Abstract
Background. Through migration, diversity of chronic hepatitis B virus (HBV) infection has changed, affecting disease burden and control. We describe clinical and viral characteristics of chronic HBV in the United Kingdom. Methods. A total of 698 individuals with chronic HBV infection were recruited from referral liver centers. Demographic, clinical, and laboratory data were collected. Results. Sixty-one percent of patients were male, 80% were not born in the United Kingdom, and the largest ethnicity was East/Southeast Asian (36%). Twenty-two percent were hepatitis B e antigen (HBeAg) seropositive; 20.4% (59/289) had cirrhosis and 10 (1.7%) had hepatocellular carcinoma. Genotype D was most common (31%) followed by A, C, B, and E (20%, 20%, 19%, and 9%, respectively). Genotype was significantly associated with country of birth, length of time in the United Kingdom, HBeAg status, and precore and basal core promoter mutations. One-third were on treatment, with men independently more likely to be treated. Only 18% of those on treatment were on recommended first-line therapies, and 30% were on lamivudine monotherapy. Among treated individuals, 27% had antiviral drug resistance. Testing rates for human immunodeficiency virus, hepatitis C virus, and delta coinfections were low. Conclusions. We demonstrated diversity of chronic HBV infections in UK patients, suggesting that optimal management requires awareness of the variable patterns of chronic HBV in countries of origin. We also found less-thanoptimal clinical management practices, possible gender-based treatment bias, and the need to improve testing for coinfections.
Original language | English |
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Pages (from-to) | 951-960 |
Number of pages | 10 |
Journal | Clinical Infectious Diseases |
Volume | 56 |
Issue number | 7 |
DOIs | |
Publication status | Published - 1 Apr 2013 |
Bibliographical note
Funding Information:Potential conflicts of interest. The study was part funded by industry through the unrestricted grants listed above. R. S. T. has received an honorarium from Gilead Sciences. A. M. J., A. J. R., and L. F. received funding from unrestricted grants as listed above, and A. M. J. is also a governor of the Wellcome Trust. A. J. R. also received nonrestricted grant funding from Gilead. T. W. has served on advisory boards and/or received honoraria from Novartis, Bristol-Myers Squibb (BMS), and Gilead. M. J. has received travel grants and consulted for Gilead. N. N. is an employee of Novartis (Basel, Switzerland). S. M. has served on advisory boards and/or received honoraria from AstraZeneca, BMS, Gilead, Janssen-Cilag, Merck Sharp & Dohme (MSD), and Roche. G. D. has received consulting fees from Abbott, Boehringer Ingelheim, BMS, GlaxoSmithKline, Human Genome Sciences, Novartis, Pharmasset, Pfizer, Roche–Genentech, Scher-ing-Plough (Merck), Tibotec, Vertex Pharmaceuticals, Janssen, ZymoGe-netics, and Gilead Sciences. His institution has received grant support from Gilead Sciences, Janssen, Novartis, Pharmasset, Hoffmann–La Roche, Schering-Plough (Merck), Tibotec, and Vertex. W. R. sits on advisory boards for Roche and Gilead and has received research support from Roche. M. B. has received travel grants and/or honoraria for presentations/ advisory boards from MSD, Gilead Sciences, Janssen, and BMS and has received fellowships from Gilead Sciences. M. T. has received consulting and lecture fees from Gilead, BMS, Abbott, and MSD. All other authors report no potential conflicts.
Funding Information:
Financial support. The work was supported through unrestricted educational grants from The Nuffield Trust, BMS, Novartis, Gilead, and Roche. The industry funders had no role in any aspect of the study other than receiving study progress updates.
Keywords
- Clinical outcomes
- Cross-sectional
- Genotypes
- Hepatitis B virus
- Virology