Publications
701 results found
Thursz MR, Zhang L, Frodsham A, et al., 2001, Polymorphisms in the IL-10 ligand and the IL-10 receptor β chain influence susceptibility to persistent HBV infection, JOURNAL OF HEPATOLOGY, Vol: 34, Pages: 14-14, ISSN: 0168-8278
Dave U, Williams A, Larkman D, et al., 2001, Endoscopic MRI in suspected oesophageal cancer, GUT, Vol: 48, Pages: A13-A13, ISSN: 0017-5749
Zhang L, Frodsham AJ, Best S, et al., 2000, Identification of a gene associated with chronic hepatitis B virus infection by genome-wide linkage analysis and family based association studies., AMERICAN JOURNAL OF HUMAN GENETICS, Vol: 67, Pages: 21-21, ISSN: 0002-9297
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- Citations: 1
Walker MM, Worku ML, Karim QN, et al., 2000, Mice are not men:: The Sydney system does not discriminate the genetically determined degree of gastritis in <i>H-felis</i> infection., GUT, Vol: 47, Pages: A62-A62, ISSN: 0017-5749
Godkin AJ, Thursz M, Openshaw P, et al., 2000, Identification of HLA-DR11-restricted CD4+T cell epitopes derived from hepatitis C virus., HEPATOLOGY, Vol: 32, Pages: 271A-271A, ISSN: 0270-9139
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- Citations: 1
Zhang L, Thursz MR, Frodsham A, et al., 2000, Identification of a gene for chronic hepatitis B virus infection by genome-wide linkage analysis family-based association studies., HEPATOLOGY, Vol: 32, Pages: 392A-392A, ISSN: 0270-9139
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- Citations: 1
Walker MM, Negus R, Rice AJ, et al., 2000, Are all five sites of the Sydney system essential to assess <i>H-pylori</i> and gastritis?, GUT, Vol: 47, Pages: A57-A57, ISSN: 0017-5749
Griffiths AE, Walker MM, Loh V, et al., 2000, Polymorphisms in IL-1 beta and IL-1 receptor antagonist genes increase the risk of gastric atrophy and intestinal metaplasia in patients infected with <i>Helicobacter pylori</i>., GUT, Vol: 47, Pages: A53-A54, ISSN: 0017-5749
Touzet S, Kraemer L, Colin C, et al., 2000, Epidemiology of hepatitis C virus infection in seven European Union countries: a critical analysis of the literature. HENCORE Group. (Hepatitis C European Network for Co-operative Research., Eur J Gastroenterol Hepatol, Vol: 12, Pages: 667-678, ISSN: 0954-691X
Hepatitis C is now recognized as the most common infection causing chronic liver disease in the European population. Our aim was to assess the prevalence of the antibody to hepatitis C virus (HCV), and the incidence of HCV seroconversion in the general population and the main risk groups, namely intravenous drug users, haemodialysis and transfused patients, in seven countries of the European Union, by carrying out a critical analysis of the literature. Data sources used were the Medline database and a manual search using the key words: hepatitis C, prevalence, incidence, transmission, risk factors and epidemiology. Articles published between January 1990 and March 1997 were reviewed. Articles were reviewed according to a critical analysis method regarding title, type of article, study design, period and population, tests, results and their consistency with data. The tests performed were mainly second- or third-generation serological tests. The average prevalence rate in blood donors was 1%, with a north-south gradient ranging from 0.04% to 2%. Prevalence varied from 20% to 30% in haemodialysis patients. The incidence in transfused patients was less than 1% after 1991. The prevalence in intravenous drug users was about 80%. Multicentre studies conducted in larger samples are needed to obtain more accurate and reliable results, in particular. However, the epidemiological studies available allowed us to assess the magnitude of HCV infection in Europe.
Touzet S, Kraemer L, Colin C, et al., 2000, Epidemiology of hepatitis C virus infection in seven European Union countries:: a critical analysis of the literature, EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY, Vol: 12, Pages: 667-678, ISSN: 0954-691X
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- Citations: 62
Pradat P, Chossegros P, Bailly F, et al., 2000, Comparison between three quantitative assays in patients with chronic hepatitis C and their relevance in the prediction of response to therapy, JOURNAL OF VIRAL HEPATITIS, Vol: 7, Pages: 203-210, ISSN: 1352-0504
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- Citations: 16
Thursz M, Rahman R, Murphy C, et al., 2000, Impairment of health-related quality of life in patients with asymptomatic chronic hepatitis B or C in the United Kingdom, JOURNAL OF HEPATOLOGY, Vol: 32, Pages: 112-112, ISSN: 0168-8278
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- Citations: 3
Thursz M, 2000, Genetic susceptibility in infectious diseases, BIOTECHNOLOGY & GENETIC ENGINEERING REVIEWS, VOL 17, Vol: 17, Pages: 253-264, ISSN: 0264-8725
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- Citations: 7
Dumpis U, Hall A, Mendy M, et al., 2000, Molecular epidemiology gives insight of the routes of transmission of HBV in the Gambia, JOURNAL OF HEPATOLOGY, Vol: 32, Pages: 106-106, ISSN: 0168-8278
Wright M, Thomas HC, Goldin R, et al., 2000, Tissue inhibitor of metalloproteinase 1 gene polymorphism and rate of liver fibrosis in chronic hepatitis C infection, JOURNAL OF HEPATOLOGY, Vol: 32, Pages: 81-81, ISSN: 0168-8278
Thursz M, Yallop R, Goldin R, et al., 1999, Influence of MHC class II genotype on outcome of infection with hepatitis C virus, LANCET, Vol: 354, Pages: 2119-2124, ISSN: 0140-6736
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- Citations: 243
Thursz M, Yallop R, Goldin R, et al., 1999, Influence of MHC class II genotype on outcome of infection with hepatitis C virus. The HENCORE group. Hepatitis C European Network for Cooperative Research., Lancet, Vol: 354, Pages: 2119-2124, ISSN: 0140-6736
BACKGROUND: The outcome of infection with hepatitis C virus (HCV) varies substantially among individuals. Host genetic factors are likely to give rise to some of this variability. Polymorphisms in the MHC class II loci may influence the outcome of HCV infection; however, reports of MHC class II allele associations have been inconsistent. We aimed to confirm these associations in a cohort of European patients with different clinical outcomes. METHODS: The distribution of MHC class II alleles was compared between patients with self-limiting infection (n=85) and matched patients with persistent infection (n=170); between patients with mild (n=321) and severe (n=321) histological injury; and between patients who responded to interferon (n=96) and those who did not (n=192). The results of these comparisons were confirmed with a second-stage study of self-limiting infection (n=52) versus persistent infection (n=152). FINDINGS: Self-limiting HCV infection was associated with HLA-DRB1*1101 (odds ratio 2.14 [95% CI 1.11-4.12]; p=0.013) and HLA-DQB1*0301 (2.22 [1.24-3.96], p=0.004). Persistent HCV infection was associated with HLA-DRB1*0701 (2.04 [1.03-4.17], p=0.027), and HLA-DRB4*0101 (2.38 [1.29-4.35], p=0.002). These results were confirmed in the second-stage study. No significant associations (p<0.05 after Bonferroni correction) were found between MHC class II alleles and severe histological injury or response to interferon therapy. INTERPRETATION: Specific MHC class II alleles influence susceptibility or resistance to persistent HCV infection.
Frodsham AJ, Best S, Young K, et al., 1999, A genome scan for major infectious disease susceptiblity genes., Publisher: UNIV CHICAGO PRESS, Pages: A250-A250, ISSN: 0002-9297
Eggleton P, Murray E, Dodds A, et al., 1999, Surfactant protein D binding to <i>Helicobacter pylori</i> lipopolysaccharide, GUT, Vol: 45, Pages: A35-A35, ISSN: 0017-5749
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- Citations: 2
Walker MM, Karim QN, Worku M, et al., 1999, Direct observation of kinetics and agglutination of <i>Helicobacter pylori</i> with the collectin, surfactant protein D, GUT, Vol: 45, Pages: A41-A42, ISSN: 0017-5749
Griffiths A, Sumiya M, Summerfield J, et al., 1999, The codon 52 mutation in the mannose binding lectin gene predispoes to Helicobacter pylori infection, GUT, Vol: 44, Pages: A67-A67, ISSN: 0017-5749
Karim QN, Thursz MR, Murray E, et al., 1999, Kinetic impairment of Helicobacter pylori by the collectin surfactant protein D., GASTROENTEROLOGY, Vol: 116, Pages: A745-A745, ISSN: 0016-5085
Griffiths AE, Sumiya M, Summerfield J, et al., 1999, The colon 52 mutation in the mannose binding lectin gene predisposes to <i>Helicobacter pylori</i> infection., GASTROENTEROLOGY, Vol: 116, Pages: A727-A727, ISSN: 0016-5085
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- Citations: 1
Walker M, Karim Q, Thursz M, et al., 1999, Kinetic impairment of Helicobacter pylori by the collectin surfactant protein D, GUT, Vol: 44, Pages: A67-A67, ISSN: 0017-5749
Bellamy R, Ruwende C, Corrah T, et al., 1999, Tuberculosis and chronic hepatitis B virus infection in Africans and variation in the vitamin D receptor gene, JOURNAL OF INFECTIOUS DISEASES, Vol: 179, Pages: 721-724, ISSN: 0022-1899
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- Citations: 343
Griffiths AE, Thursz MR, Walker MM, et al., 1998, The immcnogenetics of h. pylori, Zeitschrift fur Gastroenterologie, Vol: 36, ISSN: 0044-2771
Background The importance of the host in influencing the outcome of H. pylori (Hp) infection is becoming increasingly accepted. The identity of the host genes involved, however, remains unknown. Potential candidate genes include MHC class II genes, cylokine genes and genes involved in mucosal protection and repair. Aim The purpose of this study was to determine if certain polymorphisms, of known functional significance, in the tumour necrosis factor (TNF), Interleukin (IL)-l, IL-10 and mannose binding lectin (MBL) genes, were associated with outcome of Hp infection. Methods From a large DNA bank, matched case and control cohorts of 100150 subjects each of duodenal ulcer (DU), Hp+ non-ulcer dyspepsia (NUD) and Hp-NUD were assembled. Gene polymorphisms were screened by PCR followed by restriction fragment length polymorphism analysis (for TNF308 and IL-1 β-511 ) or by sequence specific oligonucleotide hybridisation techniques. Allele frequencies were compared between the groups using standard odds ratios and chi squared tests. Results Four TNF and two IL-10 polymorphisms were studied and showed no association with outcome. However individuals homozygous for allele 2 of the IL-1 receptor antagonist gene intron 2 VNTR did show a trend towards increased risk of ulcer (p=0,09). This is the same allele that has been associated with increased severity of inflammation in ulcerative colitis and SLE. The MBL codon 52 mutation was found in 15% of Hp+ patients but only 4% of uninfected controls; odds ratio -3.97 (95%CI 1.33-15.94), p=0.007. Conclusions A known deficiency in innate immunity has been shown to predispose to Hp infection. No genes associated with particular outcome of infection have yet been identified.
Goldin RD, Lloyd J, Thursz MR, 1998, Angiogenesis correlates with the development of dysplasia and liver cell cancer in patients with hepatitis C virus infection., Publisher: W B SAUNDERS CO, Pages: 164A-164A, ISSN: 0270-9139
Thursz MR, Hill AV, Trepo C, et al., 1998, Polymorphisms in genes affecting Th1/Th2 balance influence the outcome of HBV and HCV infection., Publisher: W B SAUNDERS CO, Pages: 565A-565A, ISSN: 0270-9139
Griffiths AE, Walker MM, Thursz MR, 1998, Allele 2 of the IL-1 receptor antagonist gene predisposes to chronic <i>H-pylori</i> infection, Publisher: BRITISH MED JOURNAL PUBL GROUP, Pages: A26-A26, ISSN: 0017-5749
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