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)

To assess whether demography is one of the important factors determining antibody response to nuclear antigens [ANA: SSA-Ro (52K and 60K), SSB-La, snRNPs (A, 70K, B'/B), and Cenp-B], we investigated 95 and 47 sera of autoimmune hepatitis (AIH) from North America and Asia, respectively, by immunofluorescent (IF) and recombinant ELISA. Correlations among nuclear IF patterns, ELISA, and disease indices were analyzed. The frequency and titer of individual antibodies differed significantly between the groups. Patients with speckled patterns were younger in both regions and had higher aspartate aminotransferase levels only in North America. HLA-A1, B8, DQ2, and DR4 or DR3 or both in North America, and A2, B61, DQ7, and DR4 in Asia were predominant. In Asia, B61 correlated with anti-70K, and DQ7 correlated with antibodies to 52K, Cenp-B, and B'/B. In North America, A1, B8, DR3 haplotype, and DQ2 correlated with antibodies to A and 70K. Anti-B'/B and DR4 in North America, and A2 in Asia, were associated with concurrent immunologic disorder. Individual ANA clusters correlated with individual HLA in the demography, and different HLA alleles might determine disease expression as well as different ANA being produced in AIH.
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PMID:Antibodies to Ro/La, Cenp-B, and snRNPs antigens in autoimmune hepatitis of North America versus Asia: patterns of immunofluorescence, ELISA reactivities, and HLA association. 963 26

HCV infection and interferon-alpha (IFN-alpha) therapy have been associated with autoimmunity. To assess whether chronic liver disease (CLD) due to HCV infection or its treatment with IFN-alpha cause autoimmune manifestations, the prevalence of tissue autoantibodies in 51 children with chronic HCV infection and 84 with other CLD was analysed by standard techniques. Sixty-five percent of patients with chronic HCV infection, 66% with chronic hepatitis B infection and 60% with Wilson's disease were positive for at least one autoantibody. In the 51 subjects with chronic HCV infection (29 treated with IFN-alpha, 22 untreated), tested on 165 occasions over a median of 9 months (range 5-42 months), autoantibodies to nuclei (ANA), smooth muscle (SMA), gastric parietal cell (GPC) and/or liver kidney microsomal type 1 (LKM-1) were similarly prevalent in treated and untreated patients (90% versus 68%, P = 0.12). Positivity for SMA was present in 67%, GPC in 32%, ANA in 10%, LKM-1 in 8% of cases. Treatment with IFN-alpha had to be suspended due to transaminase elevation in one SMA-positive, one ANA-positive but in three of four LKM-1-positive patients. Our results show that: (i) autoantibodies are common in viral-induced hepatitis and Wilson's disease; (ii) positivity for SMA, GPC, ANA is part of the natural course of chronic HCV infection, their prevalence being unaffected by IFN-alpha; and (iii) IFN-alpha should be used cautiously in the treatment of LKM-1/HCV-positive patients.
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PMID:Autoantibody prevalence in children with liver disease due to chronic hepatitis C virus (HCV) infection. 964 17

Autoimmune liver diseases comprise a number of disorders in which inflammatory damage to the liver is believed to derive from an autoimmune attack. These include autoimmune hepatitis (AIH), characterised by positive smooth muscle and/or nuclear (SMA/ANA) or liver kidney microsomal type 1 (LKM1) antibodies, autoimmune sclerosing cholangitis (ASC), usually SMA/ANA positive, and AIH after liver transplantation, which is positive for SMA, ANA, or atypical LKM. These disorders often present with symptoms indistinguishable from prolonged acute hepatitis. Less commonly the onset is insidious, with nonspecific symptoms, or with complications of portal hypertension. For AIH and ASC, experimental evidence suggests that usually in individuals genetically predisposed to autoimmunity, a liver self antigenic peptide is recognized by T lymphocytes which promote a cascade of autoaggressive processes. For AIH after liver transplantation, the pathogenic mechanisms remain to be elucidated. All types of autoimmune liver disorders appear to respond favourably to early treatment with prednisolone with or without azathioprine. For patients presenting with fulminant hepatic failure or with already advanced cirrhosis, immunosuppression is rarely effective and the only mode of treatment is liver transplantation. The role of other immunosuppressant or immunomodulatory drugs, like cyclosporin A, tacrolimus or ursodeoxycholic acid, in the treatment of autoimmune liver disorders remains to be defined.
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PMID:Immunological liver diseases in children. 977 27

A 27-year-old woman was successfully treated with a highly dosed steroid therapy over several months during summer 1994 in the event of urticaria. In October 1994, when the patient was complaint free, therapy was abruptly terminated. In November 1994 jaundice, nausea and loss of appetite occurred. Biochemical results showed markedly elevated serum transaminases, negative hepatitis serology, normal immunoglobulins and inconspicious autoantibodies. Histology showed a florid hepatitis. In January 1995 the patient was hospitalized again in very low general and nutritional condition with a marked jaundice, high serum transaminases, insufficient liver synthesis function, established ANA(+), ASMA(+2) and normal immunoglobulins. This time histology painted out an active hepatitis going into liver cirrhosis. Evaluation in view of liver transplantation was carried out in this case of liver failure. At that time, tests showed a distinct gamma globulin fraction increase although the antibody pattern had remainded identical. An immunosuppressive therapy with azathioprine and steroids was decided upon under suspicion of an autoimmune hepatitis leading to a prompt positive response and therefore confirmation of the diagnosis. Complete biochemical remission was attained in April 1995 and a complete histological remission in March 1998.
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PMID:[Jaundice and progressive liver failure: delayed diagnosis of autoimmune hepatitis due to abrupt termination of steroid therapy?]. 979 14

The clinical and evolutive characteristics and the response to treatment of a series of 49 patients with autoimmune hepatitis (AIH) diagnosed in the Liver Unit of a tertiary hospital from 1979 to 1996 and followed over 5.6 +/- 0.7 years were reviewed. Forty cases (80.4%) were AIH type 1 (ANA/AML positive), 7 (14%) type 2 (ALKM positive) and 2 (5%) of an undetermined type (absence of detectable antibodies). In 13 (26.6%) the disease presented as acute hepatitis and 16 (32%) presented extrahepatic manifestations. The AIH type 2 was observed in younger patients with the debut being more acute than in AIH type 1, but no significant differences were observed between the two groups with regard to the results of laboratory tests, frequency of a systemic manifestations and histologic lesions. Immunosuppressive treatment was effective in 90% of the cases, but 11 (30%) out of 37 relapsed on suppression of prednisone or reduction of the dosis. All showed response on reinitiation or an increase in the dosis of prednisone. Progression to cirrhosis was observed in 17% of the patients without cirrhosis at the time of diagnosis despite biochemical remission induced by treatment. No patient died during the follow up but 4 required liver transplantation.
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PMID:[Autoimmune hepatitis. Clinical characteristics and response to treatment in a series of 49 spanish patients]. 984 74

Autoimmune hepatitis is a chronic inflammatory liver disorder of unknown etiology associated with serum autoantibodies and hypergammaglobulinemia. This disease has a broad spectrum of presentations ranging from asymptomatic to fulminant hepatic failure. A 36 year old female with past history of hypothyroidism developed jaundice 2 months prior to admission. Outpatient evaluation revealed ANA and anti-SMA antibodies in high titers, negative viral markers for hepatitis, and hypergammaglobulinemia. A presumptive diagnosis of autoimmune hepatitis was made; steroids were recommended but the patient did not take them. She was admitted to the University Hospital due to increased jaundice, general malaise and ascites 5 weeks later. She deteriorated developing coagulopathy, encephalopathy and increasing hyperbilirubinemia. Intravenous corticosteroids were started. The patient improved and was discharged 3 weeks after admission. Fulminant hepatic failure has a high mortality and may require liver transplant. Our patient survived fulminant hepatic failure that resolved after corticosteroid therapy. It is important to identify and distinguish autoimmune hepatitis from other forms of liver disease because of the high percentage of response to immuno-suppressive therapy. Early diagnosis and treatment of this condition could improve survival, quality of life, and defer liver transplantation.
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PMID:Steroid therapy in fulminant hepatic failure secondary to autoimmune hepatitis. 988 78

ANA IIF is an effective screening assay in patients with clinical features of SLE and will detect most anti-ssDNA, anti-dsDNA, ENAs, and other autoantibodies. False positives are common. The clinical importance cannot be extrapolated from the ANA titre or pattern, although higher titres (> 1/160) are more likely to be important. HEp-2 cells are the most sensitive substrate for ANA detection, but this must be balanced against an increased incidence of insignificant positivity. ANA positive samples should be subjected to more specific assays for the diagnosis of SLE. A combination of ENA (Ro/La/Sm/RNP) and dsDNA assays will detect most patients with SLE as long as the characteristics of the assays used are well understood. ESR and CRP measurements provide useful additional information. Sjogren's syndrome and MCTD will produce overlapping serology with SLE, and anti-dsDNA titres are sometimes seen in autoimmune hepatitis and rheumatoid arthritis. All results should be reported in the light of the clinical details, by an experienced immunologist. A suggested diagnostic protocol is outlined in fig 1. The type of assay used crucially influences the predictive value of the tests. ELISA technology dominates routine laboratory practice, but tends to produce more false positive and true weak positive results, which may reduce the PPV of the test. This can be minimised by using IgG specific conjugates and careful assay validation. The NPV for SLE [figure: see text] is high for most assays but the PPV varies. Where necessary, laboratories should use crithidia or Farr dsDNA assays to confirm dubious ELISA dsDNA results, and ID/IB to confirm dubious ENA results. For monitoring, a precise, quantitative assay is required. It is unclear whether the detection of IgM or low affinity antibodies has a role here. A combination of anti-dsDNA, C3, C4, CRP, and ESR assays provides the most useful clinical information. Anti-ssDNA assays are likely to be useful, and are potentially more robust than anti-dsDNA assays, but require more validation. Local validation of individual assays and EQA participation is essential. Not all assays that apparently measure the same antibody specificities have equal clinical relevance, even within a single technology. Insufficient international or national reference preparations are currently available for many antibody specificities to enable effective standardisation. Quality assurance schemes reveal large differences in units reported by different assays for some analytes, even when calibrated against an IRP or equivalent reference preparation. Serial results can therefore only be compared from the same laboratory at present. Most autoantibodies increase during active disease, but few prospective data are currently available to justify treatment on the basis of rising titres. Further randomised prospective studies are required to examine the importance of antibody isotype and affinity in the monitoring of SLE by individual assay methods. The most important aspect of the appropriate use of laboratory assays is to become familiar with the limitations of the technology currently in use in your local laboratory, and to consult with your clinical immunologist in cases of doubt, preferably before commencing serological screening.
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PMID:The use of laboratory tests in the diagnosis of SLE. 1091 99

A 66 year-old obese woman with arthrosis, self-medicated with oral nimesulide, 200 mg daily. After 6 weeks she developed nausea, jaundice and dark urine. Two weeks later she had recurrent hematemesis and was hospitalized. Besides obesity and anemia her physical examination was unremarkable. An upper GI endoscopy revealed 3 acute gastric ulcers and a 4th one in the pyloric channel. Abdominal ultrasonogram showed a slightly enlarged liver with diffuse reduction in ecogenicity; the gallbladder and biliary tract were normal. Blood tests demonstrated a conjugated hyperbilirubinemia (maximal total value: 18.4 mg/dl), ALAT 960 U/l, ASAT 850 U/l, GGT 420 U/l, alkaline phosphatases mildly elevated, pro-time 49% and albumin 2.7 mg/dl. Serum markers for hepatitis A, B and C viruses were negative. ANA, AMA, anti-SmA, were negative. Ceruloplasmin was normal. A liver biopsy showed bridging necrosis and other signs of acute toxic liver damage. Gastric ulcers healed after conventional treatment and hepatitis subsided after 2 months leaving no signs of chronic liver damage. The diagnosis of toxic hepatitis due to nimesulide was supported by the time-course of drug usage, sex, age, absence of other causes of liver disease, a compatible liver biopsy and the improvement after drug withdrawal. Peptic ulcers or toxic hepatitis have been previously described as independent adverse reactions in patients taking nimesulide or other NSAIDs but their simultaneous occurrence in a single patient is a unique event that deserves to be reported.
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PMID:[Bleeding gastric ulcers and acute hepatitis: 2 simultaneous adverse reactions due to nimesulide in a case]. 1122 44

The paper presents a case of a 17-year-old girl with type 1 autoimmune hepatitis in whom biochemical, serological and histopathological markers of chronic hepatitis A were observed for the last 4 years. The diagnosis was based on elevated levels of gammaglobulins, IgG and the presence of autoantibodies (ANA, SMA). At first, the patient was treated with the pulses of corticosteroids and then, as no improvement was observed, continuous steroid therapy was involved. Relatively mild clinical course of the disease and good response to treatment with prednisone were recorded. Our observations suggest that HAV is capable of inducing autoimmune reactions and they indicate possible development of chronic hepatitis A.
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PMID:Autoimmune hepatitis in the course of chronic HAV--four year observation. 1221 21

The diagnosis of autoimmune hepatitis (AIH) relies on the exclusion of viral, metabolic, genetic, and toxic etiologies of chronic hepatitis or hepatic injury. There are few parameters that positively predict the presence of AIH. Autoantibodies have been intensively evaluated in this respect and have led to the classification of AIH into three serological subgroups: antinuclear and smooth muscle antibody-positive (ANA/SMA, type 1), liver-kidney microsomal antibody-positive (LKM-1, type 2), and soluble liver antigen/liver-pancreas antigen antibody-positive (SLA/LP, type 3) AIH. Although there are few clinical implications resulting from this classification, autoantibody profiles indicate that AIH is a heterogenous group of entities. The molecular characterization of B cell autoimmunity has led to the identification of major phase I and phase II metabolic enzymes as well as structural and functional components of the cell nucleus as immunologic targets. Autoantibodies and their corresponding autoantigens are intensively studied to provide clues to the understanding of disease initiation, tissue specificity, and propagation of hepatic autoimmune diseases.
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PMID:Autoantibodies and autoantigens in autoimmune hepatitis. 1244 6


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