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)

Thalassemia major is a progressive disease. Modern therapy with transfusions and iron chelation has greatly improved both the quality and length of thalassemics life. Nevertheless, progressive overload of iron in the organs, hepatitis and other infections acquired randomly imply the risk of mortality that increases with age. Bone marrow transplant from an HLA identical donor (a possibility for about 45%) represents the only form of radical cure of the disease. With the classification of the classes of risk we know today that a thalassemic child has a chance to die from transplant 3 to 100 with probability of being cured 94%. Thalassemics that receive the transplant at a more advanced stage of complications of the disease have a major risk of death due to the transplant of class 2 (14% probability of death due to the transplant against 83% chance of being cured). Class 43 patients have 9 chances out of 100 to die of transplant and 60% probability of being cured of thalassemia.
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PMID:[Bone marrow transplantation in thalassemia]. 830 17

Molecular biology techniques are now a vital part of hepatitis virology, with a central role in studies of diagnosis, epidemiology, virology, pathogenesis, and natural history of infection. Cloning of the genome of hepatitis E virus has allowed its tentative classification as a calici- or related virus, and is the first step toward the development of a vaccine. Long-term implications of hepatitis C for groups such as children with hemophilia, thalassemia, and even leukemia can be better understood by comparison of virus load measured by molecular amplification of the plasma viral RNA with the serologic and clinical status of the respective cohorts of children. A new vaccine for hepatitis A has been licensed in several European countries, and recent experience with severe hepatitis in infants after unexpected transmission of hepatitis B from anti-hepatitis B e positive mothers reemphasizes the value of universal hepatitis B immunization programs. Mother-to-infant transmission of hepatitis C virus has now been well documented, but there are still insufficient data on the dynamics of this, particularly in the absence of passive immunoprophylaxis or a vaccine, to permit recommendations regarding the management of individual pregnancies or deliveries. There is especially too little information to suggest whether breast feeding may be an important mechanism for transmission.
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PMID:Hepatitis viruses and protection against infection in children. 837 24

Hepatitis C virus (HCV) is responsible for the majority of cases of post transfusion non-A non-B (NANB) hepatitis in thalassaemia major (TM). Twelve multi-transfused TM patients with serological, biochemical, histological and molecular biological evidence of HCV infection have been treated for 6 months with recombinant alpha-interferon (IFN). Ten (83%) responded as assessed by a fall of at least 50% of pre-treatment serum transaminase levels. Histological improvement was observed in 6/7 responders tested. Natural killer (NK) cell activity 24 h after the first dose of IFN was significantly increased in responders as compared to non-responders (P < 0.05). HCV RNA disappeared from serum in 5/12 and from liver tissue in 2/5 of the responders. The degree of induction of peripheral blood mononuclear cell 2'5' oligoadenylate synthetase messenger RNA (2-5 OAS mRNA), an enzyme induced by IFN, after the first dose of IFN did not correlate with response. IFN was generally well tolerated. We conclude that the response rate in multi-transfused TM patients infected with HCV and treated with IFN is similar to that in non-multi-transfused patients.
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PMID:Alpha interferon in the treatment of chronic hepatitis C infection in thalassaemia major. 838 24

Hepatitis C virus (HCV) is responsible for the majority of cases of post transfusion non-A non-B (NANB) hepatitis in thalassaemia major (TM). Fifteen multi-transfused TM patients with serological, biochemical, histological and molecular biological evidence of HCV infection have been treated for six months with recombinant alpha interferon (IFN). Eleven (73%) responded, 8 (53%) had complete response (CR), 3 (20%) partial response (PR) and 4 (27%) did not respond (NR) to IFN. Natural killer (NK) cell activity 24 hours after the first dose of IFN was significantly increased in responders as compared to non-responders. Liver histology showed an overall reduction of portal inflammation and periportal necrosis in the responding patients. HCV RNA disappeared from serum in 8 (15) responders and partial responders. Non responders remained positive. HCV RNA was tested and found to be positive in liver tissue material in 7 patients, five of those were re-tested after IFN treatment. Two became negative (both CR) 3 remained positive despite biochemical response to IFN. The degree of induction of peripheral blood mononuclear cell 2'5' oligoadenylate synthetase messenger RNA (2-5 OAS mRNA), an enzyme induced by IFN, after the first dose of IFN did not correlate with response neither was any significant interaction with cytokines observed; tumour necrosis factor (TNF), interleukin-1. (IL-1) and CD4:CD8 ratios did not change. We conclude that IFN should be given to all TM patients with chronic active hepatitis due to HCV.
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PMID:Recombinant alpha 2B interferon (IFN) in the treatment of chronic hepatitis C disease in thalassaemia major (TM). 839 33

Some 20% of cases of posttransfusion and sporadic hepatitis non-A, non-B are anti-HCV negative. In 1995 it proved possible in collaboration of Genelabs with Boehringer Co. Mannheim to identify a new RNA virus which causes acute and chronic hepatitis in humans and tamarins. The genome of the virus contains some 2900 amino acids, and as to its structure, it resembles flaviviruses. It was described as hepatitis G virus (HGV). It differs from the hepatitis C, virus as it has only a 26% homology of amino acids. It is transmitted through blood during transfusion along with other parenteral routes of infection. Risk groups comprise i.v. drug addicts, blood donors and patients with thalassaemia and repeated blood transfusions. HGV can infect the liver as an independent virus or along with the virus of hepatitis B or C (dual infection). As to clinical aspects, hepatitis G is very mild and not associated with jaundice. Some patients develop chronic hepatitis. About half the patients infected with HGV have only a slightly raised transaminase activity, the remainder have normal liver enzymes. As compared with hepatitis C, the mean transaminase activity is one half. It can be diagnosed by assessment of HGV RNA by means of PCR. In the USA the prevalence of HGV RNA in blood donors with normal ALT activity is 1.7% and in donors with increased ALT activity 1.5%. The virus is sensitive to interferon, after treatment the serum concentration of HGV RNA declines rapidly but after withdrawal of treatment the values return to pre-treatment levels. This is the first report on the newly discovered hepatitis G virus.
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PMID:[The discovery of hepatitis G virus]. 862 84

The study group screened for anti-HCV comprised 789 subjects of hepatitis, renal failure, thalassaemia and healthy voluntary blood donors coming from Central India during July 1992 to November 1995. The prevalence of HCV was low (4.85%) among 103 patients of acute viral hepatitis (AVH) while it was higher (25.64%) among 117 patients of chronic liver disease (CLD) with the highest rate of 31.57 percent in 57 patients of cirrhosis. The anti-HCV positivity among 101 patients with hepatic failure was around 10 percent. High risk groups such as chronic renal failure (CRF) patients mainly on haemodialysis and thalassaemics receiving multiple blood transfusions showed the prevalence of anti-HCV in 41.9 and 25.45 percent respectively. Only 1.78 percent of the 280 voluntary blood donors showed positivity for anti-HCV. Comparison of the data on HCV in the present study with data from other parts of India showed a wide variation in the different centers. The higher prevalence of HCV among CRF patients and thalassaemics indicates the need for screening of the blood units for anti-HCV before transfusion to these high risk patients.
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PMID:Prevalence of anti-HCV antibodies in central India. 884 Jun 56

The aim of the study was to determine the prevalence of hepatitis E virus (HEV) infection among individuals at high risk of transmission of non-A, non-B hepatitis or sexually transmitted diseases (STDs), and to evaluate whether they have an increased risk of exposure to HEV. Serum samples from 125 thalassemia patients, 300 intravenous drug users, 420 hemodialysis patients, 263 individuals with STDs, 47 human immunodeficiency virus (HIV) infected homosexual men, and 316 healthy volunteers were tested for immunoglobulin G (IgG) and M (IgM) antibodies to HEV (anti-HEV) by enzyme immunoassays (EIAs) following a predetermined algorithm (Abbott Labs). Anti-HEV IgG was confirmed in 3/125 (2.4%) thalassemia patients, 5/300 (1.7%) intravenous drug users, 27/420 (6.4%) hemodialysis patients, 4/263 (1.5%) STD patients, 1/47 (2.1%) homosexual men, and 7/316 (2.2%) of the reference group. No patient was found positive for anti-HEV IgM. The higher prevalence which was observed in hemodialysis group was due to the confounding effect of age, as multivariate analysis showed. The anti-HEV prevalence increased significantly with age (p = 10(-4)). No significant association was found between anti-HEV, anti-HCV, and anti-HBc. In conclusion, individuals at high risk of non-A, non-B hepatitis and STDs have no increased risk of exposure to HEV and the higher prevalence of anti-HEV IgG among older subjects may be due to an epidemic form of HEV infection which occurred some decades ago, when the sanitary conditions in our country were poor.
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PMID:Hepatitis E virus infection in individuals at high risk of transmission of non-A, non-B hepatitis and sexually transmitted diseases. 895 70

The study was conducted on 75 multitransfused children aged between 2 and 13 years who attended the Department of Paediatrics, LNJPN Hospital, New Delhi from July 1990 to July 1991. These included 64 cases of thalassaemia major, 4 cases of haemophilia, 3 patients of acute lymphatic leukaemia and one each of acute myeloid leukaemia, aplastic anemia, chronic idiopathic thrombocytopenic purpura and acute haemorrhagic pancreatitis. HBsAg was tested in all, Anti-HBc was tested in 44 patients and Anti-HCV in 43 patients. Anti HDV was tested in HBsAg positive patients and IgM anti-HAV was tested in patients suffering from hepatitis. Liver function tests were evaluated in all patients. HBsAg was positive in 31% of patients; 40% of males and 15% of females were HBsAg positive, the difference being statistically significant. 84% of patients were Anti-HBc positive, 21% were anti HCV positive, 4% were Anti HDV positive. 15% of the patients had post transfusion hepatitis. Anti HCV was present in 57% of the hepatitis patients; none had anti-HAV IgM.
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PMID:Hepatitis B and hepatitis C in multitransfused children. 964 Oct 34

Two women, aged 27 and 42 years, both born in Surinam and both suffering from heterozygous thalassemia, developed cholestatic hepatitis three and two weeks respectively after the start of a two-day course of thiabendazol for Strongyloides stercoralis infection. Other causes of cholestasis were unlikely in view of the results of blood tests, echography and the endoscopic retrograde cholangiopancreaticography. The symptoms persisted for several months, and the liver function disorders for 7 years and one year, respectively. The incidence of thiabendazole-induced cholestatic hepatitis is unknown, but probably low.
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PMID:[Cholestatic hepatitis ascribed to the use of thiabendazole]. 975 41

Although the risk of transfusion-transmitted hepatitis has been recently reduced, transfusion-dependent beta-thalassemia patients may still develop liver disease due to viral infection or iron overload. We assessed the frequency and causes of liver dysfunction in a cohort of anti-hepatitis C virus (HCV) negative thalassemics. Of 1,481 thalassemics enrolled in 31 centers, 219 (14.8%) tested anti-HCV- by second-generation assays; 181 completed a 3-year follow-up program consisting of alanine-aminotransferase (ALT) measurement at each transfusion and anti-HCV determination by third-generation enzyme-immunoassay (EIA-3) at the end of study. Serum ferritin levels were determined at baseline and at the end of follow-up. Ten patients were anti-HCV+ by EIA-3 at the end of follow-up. Of them, seven were already positive in 1992 to 1993 when the initial sera were retested by EIA-3, one tested indeterminate by confirmatory assay, and two had true seroconversion (incidence, 4. 27/1,000 person years; risk of infection, 1/7,100 blood units, 95% confidence interval [CI], 1 in 2,000-1 in 71,000 units). At baseline, 67 of 174 thalassemics had abnormal ALT. Of those with normal ALT, seven subsequently developed at least one episode of moderate ALT increase (incidence, 24.6/1,000 person-years). All of the 20 patients with ferritin values >/=3,000 ng/mL had clinically relevant ALT abnormalities, as compared with 53 of 151 with <3,000 ng/mL (P < .005). Hepatic dysfunction is still frequent in thalassemics. Although it is mainly attributable to siderosis and primary HCV infection, the role of undiscovered transmissible agents cannot be excluded.
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PMID:A multicenter prospective study on the risk of acquiring liver disease in anti-hepatitis C virus negative patients affected from homozygous beta-thalassemia. 978 88


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