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)

The recent observation by Arndt-Hansen et al. (1974) of increased frequency of blood group A over group O in blood donors positive for the hepatitis associated antigen has been investigated in Down's syndrome, in order to establish if this could account for the increased frequency of the antigen in that syndrome. Seventy-one of 227 subjects with Down's syndrome (31.3%) were found to be positive for the antigen by haemagglutination, and comparison of these with the HAA-subjects failed to reveal any differences in the ABO blood groups.
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PMID:Hepatitis associated antigen and the ABO locus in Down's syndrome. 12 67

Hepatitis-Associated (Australia) Antigen (HAA) was detected in 13 (5.8%) of 223 patients with Down's syndrome and in 14 (3.7%) of 378 patients with other forms of mental retardation. The frequency of HAA was 2.4 per cent in 127 noninstitutionalized patients with Down's syndrome, and 10.4 per cent in 96 institutionalized patients. The frequency of HAA with Down's syndrome was lower on the average in Japan than in the United States or Germany. HAA was detected in one (1.3%) of 78 mothers of infants with Down's syndrome. Our study suggests that maternal exposure to HAA, as reflected by the presence of either HAA or anti-HAA, was not associated with the subsequent birth of an infant with Down's syndrome.
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PMID:Hepatitis-associated (Australia) antigen and Down's syndrome. 12 83

In 50 patients with acute hepatitis serum lipide and lipoproteins were determined at regular intervals and the results were compared with the usual liver function tests. Australia-antigen was established in 26 patients. During the first three weeks of the disease the most striking finding was a significant increase in the triglycerides, which was most pronounced at the end of the second week. Triglyceride levels usually returned to normal during the fourth week. In the course of the disease, lipoprotein electrophoresis showed marked decrease or absence of alpha- and pre-beta-lipoproteins during the first two weeks. During the third week faint alpha and pre-beta bands recurred in most patients. By the end of the fourth week lipoprotein electrophoretic findings were back to normal. There was general correlation between routine tests of liver function and results of lipid analyses throughout the course of the disease. This typical pattern of serum lipid and lipoprotein changes was found with near-consistency in patients with HAA-positive hepatitis. It was also present in the majority of HAA-negative patients, though in these the characteristic discrepancy between hypertriglyceridemia and simultaneous decrease of the pre-beta-lipoprotein band in eletrophoresis was, on the average, absent.
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PMID:[Changes in serum lipids and lipoproteins in acute hepatitis]. 18 24

Due to its high sensitivity, radioimmunoassay has become of great importance in the detection and measurement of levels of proteins and steroids in body fluids. However, this method involves the use of expensive equipment and radioactive material. Herein is described an alternate method to radioimmunoassay, which uses an enzyme-labeled rather than a radioactively-labeled antibody. An enzyme immunoassay procedure, the Cordia HAA-enzyme Immunoassay, for the detection of hepatitis-associated antigen has been evaluated. With this technique a sandwich type immunoassay with an alkaline phosphatase tagged second antibody is used. The presence of antigen is detected by the p-nitrophenyl phosphotase activity of the bound enzyme. In 1083 clinical samples from patients of Jackson Memorial Hospital, only 19 discrepant results were found when tested by both the Cordia and the Ausria II methods. Eight had sufficient sera for retesting, yielding two positive Cordia, negative Austia; one negative Cordia, positive Ausria; one borderline positive; and four unconfirmed false positives by Cordia.
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PMID:Enzyme immunoassay of hepatitis associated antigen (HAA). 32 Jun 36

A patient of 50 years is admitted to hospital. He is found to be suffering from infectious hepatitis complicated by thrombocytopenia, the initial platelet count being 10 000 per mul soon falling to 2000 per mul. A prompt increase in the number of platelets is seen during treatment with prednisone, but a sudden fall is observed after a gradual reduction of prednisone to zero, the reaction for hepatitis associated antigen at that point still being positive. After a renewed therapy with adrenocortical steroid, the platelet count is within normal limits, and the patient is discharged with a small dose of prednisone. At the time of discharging, the HAA reaction had been negative for 3 weeks. After treatment with a small dose of prednisone for 2 months, the patient was taken into hospital. In the course of one week the dose of prednisone was gradually reduced without any fall in the platelet count. The possibility of lysis of a platelet-virus antigen as an explanation of thrombocytopenia complicating infectious hepatitis is discussed.
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PMID:Thrombocytopenia complicating infectious hepatitis. 113 Jan 62

A radioimmunologic test system for determining the subtypes D and Y of the hepatitis-B surface antigen (HBs-Ag, Australia antigen, HAA) is described. This technique uses the immunoadsorption principle. The antigen to be subtyped is incubated with an antiserum which contains (125)I-labeled antibodies to the antigenic determinants a, d, and y. The specificity of the antibody which is not consumed in forming the antigen-antibody complex is determined by absorption on agarose to which HBs-Ag of subtypes D and Y is coupled. This specificity permits conclusions as to the subtype of the hepatitis-B surface antigen which is being investigated.
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PMID:A radioimmunoassay to determine the subtypes D and Y of the hepatitis-B surface antigen. 127 Aug 83

In a significant percentage of examined cases of fulminant hepatitis, subacute hepatitis, chronic aggressive hepatitis, liver cirrhosis and chronic persistent hepatitis, Australia (hepatitis-associated) antigen (Au HAA) was identified in the liver and in extrahepatic locations. The several immunofluorescent patterns of Au HAA localization in hepatocytes strongly suggested various stages of Au HAA accumulation and release. Deposits of a mixture of immunoglobulins G and M and occasionally beta1C-globulin were found in the cytoplasm of Au HAA containing hepatocytes, on their plasma membranes, on or in the nuclei, in the cytoplasm of Kupffer cells and, rarely, in the sinusoids. The accompanying tissue changes were hepatocellular degeneration and necrosis. These intra- and extracellular complexes of Au HAA and immunoglobulins displayed strong affinity for guinea pig complement in the immunohistochemical complement fixation reaction. When tested by immunodiffusion in agar, IgG dissociated from these complexes by potassium thiocyanate (KSCN) treatment showed anti-Au HAA specificity. In fulminant hepatitis neither Au HAA nor immunoglobulins and complement were found in the liver. In chronic aggressive hepatitis and subacute hepatitis the amount of the Au HAA immune complexes identified in the liver was approximately inversely proportional to the extent and severity of the parenchymal lesions. In liver cirrhosis and chronic persistent hepatitis there was a positive correlation between the amount of the Au HAA immune complexes found in the liver and the degree of hepatocellular damage. The deposits of Au HAA, identified in extrahepatic locations including germinal centers of lymph nodes and spleen, kidney glomeruli and blood vessel walls, were as a rule accompanied by deposits of IgG, IgM, beta1C-globulin and fibrin. All these deposits showed strong affinity for guinea pig complement in the immunohistochemical reaction of complement fixation. Germinal center activation, chronic membraneous glomerulonephritis, panarteritis and simple arteriolar hyalinosis were found at sites of localization of these deposits.
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PMID:Tissue localization of Australia antigen immune complexes in acute and chronic hepatitis and liver cirrhosis. 462 11

Hepatitis-associated (Australia) antigen (HAA) was detected in the sera of 16 (50%) of 33 patients with Hodgkin's disease; all of these patients had received the same treatment for approximately two years, and they had been in complete remission for at least two years. The HAA-positive patients had significantly higher levels of serum SGPT and significantly lower bromsulphalein clearance than the HAA-negative patients. Histological changes compatible with a diagnosis of chronic persistent hepatitis were found in the livers of 12 of the 16 HAA-positive patients and in five of the 17 HAA-negative patients (p < 0.05). In 128 patients with Hodgkin's disease who had received various forms of treatment and who were studied at various stages of remission, HAA was found in the sera of 42 (33%). Tests for HAA repeated four months later in positive reactors of both groups showed persisting antigenaemia. Hepatitis-associated antigen was not present in the sera of any of 36 patients with Hodgkin's disease studied when the diagnosis was first made and before treatment had begun. These observations suggest that persistence of HAA and the presence of chronic persistent hepatitis were more likely to be related to the treatment the patients had received than to the disease itself.
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PMID:A possible relationship to treatment between hepatitis-associated antigen and chronic persistent hepatitis in Hodgkin's disease. 471 8

We discuss the case of a 24-year-old black woman at 33--34 weeks gestation, who after intravenous injection of Talwin presented with the following symptom complex: pyrexia, nausea, vomiting, shaking, chills, headache, myalgias, polyarthralgias, severe abdominal pain and "contractions." This symptomatology presents a complex diagnostic problem. Systematic laboratory evaluation eliminated more common etiologies, i.e., sub-acute bacterial endocarditis, HAA + hepatitis, placental abruption, chorioamnionitis, and urinary tract infection. The Talwin had been filtered through cotton ball. History plus exclusion of other etiologies led to the diagnosis of "cotton fever." The available literature is reviewed, and the importance of recognizing this entity when servicing a pregnant population with a high rate of drug abuse is discussed.
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PMID:Cotton fever and pregnancy. A confusing clinical problem. 721 12