Hepatitis: Taylor C

O'Grady J, Taylor C, Brook G. · King's College Hospital, London, UK. · HIV Med. · Pubmed #16011540 No free full text.

This publication has no abstract.

Brant LJ, Hurrelle M, Balogun MA, Klapper P, Ahmad F, Boxall E, Hale A, Hollyoak V, Ibrahim IB, Irving W, Meigh R, Mutton KJ, Patel BC, Paver WK, Pugh S, Taylor C, Turner AJ, Ramsay ME. · Health Protection Agency, Centre for Infections, Colindale, London, UK. · Epidemiol Infect. · Pubmed #16836798 No free full text.

Abstract: This paper describes sentinel laboratory surveillance of hepatitis C antibody testing in England. Demographic and test result data were supplemented by follow-up questionnaires sent to the requesting clinician. Between October 2002 and September 2003 almost 75000 anti-HCV tests were performed in eight sentinel centres. More males were tested than females and over half of those tested were aged 25-44 years. Overall 5.7% (3333/58144, range 2.8-7.7%) individuals tested positive. Follow-up questionnaire data showed that 82% (1043/1277) of the positives had injecting drug use reported as the main risk exposure. The majority of negative individuals were undergoing routine screening as recommended for specific patient groups. Most individuals were asymptomatic. Antibody prevalence was estimated to be 34% in current injecting drug users and 42% in former injectors. Comparing positives to routine national surveillance suggests that only 53% (1782/3333) of diagnosed cases were reported. Sentinel laboratory data can provide valuable supplementary data to national surveillance.

Clark SJ, Creighton S, Horner M, Smith HM, Portmann B, Taylor C, Cramp ME. · Department of Liver Studies, King's College Hospital, Denmark Hill, London, UK. · Int J STD AIDS. · Pubmed #16409685 No free full text.

Abstract: The effect of HIV-related immunosuppression and antiretroviral therapy on the reactivation of latent hepatitis B virus (HBV) infection is unclear. We report four patients with advanced HIV-related immunosuppression and abnormal liver function tests who had evidence of HBV reactivation. Reclearance of hepatitis B occurred in two cases with HIV treatment regimens not containing lamivudine, suggesting that improved immune function may be responsible. In three cases, HBV reactivation was recognized during investigation for abnormal liver function initially attributed to drug toxicity. The possibility of HBV reactivation must be considered in the differential diagnosis of abnormal liver function in cases with advanced HIV.

Taylor C, Waters K. · Kansas Department of Health and Environment, USA. · Kans Nurse. · Pubmed #16381345 No free full text.

Abstract: The hepatitis C (HCV) infection prevalence in Kansas is concentrated in populations with increased risk factors for acquiring the virus. Testing the appropriate population and providing counseling and medical referral to these high risk individuals is accomplished by offering HCV testing at HIV Counseling and Testing sites across the state. Such public health programs along with the medical community allow the at risk populations of Kansas an opportunity to improve their health and decrease the spread of HCV

Semmo N, Barnes E, Taylor C, Kurtz J, Harcourt G, Smith N, Klenerman P. · Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, UK. · Lancet. · Pubmed #15664228 No free full text.

Abstract: Blood donors are routinely screened for hepatitis C virus infection. Some individuals have weak or restricted virus-specific antibody responses, and are classed as indeterminate. Such donors are almost always negative for viral RNA in blood. We postulated that previous transient virus exposure might account for some of these cases. With sensitive ex-vivo analyses of T-cell responses, we identified virus-specific responses in 15 of 30 indeterminate blood donors tested, compared with none in controls (p=0.0013). Additionally, these responses were typically focused on core-derived peptides. These findings suggest previous exposure to the virus in many indeterminate blood donors.

Norris S, Taylor C, Muiesan P, Portmann BC, Knisely AS, Bowles M, Rela M, Heaton N, O'Grady JG. · Institute of Liver Studies, King's College Hospital, London, UK. · Liver Transpl. · Pubmed #15376307 links to  free full text

Abstract: Liver transplantation (LT) in human immunodeficiency virus (HIV)-positive individuals is considered to be an experimental therapy with limited reported worldwide experience, and little long-term survival data. Published data suggest that the short-term outcome is encouraging in selected patients. Here, we report our experience in 14 HIV-infected liver allograft recipients, and compare outcomes between those coinfected with hepatitis C virus (HCV) and the non-HCV group. A total of 14 HIV-infected patients (12 male, 2 female, age range 26-59 years) underwent LT between January 1995 and April 2003. Indications for LT were HCV (n = 7), hepatitis B virus (HBV; n = 4), alcohol-induced liver disease (n = 2), and seronegative hepatitis (n = 1); 3 patients presented with acute liver failure. At LT, CD4 cell counts (T-helper cells that are targets for HIV) ranged from 124 to 500 cells/microL (mean 264), and HIV viral loads from <50 to 197,000 copies/mL. Nine of 12 patients were exposed to highly active antiretroviral therapy (HAART) before LT. In the non-HCV group (n = 7), all patients are alive, all surviving more than 365 days (range 668-2,661 days). No patient has experienced HBV recurrence, and graft function is normal in all 7 patients. However, 5 of 7 HCV-infected patients died after LT at 95-784 days (median 161 days). A total of 4 patients died of complications due to recurrent HCV infection and sepsis, despite antiviral therapy in 3 of them. A total of 3 patients experienced complications relating to HAART therapy. In conclusion, outcome of LT in HIV-infected patients with HBV or other causes of chronic liver disease indicates that LT is an acceptable therapeutic option in selected patients. However, longer follow-up in larger series is required before a conclusive directive can be provided for HCV / HIV coinfected patients requiring LT.

Antoniades C, Macdonald C, Knisely A, Taylor C, Norris S. · Institute of Liver Studies, King's College Hospital, Denmark Hill, London SE 5 9RS, UK. · Liver Transpl. · Pubmed #15108264 links to  free full text

Abstract: Antiretroviral therapy is not uncommonly associated with drug toxicities, and hepatotoxicity occurs in approximately 20% of individuals prescribed antiretroviral therapy. Mitochondrial toxicity causing lactic acidosis is a rare but fatal complication that has been described in some HIV-infected patients treated with nucleoside analogue reverse transcriptase inhibitors. In this report, we describe the course of an HIV-infected patient receiving antiretroviral therapy who developed lactic acidosis after liver transplantation for HCV-induced liver disease.

Mohsen AH, Easterbrook PJ, Taylor C, Portmann B, Kulasegaram R, Murad S, Wiselka M, Norris S. · Department of HIV/GU Medicine, The Guy's King's and St Thomas School of Medicine, Weston Education Centre, Denmark Hill Campus, Cutcombe Road, London SE5 9RJ, UK. · Gut. · Pubmed #12801963 links to  free full text

Abstract: OBJECTIVES: To compare the rate of hepatic fibrosis progression in hepatitis C virus (HCV) infected and human immunodeficiency virus (HIV)-HCV coinfected patients, and to identify factors that may influence fibrosis progression. PATIENTS AND METHODS: A total of 153 HCV infected and 55 HCV-HIV coinfected patients were identified from two London hospitals. Eligible patients had known dates of HCV acquisition, were HCV-RNA positive, and had undergone a liver biopsy, which was graded using the Ishak score. Univariate and multivariate logistic regression analyses were used to identify factors associated with fibrosis progression rate and the development of advanced fibrosis (stages 3 and 4). RESULTS: The estimated median fibrosis progression rate was 0.17 units/year (interquartile range (IQR) 0.10-0.25) in HIV-HCV coinfected and 0.13 (IQR 0.07-0.17) in HCV monoinfected patients (p=0.01), equating to an estimated time from HCV infection to cirrhosis of 23 and 32 years, respectively. Older age at infection (p<0.001), HIV positivity (p=0.019), higher alanine aminotransferase (ALT) level (p=0.039), and higher inflammatory activity (p<0.001) on first biopsy were all independently associated with more rapid fibrosis progression. ALT was correlated with histological index (r=0.35, p<0.001). A CD4 cell count < or =250 x 10(6)/l was independently associated with advanced liver fibrosis (odds ratio 5.36 (95% confidence interval 1.26-22.79)) and was also correlated with a higher histological index (r=-0.42, p=0.002). CONCLUSION: HIV infection modifies the natural history of HCV by accelerating the rate of fibrosis progression by 1.4 fold, and the development of advanced fibrosis threefold. A low CD4 cell count was independently associated with advanced disease and correlated with higher histological index, which suggests that early antiretroviral therapy may be of benefit in slowing HCV progression in coinfected patients.

Prachalias AA, Pozniak A, Taylor C, Srinivasan P, Muiesan P, Wendon J, Cramp M, Williams R, O'Grady J, Rela M, Heaton ND. · Institute of Liver Studies, King's College Hospital, Denmark Hill, London, SE5 9RS, United Kingdom. · Transplantation. · Pubmed #11726833 No free full text.

Abstract: OBJECTIVE: To report our experience of prospectively identifying and transplanting livers into HIV-positive patients. DESIGN: Liver transplantation in HIV-positive patients remains controversial. The finding of HIV is usually considered a contraindication to any form of transplantation. Previously reported cases are few and refer to patients who tested HIV positive after they had their liver transplantations or who seroconverted in the posttransplantation period. This is, to our knowledge, the only report of patients who were known to be HIV positive at the time of decision for listing for transplantation. METHODS: The medical records of five HIV-positive patients who received liver transplants in King's College Hospital, London, during a 5-year period (January 1995-December 1999) were reviewed. All five were known to be HIV positive at the time of listing for liver replacement. Three of them had end-stage liver disease due to hepatitis C (two of them had underlying Hemophilia A) while the other two had acute liver failure, one due to hepatitis B infection and one due to nonA-nonB-nonC hepatitis. In all but one patient the HIV infection had been asymptomatic. RESULTS: All patients survived the immediate posttransplantation period, but the three patients with hepatitis C died of complications of recurrent hepatitis C between 6 and 25 months posttransplantation. The other two patients are currently alive 4 and 34 months posttransplantation with good graft function and without complications from their HIV infection. CONCLUSION: The early outcome of liver transplantation in HIV seropositive patients can be good, and patients should not be excluded from transplantation if their liver disease determines their prognosis. More effective antiviral therapy for hepatitis C given posttransplantation, and for hepatitis B reinfection, should improve the longer-term outcome of HIV patients with end-stage liver disease due to hepatitis.

Edwards S, Tenant-Flowers M, Buggy J, Horne P, Hulme N, Easterbrook P, Taylor C. · Department of Genitourinary/HIV Medicine, Caldecot Centre, King's College Hospital, London SE5 9RS. · BMJ. · Pubmed #11179158 links to  free full text

This publication has no abstract.

Taylor C, Burns DA, Wiselka MJ. · Department of Infection and Tropical Medicine, Leicester Royal Infirmary, Infirmary Square, Leicester LE1 5WW, UK. · Postgrad Med J. · Pubmed #10824054 links to  free full text

Abstract: A 47 year old man with chronic hepatitis C was treated with interferon alfa, 3 million units three times a week, and developed widespread plaque psoriasis within weeks of starting interferon therapy. There was no previous history of psoriasis. The psoriasis was characterised by extensive nail involvement and plaques at the interferon injection sites. The patient relapsed after a total of 12 months of interferon and was subsequently treated with interferon and tribavirin (ribavirin) with recurrence of the psoriasis.