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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A prospective study of post-transfusion hepatitis was conducted in 97 adult patients undergoing open heart surgery. Twelve patients developed presumed non-A, non-B hepatitis (five of these were hospitalized and three were jaundiced), and all 12 had received clotting factors from pooled plasma (fibrinogen, factor VIII, factor IX complex) from different manufacturers. Of the remaining 85 patients none received these high risk plasma derivatives and none developed hepatitis. Multiple peak ALT elevation seems to be an indication of development of chronic non-A, non-B hepatitis. In addition to the 12 cases of presumed non-A, non-B hepatitis, nine cases of serological changes related to hepatitis B virus were observed as follows: six early booster reactions of anti-HBs, but not anti-HBc, in anti-HBs and anti-HBc positive persons; one late immunization-like response for anti-HBs and two serological hepatitis B infections without transaminase elevation. Five of the nine cases were also associated with the administration of pooled clotting factors.
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PMID:Post-transfusion hepatitis and its association with pooled clotting factors. 640 30

We report immunohistological findings in liver, spleen, brain, and skeletal muscle of a 23-year-old woman with hepatitis nonA/nonB caused by contaminated anti-D-globulin. She died in a liver coma. At autopsy, a chronic liver dystrophy with cirrhosis was diagnosed. The necrotic areas of the liver showed a collapse of the reticulin framework, newly formed collagen fibres, and diffuse inflammation with immunohistological evidence of IgG, CIq, C9, and fibrinogen. C4 and C9 could be localised in bile thrombi and in the cytoplasm of pseudotubular transformed hepatocytes. In addition, C9 was found in blood vessel walls. A local distribution of HBsAg was found in the cytoplasm and/or the periphery of liver cells. HBcAg could not be detected in any of 5 different regions of the liver. A serum with antibodies to acute phase antigen of nonA/nonB hepatitis stained the cytoplasm and nuclei of (mostly intact) liver cells focally and their cell membranes diffusely. Patchy deposits of IgA and IgM were demonstrated in liver, brain und spleen. Circulating antibodies to cell nuclei and smooth muscle reacted with the patient's own liver and brain but not with spleen and skeletal muscle.--It is suggested that the manifold immunohistological findings in this patient are an expression of the vain attempt of the organism to clear away antigenic material, probably induced by different hepatitis viruses.
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PMID:[Immunohistologic findings in the liver, spleen, brain and skeletal muscles in fatal cholestatic viral hepatitis (following double infection with hepatitis B and non-A/non-B?)]. 641 98

HBsAg has been detected by direct immunofluorescence in the small bowel biopsy specimen of a 16 a old male patient with diarrhoea and HBsAg seronegative (autoimmune) chronic aggressive hepatitis. HBsAg was localized focally in apical regions of intestinal crypts, in the cytoplasm, and on their cell membranes as well as in vascular endothelium. Pretreatment of the tissue sections with unlabelled anti-IgM, anti-IgG, and fresh human serum did not block the direct staining for HBsAg. Antisera to IgG, the complement components C1q, C4, and C5 as well as to fibrinogen and FITC-Staphylococcus protein A were bound in a similar manner. Therefore, it may be reasonable to assume, that hepatitis B virus can infect the human small intestine and could be regarded as one of rare gastroenteritic viruses.
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PMID:[Immunofluorescent optical detection of HBSAG in the human small intestine in chronic aggressive HBSAG-seronegative hepatitis with diarrhea]. 642 Oct 68

Titrated stocks of hepatitis B virus and Hutchinson strain non-A, non-B hepatitis virus were diluted in normal serum to contain, respectively, greater than or equal to 10(6) and greater than or equal to 10(4) chimpanzee infectious doses (CID50) per milliliter and exposed to 1% Tween 80 and 20% ether at 4 degrees C for 18 h. After evaporation of the ether, the treated sera were each inoculated into two chimpanzees. The animals remained free of serologic and biochemical evidence of hepatitis during a 6-month follow-up period, and were then shown to be susceptible to infection by challenge with the original untreated inocula. To assess the effect of exposure to Tween 80/ether on coagulation factors, four lots of antihemophilic factor (AHF) concentrate and 2 lots of commercial factor IX concentrate were treated as above. For the AHF concentrate there was an average of 70% recovery of factor VIII procoagulant activity, 93% recovery of factor VIII-related antigen, and 73% recovery of fibronectin opsonin activity and no detectable change in ristocetin cofactor activity or in fibronectin antigen. Crossed immunoelectrophoresis revealed no change in migration rate of fibrinogen, fibronectin, and von Willebrand factor (vWF), although the quantity of fibrinogen was reduced. Factor VIII procoagulant activity and vWF activity remained associated during chromatography on BioGel A15.
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PMID:Inactivation of hepatitis B and Hutchinson strain non-A, non-B hepatitis viruses by exposure to Tween 80 and ether. 642 34

Evidence supporting the existence of two agents of human non-A, non-B hepatitis was obtained by the inoculation of chimpanzees sequentially with serum from a chronically infected human (Inoculum I) and with fibrinogen prepared from pooled plasma (Inoculum IV), each of which had transmitted non-A, non-B hepatitis to humans. Passage inoculations of serum samples obtained during the acute stages of chimpanzee infections transmitted by either the agent in Inoculum I or IV also transmitted non-A, non-B hepatitis to additional chimpanzees. Transmission and passage of the agent in Inoculum IV were conducted in chimpanzees which previously had recovered from infection by the agent in Inoculum I. Cytoplasmic tubules in hepatocytes, which have been described during non-A, non-B hepatitis, were observed by electron microscopy in liver biopsies obtained during all infections transmitted by the agent in Inoculum I. These cytoplasmic tubules were not detected in liver biopsies from chimpanzees infected by Inoculum IV, except in one chimpanzee inoculated by Inoculum IV without prior exposure to the agent in Inoculum I. The cytoplasmic tubules observed in this study were found to be composed of transverse bands arranged with a periodicity of approximately 17 nm. These studies suggest that two different agents or distinct serotypes of human non-A, non-B hepatitis may have been present in these inocula, although reactivation of latent infection or reinfection could not be ruled out completely.
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PMID:Additional evidence for more than one agent of human non-A, non-B hepatitis. Transmission and passage studies in chimpanzees. 642 90

Large amounts of Factor VIII concentrates are required for the treatment of haemophiliacs. Two batches each of nine commercial preparations were examined for their in vitro properties. The parameters studied were Factor VIII coagulation activity (F VIII: C), ristocetin cofactor activity (F VIII R: CoF), the Factor VIII antigen content (F VIII R: Ag), fibrinogen, fibronectin and immunoglobulins. The preparations were also tested to determine their hepatitis A and B marker content. In none of the investigated concentrates compared to the data given by the manufacturers was a marked F VIII: C deficit. All the preparations showed higher values for F VIII R: Ag than for F VIII: C. Factor VIII concentrate HS was the only concentrate in which the fibrinogen concentration was below the detection limit and only small amounts of fibronectin and immunoglobulins were detected. In two of the nine preparations tested possible contamination with hepatitis B viruses was more or less ruled out by means of hepatitis serology.
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PMID:[Comparative protein chemistry studies on Factor VIII concentrates]. 643 15

An analysis of findings of laboratory examinations of 36 patients with a cholestatic form of virus hepatitis and 35 patients with carcinoma of the hepatopancreatoduodenal zone enabled the authors to establish the differential-diagnostic significance of the activity of gamma glutamyl transpeptidase, time of plasma recalcification, plasma tolerance to heparin, fibrinogen content in plasma and fibrinolytic activity in cholestatic hepatitis and mechanical jaundice.
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PMID:[Differential diagnosis between the cholestatic form of viral hepatitis and tumor-caused obstructive jaundice]. 664 68

The addition of excess sodium citrate to plasma was found to inhibit fibrin polymerisation (clot opacity) from patients with cirrhosis, hepatitis and hepatoma but not from normal controls. Abnormal clot opacity in plasma from patients with liver disease could be partly or completely abolished by removal of citrate ions by dialysis against citrate-free buffer, but not by dialysis against buffer containing citrate. Similar results were observed in plasma freed of calcium ions by treatment with EGTA. Treatment of plasma with neuraminidase largely abolished the inhibitory effect of excess citrate, and the thrombin times and clot opacity of asialofibrinogen were less affected by citrate than native fibrinogen. In addition, the effects of citrate on the clotting of purified, calcium-free fibrinogen from cirrhotic patients correlated with the sialic acid content. It is concluded that binding of citrate ions to fibrinogen renders the molecule acutely more sensitive to elevations in the sialic acid content, and that a simple plasma clot opacity test in the presence of excess citrate may be a useful aid in the differential diagnosis of liver disease. These findings may also explain why defects in fibrin polymerisation observed in plasma are not always reproduced in purified fibrinogen or fibrin monomer preparations.
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PMID:The role of sodium citrate in the dysfibrinogenaemia of liver disease. 672 77

Two patients who had received a fibrinogen preparation contracted hepatitis of non-A/non-B etiology 3 and 8 wk after the injection. A chimpanzee inoculated with the same preparation developed hepatitis 11 wk later, with an increase in SGPT and a liver pathology compatible with acute viral hepatitis. His preacute serum containing the presumptive etiologic agent induced hepatitis in another chimpanzee. Electron microscopic observation of the liver of these chimpanzees biopsied during preacute and acute stages revealed peculiar tubular structures composed of two unit membranes with electron-opaque material in between. Using the serum obtained from infected chimpanzees at convalescence as an antibody reagent, viruslike particles were identified in the fibrinogen preparation by immune electron microscopy. When the serum of 100 apparently healthy blood donors with SGPT value of 80 Karmen units/ml or higher was tested for viruslike particles, eight were found to be positive. Furthermore, one of these sera, when a 5-ml amount was injected into each of two chimpanzees, induced hepatitis with viruslike particles in the circulation and characteristic tubular changes in the liver. On the basis of the results obtained, the viruslike particles in the fibrinogen preparation, as well as in the circulation of apparently healthy donors, were capable of inducing hepatitis of non-A/non-B category with a liver pathology characterized by tubular structures. The detection of non-A/non-B viral particles, especially when refined to routine laboratory tests, may open the way for the specific diagnosis, exclusion of contaminated blood from transfusion, and eventual prophylaxis by vaccination.
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PMID:Viruslike particles in a plasma fraction (fibrinogen) and in the circulation of apparently healthy blood donors capable of inducing non-A/non-B hepatitis in humans and chimpanzees. 677 3

During a period when screening for hepatitis B surface antigen (HBsAg) was performed by immunodiffusion using dextran-containing agarose gel, a diffuse precipitation (DP) zone was observed when citrate plasma samples were reacted with certain serum specimens. The DP reaction was noted with a significantly larger number of sera from patients with renal disorders, hepatitis, or certain other virus infections than with sera from apparently healthy blood donors, indicating that it was associated with some type of pathological condition. Highly purified fibrinogen used as detector reagent instead of plasma was sufficient to elicit a precipitation zone similar to that of the DP reaction. In the presence of coagulation inhibitors such as heparin, hirudin and antithrombin III the DP reaction was inhibited, suggesting that the precipitation zone represents coagulation. Cross-linked fibrin was demonstrated in the precipitates of DP-positive sera but not in the corresponding zone of a DP-negative serum.
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PMID:Fibrin formation induced in agarose gel in the presence of plasma by sera from patients with certain diseases. 679 95


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