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)

Medical histories of themselves and their first-degree relatives were obtained from parents of 82 leukaemic children (54 acute lymphoblastic (ALL), 28 acute myeloblastic (AML)) and from control couples matched for age. The possibility of a primary familial immunological abnormality as an aetiological factor in childhood leukaemia was suggested by binding some infections significantly more frequently reported in parents than in controls, but more strongly supported by the finding of a significantly (P less than 0.02) increased prevalence of disorders associated with autoimmunity (but not of other conditions such as peptic ulceration, infective hepatitis, tuberculosis or malignancy) amongst members of ALL families compared to those of controls. Analogy with Down's syndrome and the strain of NZB mice, in which diminished T-cell function is associated with autoimmune disease and lymphoid neoplasia, is discussed. Varicella and herpes zoster occurred respectively in 2 ALL mothers during their pregnancies involving the patients and in none of the other 388 pregnancies here reported. This supports previous evidence that antenatal varicella infections may be of aetiological importance in some cases of ALL.
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PMID:Family studies in acute leukaemia in childhood: a possible association with autoimmune disease. 28 5

A solid-phase enzyme linked immunosorbent assay was developed for the detection of immunoglobulin M antibody to hepatitis A virus. The system was capable of detecting hepatitis A-specific immunoglobulin M in a single dilution of serum and appears to be a reliable and rapid means of establishing a diagnosis of hepatitis A infection. Specific immunoglobulin M was only detected in patients with serologically confirmed hepatitis A and not in patients with other forms of hepatitis, chronic liver disease, or autoimmune disease. In patients with hepatitis A, specific immunoglobulin M was usually detectable for 6 weeks after the onset of dark urine, and the longest period for which it was present in any patient was 115 days. This enzyme-linked immunosorbent assay is rapid, simple to perform, and does not require complicated equipment. Provided adequate supplies of purified reagents can be obtained, this enzyme-linked immunosorbent assay procedure is likely to simplify hepatitis A serology, because the same antibody-coated plates can be utilized to detect hepatitis A virus, anti-hepatitis A virus, and hepatitis A-specific immunoglobulin M.
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PMID:Solid-phase enzyme-linked immunosorbent assay for detection of hepatitis A-specific immunoglobulin M. 37 36

Twenty-six of 388 patients (6.7%) followed prospectively after open-heart surgery developed non-A, non-B hepatitis. Of these 26, 12 had an elevated (often fluctuating) serum alanine aminotransferase (SGPT) for greater than 1 year. Liver biopsy, done in eight of 12, showed chronic active hepatitis in six and chronic persistent hepatitis in two; one patient with chronic active hepatitis had early cirrhosis. Anicteric patients with peak SGPT greater then 300 IU/L were at greatest risk of developing chronic hepatitis. Chronic non-A, non-B hepatitis was symptomatically mild and unaccompanied by physical signs or laboratory evidence of autoimmune disease or severe chronic liver disease. In all 12 patients there was spontaneous improvement in serum transaminase over a period of 1 to 3 years, and four patients had sustained normalization of SGPT. Thus chronic active hepatitis is a common sequela of acute non-A, non-B hepatitis but may have a better prognosis than chronic active hepatitis of other causes.
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PMID:The chronic sequelae of non-A, non-B hepatitis. 46 17

The hypothesis that "halothane hepatitis" is related to hypersensitivity to the agent is widely accepted. The hypothesis is based, in part, on reports ostensibly demonstrating cell mediated immunity to halothane in such patients. These reports, however, are open to criticism and have not been confirmed. Halothane is unlikely to be capable of antigenicity in its own right, although reactive metabolites may be involved. We have further investigated cell mediated immunity in patient with alleged halothane hepatitis. Human serum albumin and liver specific protein were chemically trifluoroacetylated and these complexes were used as potential antigens in lymphocyte transformation and leucocyte migration inhibition tests. Using these in vitro indices, cell mediated immunity was not demonstrated in any of the patients studied. It is possible that other metabolites and/or carrier molecules may be involved, and that patients predisposed to autoimmune disease may be particularly at risk.
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PMID:Immunological aspects of halothane hepatitis. Possible relevance of biotransformation. 123 79

The patient (a 49 year-old, female) had been diagnosed in Apr. 1987 as having rheumatoid arthritis (RA) following the history as chronic non-A, non-B hepatitis for 4 years. Progressive systemic sclerosis (PSS) and primary biliary cirrhosis (PBC) were also defined on 1989 in the same patient mainly due to proximal scleroderma and histological findings of liver biopsy. On the other hand, the coexistence of rheumatoid factor, anti-Scl-70 antibody, anti-mitochondrial antibody (anti-MC, anti-MD and an unidentified fraction) and anti-centromere antibody have been observed with marked polyclonal hypergammopathy in her sera since July 1990. Her disease activity has been controlled well with the administration of D-penicillamine and ursodeoxycholic acid during recent clinical course. Few cases of RA associated with PSS and PBC, showing various autoantibodies as a disease marker in sera, have been reported. In order to evaluate the mechanisms of autoimmune disease especially chain reaction of autoimmunity, it should be important to accumulate the reports concerning such cases.
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PMID:[A case of rheumatoid arthritis associated with progressive systemic sclerosis and primary biliary cirrhosis in the presence of various autoantibodies]. 144 89

Anti-liver microsomes (anti-LM) autoantibodies in patients with dihydralazine-induced hepatitis were found to react specifically with cytochrome P4501A2 (P4501A2) but not with P4501A1 expressed in yeast and bacteria. These results were confirmed by immunoinhibition of methoxyresorufin-O-demethylase activity (supported by the P4501A subfamily); anti-LM antibodies more strongly inhibited this activity in yeast expressing P4501A2 than in yeast expressing P4501A1. Anti-LM were shown to be specific to the disease; in three cases, these autoantibodies were present at high titers during disease, whereas the titers decreased upon recovery and became undetectable a few months after recovery. Thus, there exists a time-dependent relationship between the disease and the autoantibodies, which does not prove that the autoantibodies are causative of the hepatitis; they might only be a marker. The inductive capacity of dihydralazine toward P450 was also studied. In rats treated in vivo and in human hepatocytes treated in vitro with dihydralazine, a 2-fold increase in P4501A2- and P4501A-supported monooxygenase activities was found. The levels of the other P450 isoforms tested were unchanged during treatment, both in vivo in rats and in vitro in cultures of human hepatocytes. In human hepatocytes, dihydralazine produced a dose-dependent increase in the level of P4501A up to 0.1 mM; induction of P4501A was less strong at 0.2 mM and disappeared at 0.5 mM. The same treatment did not change the level of P4503A4, taken as control. The strong heterogeneity in the expression of P4501A enzymes in human liver and the capacity of these enzymes for induction by dihydralazine and by other compounds might be predisposing factors in this autoimmune disease.
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PMID:Anti-liver microsomes autoantibodies and dihydralazine-induced hepatitis: specificity of autoantibodies and inductive capacity of the drug. 151 26

At least since the discovery of the acquired immune deficiency syndrome and the "human immune deficiency virus" (HIV) it has been widely accepted, that viruses infect lymphocytes (mainly especially CD 4 positive helper lymphocytes) and can also be responsible for their deletion. However, since the HIV can only be found in a small proportion of the dying lymphocytes, other viruses as well as other (nonviral) cytotoxic agents and mechanisms must be taken into consideration. The conception of involved autoimmune phenomena is being accepted increasingly. Storch's hypothesis put forward in 1975, of primary or secondary viral infection of lymphocytes as pathogenetical principle of autoimmune hepatitis (infected B- and T-lymphocytes stimulate directly or indirectly the antibody synthesis and also trigger abnormal cellular immune reactions) was confirmed. Teleologically regarded, in most cases it remains open if the demonstrable autoantibodies and immune cells are pathogenic, protective, or indifferent for the individual. Analogous to symbiosis and parasitism, this postulate can be extended to pathogenic viral infections. Assuming that the human organism is anxious to remain unharmed and, like viruses maintain its adaptability by a system of multiform control systems one can imagine, that the autoimmunity induced by and therefore directed primarily against viruses can be regarded as "physiological", thus representing a protective mechanism against disturbing exogenous and endogenous factors. It can be considered part of the "prophylaxien" (Holle, 1989). Likewise, in autoimmune hepatitis as well, new findings speak for a participation of several (various) viruses in its aetiopathogenesis. It is hypothesized, that so-called "autogenes" exist which lead to autoimmune disease (like oncogenes involved in the pathogenesis of malignancies).
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PMID:[Virus and autoimmune disease. An excursion exemplified by autoimmune hepatitis]. 156 9

Giant-cell hepatitis is a frequent pattern of liver injury in the neonate, but it is rare after infancy. Such cases have been attributed to autoimmune disease, to non-A, non-B hepatitis and, most recently, to paramyxovirus infection. To better define the entity of postinfantile (syncytial) giant-cell hepatitis, we reviewed 24 biopsy specimens from 20 patients with this finding, either alone or in combination with other diagnoses. The number of multinucleated giant cells varied greatly from one specimen to another. Varying degrees of portal inflammation appeared in all but one of the patients, and all had hepatitislike acinar inflammation associated with hepatocellular injury. Fibrosis was a common finding, varying from mild periportal fibrosis to established cirrhosis (33%). The changes were interpreted as acute giant-cell hepatitis in 25%, as CAH in 42% and as active cirrhosis in the remainder. The patients ranged in age from 2 to 80 yr, with a mean of 35 yr and a male/female ratio of approximately 1:1. The signs and symptoms of liver disease were present for more than 1 mo in most patients. A positive antinuclear antibody titer was found in seven of the patients. Three patients had a direct Coombs reaction and anemia. Overall, evidence of autoimmune disease was found in 40% of the patients. One patient had non-Hodgkin's lymphoma involving the liver. Only one patient had a history of blood transfusion or risk factors for hepatitis C. No patient underwent serological study for paramyxovirus antibodies. Liver tissue from one patient was examined ultrastructurally, but no viral particles could be identified.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postinfantile giant-cell transformation in hepatitis. 163 41

A cDNA clone (GOR47-1) bearing an epitope with an aminoacid sequence GRRGQKAKSNPNRPL (GOR epitope) was isolated from the plasma of a laboratory chimpanzee infected with human non-A, non-B hepatitis (NANBH) agent. The epitope was not encoded by reported sequences of hepatitis C virus (HCV) but instead was coded for by a host cellular sequence. An enzyme-linked immunosorbent assay (ELISA) was developed for antibodies to the GOR epitope (anti-GOR). A patient with acute NANBH produced both IgM and IgG classes of anti-GOR in the acute phase of the illness, with concentrations of IgG class anti-GOR rising when anti-HCV became detectable. Anti-GOR was detected in serum from 59 (81%) of 73 patients with chronic NANBH, 40 (65%) of 62 with NANB liver cirrhosis, and 25 (63%) of 40 NANB patients with primary hepatocellular carcinoma, but in only less than 10% of patients with chronic liver diseases due to hepatitis B virus, alcohol, or an autoimmune disorder, and in only 2% of voluntary blood donors. Circulating HCV-RNA was detected by polymerase chain reaction (PCR) in most patients seropositive for anti-GOR but negative for anti-HCV. Detection of anti-GOR would therefore help in the diagnosis of NANBH and in reducing the occurrence of post-transfusion hepatitis.
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PMID:Non-A, non-B hepatitis specific antibodies directed at host-derived epitope: implication for an autoimmune process. 167 Jun 64

GOR, an epitope borne by the amino acid sequence, GRRGQKAKSNPNRPL, is recognized by anti-GOR antibodies specifically found in patients with non-A, non-B hepatitis (NANBH). The epitope is not coded for by the hepatitis C virus (HCV), the presumed causative agent for NANBH, but by a single copy gene of the host. Anti-GOR antibodies, distinct from anti-HCV (c100-3) antibodies, were revealed to have dual specificities; they target both the presumed core gene product of HCV and a host component. This cross recognition is probably derived from homologous regions between the GOR epitope and a viral epitope on the core protein in HCV. It is therefore suggested that anti-GOR is an autoantibody induced by HCV infection. This may explain the autoimmune disease like aspect of NANBH pathogenesis.
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PMID:An autoantibody cross-reactive to hepatitis C virus core and a host nuclear antigen. 172 1


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