collagen or epinephrine), despite the binding of the antibodies to platelet actin under such circumstances. AAA also bind to platelets when aggregation is inhibited by EDTA. The incubation of "reversibly" aggregated platelet with AAA results in a small but definite binding of AAA to platelets. These findings suggest that during "irreversible" and/or "reversible" aggregation, changes take place at the surface of platelets which expose the antigen at the surface of the cell.
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PMID:Binding of anti-actin autoantibodies to platelets. 40 89

Coagulation pyelolithotomy provides an effective means to remove multiple calculi from the renal collecting system. The strength of the coagulum is directly proportional to the concentration of fibrinogen and inversely proportional to the concentration of thrombin. Because of the fear of hepatitis fibrinogen may soon be unavailable commercially. It will then become necessary to use plasma from the patient as the source of fibrinogen. By the process of cryoprecipitation fibrinogen levels can be increased about 10-fold, yielding clots of greater tensile strength than would be obtained from non-concentrated plasma.
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PMID:Commercial fibrinogen, autogenous plasma, whole blood and cryoprecipitate for coagulum pyelolithotomy: a comparative study. 64 80

Coagulation studies were made on 22 pregnant women with acute infective hepatitis and on 15 normal control pregnant women in third trimester. Fourteen hapatitis patients had clinical evidence of liver failure and all of them had a haemorrhagic diathesis; none of the patients without liver failure showed clinical evidence of haemostatic defects. Coagulopathy was present in most patients, its severity being greater in those with hepatic failure. Significant alterations were observed in bleeding time, whole blood clotting time, prothrombin time, thrombin time, plasma fibrinogen and serum levels of fibrinogen degradation products. The last three disturbances were most frequent in patients with liver failure. Increased fibrinolysis and disseminated intravascular coagulation also appeared to play a contributory role, particularly in patients with hepatic failure.
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PMID:Blood coagulations studies in pregnant patients with infective hepatitis. 88 47

A study of coagulation disorders due to hepatitis A infection occurring during pregnancy was undertaken to determine if the unique coagulation status produced by pregnancy (elevated clotting factors and decreased fibrinolytic activity) was responsible for the increased severity of hepatitis A infections reported for pregnant women from various parts of the world. Of 49 patients studied, 12 (24%) developed hepatic failure and 9 (18%) died. A prolonged prothrombin time and low fibrinogen level were found to be as frequent as previously reported for nonpregnant patients with and without hepatic failure. Thrombocytopenia was less common and a long thrombin time was more common. Although intravascular coagulation was suggested by a lower mean fibrinogen level than expected in late pregnancy, mean platelet counts were similar to controls. The frequency of a positive protamine sulfate paracoagulation test for intravascular coagulation (DIC) was similar to that reported for uncomplicated pregnancy, and was of no prognostic value when performed on admission. We conclude that the severe clinical course of hepatitis during pregnancy in this epidemic was not attributable to a predisposition for DIC. However, once fulminant hepatitis occurred, DIC may have been a clinically significant factor.
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PMID:Coagulation studies of viral hepatitis occurring during pregnancy. 100 76

A bedside method of measurement of the whole-blood thrombin time for the determination of heparin activity was used in 300 dialyses. It was easily performed by the whole staff despite the absence of previous training in laboratory work. This test, using a clot timer with an automatic pipette device, gives a minimum risk of exposure to hepatitis virus. An increase of the thrombin time of 50-100 per cent above the starting value (3.7-6.6 sec) was aimed at during the heparin infusion. Bleeding complications, which were minor, were seen only on 18 and fibrin formation only on 26 occasions out of 1500 observations. Within the 50-100 per cent limits bleeding complications were observed on 2 and fibrin formation on only 13 occasions. No protamine was given.
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PMID:Whole-blood thrombin time: a bedside method for determination of heparin activity. 100 99

In this presentation we have contrasted the normal blood-clotting mechanism with the failure to form blood clots in hemophiliacs due to the absence of protein factors necessary for conversion of prothrombin to thrombin. The statistics, hereditary basis, and long-term disabling consequences of hemophilia to the severely ffected patient are described. The systemic means of minimizing severe joint disabilities and serious internal bleeding hazards by employing concentrates of antihemophilic factors to reverse the bleeding defects are discussed. Availability and advantages of the types of concentrates are explained. The fatalistic attitude of hemophiliacs toward hepatitis is discussed, along with admonitions to avoid the use of aspirin, alcohol, and buttock injections. Alternative medications for pain are recommended; and injection sites for pediatric patients are suggested. The details of simplified oral surgical management of hemophilic patients without hospitalization are described, including local anesthetic injection technique, method of performing extractions, general anesthesia techniques when indicated, materials for packing of extraction sockets, regimen and precautions in use of Amicar administration for clot maintenance, postoperative diet, and postsurgical activity guidelines. Also noted is the self-administration of intravenous concentrate infusions at home in the event of hemorrhagin, so that bleeding is on the way to bein controlled even before the patient reaches the hospital. We avoided orthodontic treatment of hemophilic patients in the past; however, recently developed bracket-fixation techniques and auxiliary aids; along with an enlightened understanding that gingival bleeding is ot to be feared, have changed our attitude, and we now treat hemophilic patients in much the same manner as otherwise normal orthodontic patients...
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PMID:Orthodontics and dentistry for the hemophilic patient. 110 95

The authors have analysed the development of various coagulation factors in 104 cases of common virus hepatitis in young adults. Total plasma coagulability, the prothrombin complex, factors VIII and IX, fibrination and fibrinolysis were followed up during this evolution and compared, using the usual statistical methods, with the results of the same investigations carried out on 100 healthy subjects belonging to the same age-group and on 31 patients suffering from cirrhosis of the liver. Statistical methods showed up the slightest disturbances of any significance which would have been overlooked if individual results only had been examined. As it was, there was total plasma hypercoagulability which was at its maximum at the onset of development but which persisted until the 7th week. It was mainly connected with an abnormality at the second stage of fibrination, that is : polymerisation of the fibrin monomers. The results obtained do not allow a conclusion to be drawn as to whether there exists an antipolymerase or dysfibrinogenaemia. Later research dealing specifically with the chemical structure of fibrinogen in hepatitis should provide further information. In practice, assessment of total plasma coagulability, using cephalinkaolin time, and analysis of fibrination by thrombin time are of definite value on account of their sensitivity.
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PMID:[Coagulation factors during the development of common viral hepatitis]. 121 72

The objective of this study was to characterize the hemostatic defect in dogs with infectious canine hepatitis (ICH), a naturally occurring viral disease of dogs. Five littermate dogs were inoculated with 10(3) TCID50 of ICH virus intravenously. Two littermates were controls. The clinicopathologic manifestations of ICH were fever, depression, anorexia, hematemesis, melena, widespread mucocutaneous petechiae, prolonged bleeding from venipunctures, faceial edema, leukopenia, and proteinuria. The hemostatic defect of ICH was characterized by thrombocytopenia, abnormal platelet function, prolonged one-stage prothrombin time and activated partial thromboplastin time, normal thrombin times, depressed factor VIII activity, and increased fibrin-fibrinogen degradation products. These findings suggested that the central pathologic mechanism of the abnormal hemostasis in ICH was disseminated intravascular coagulation (DIC). ICH is an example of DIC induced by viral infection. This disease is a suitable model for investigation of the detection, pathogenesis, and therapy of DIC.
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PMID:Infectious canine hepatitis: animal model for viral-induced disseminated intravascular coagulation. 124 23


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