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Barry Evans

Publications and source records attributed to Barry Evans.

8 recordsLinked to original sources
PubMed2006

UK Guideline for the use of post-exposure prophylaxis for HIV following sexual exposure.

We present the British Association for Sexual Health and HIV (BASHH) guidelines for post-exposure prophylaxis after sexual exposure (PEPSE) to HIV. This document includes a review of the current data to support the use of PEPSE, considers how to calculate the risks of HIV infection after a potential exposure, and provides recommendations on when PEPSE would and would not be considered. Other areas included are the possible impact on sexual behaviour, cost-effectiveness, and issues relating to service provision. Throughout the document, consideration is given to the place of PEPSE within the broader context of HIV prevention strategies and sexual health.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Time trends in primary resistance to HIV drugs in the United Kingdom: multicentre observational study.

OBJECTIVE: To examine whether the level of primary resistance to HIV drugs is increasing in the United Kingdom. DESIGN: Multicentre observational study. SETTING: All virology laboratories in the United Kingdom carrying out tests for HIV resistance as part of routine clinical care. PARTICIPANTS: 2357 people infected with HIV who were tested for resistance before receiving antiretroviral therapy. MAIN OUTCOME MEASURE: Prevalence of drug resistance on basis of the Stanford genotypic interpretation system. RESULTS: Over the study period (February 1996 to May 2003), 335 (14.2%, 95% confidence interval 12.8% to 15.7%) samples had mutations that conferred resistance to one or more antiretroviral drugs (9.3% high level resistance, 5.9% medium level resistance). The prevalence of primary resistance has increased markedly over time, although patterns are specific to drug class; the largest increase was for non-nucleoside reverse transcriptase inhibitors. In 2002-3, the prevalence of resistance to any antiretroviral drug to nucleoside or nucleotide reverse transcriptase inhibitors, to non-nucleoside reverse transcriptase inhibitors, or to protease inhibitors was 19.2% (15.7% to 23.2%), 12.4% (9.5% to 15.9%), 8.1% (5.8% to 11.1%), and 6.6% (4.4% to 9.3%), respectively. The risk of primary resistance was only weakly related to most demographic and clinical factors, including ethnicity and viral subtype. CONCLUSIONS: The United Kingdom has one of the highest reported rates of primary resistance to HIV drugs worldwide. Prevalence seems still to be increasing and is high in all demographic subgroups.

Adolescent↗
PubMed2005

Estimating HIV-1 drug resistance in antiretroviral-treated individuals in the United Kingdom.

Good estimates of the prevalence of human immunodeficiency virus drug resistance are important for assessing requirements for new drug classes and modeling the spread of resistance. However, little consensus exists on optimal methodologies to generate such data. To compare methodologies, we used the national data set of resistance tests from >4000 patients in the United Kingdom performed between 1998 and 2002. When single-time-point analysis (method 1) was used, the proportion of tests with any form of resistance was approximately 80%, with little time trend. When a cumulative model of resistance (method 2) was used and placed in the context of all treated patients, the prevalence of any resistance increased by year, reaching 17% of treated patients in 2002. Method 2 also nearly doubles estimates of numbers of individuals infected with multiclass drug-resistant virus. Our results identify an urgent need for new drugs within existing classes and new classes of antiretroviral therapy.

Anti-HIV Agents↗
PubMed2004

Surveillance of HIV antiretroviral drug resistance in treated individuals in England: 1998-2000.

OBJECTIVES: To establish a surveillance programme for HIV drug resistance within the UK covering the years from 1998 to 2000, following the introduction of triple combination antiretroviral therapy. METHODS: Sentinel sites included large, medium sized and small clinical centres. Data were analysed until December 2000. RESULTS: Of nearly 300 samples tested, results from 91, 92 and 92 patients, respectively in 1998, 1999 and 2000, who were receiving HIV therapy with a viral load >2000 copies/mL, the majority had viruses with some degree of drug resistance. Overall, the presence of any resistance increased between 1998 and 1999, and fell again in 2000 (69% versus 88% versus 55%). However, major differences were observed between drug classes, such that non-nucleoside analogue reverse transcriptase inhibitor (NNRTI) resistance rose dramatically over the period studied. We show that this correlated with increased NNRTI prescribing. Furthermore, an overall increase in prevalence of viruses with resistance to one or more drugs within all three available classes was observed. A higher prevalence of drug resistance was observed in patients from smaller clinical centres. CONCLUSIONS: This is the first such sentinel surveillance dataset from the UK, and is unique in correlating these data with national antiretroviral prescribing patterns. Our findings are relevant to the increased transmission of HIV drug resistance observed over this period.

Anti-HIV Agents↗
PubMed2004

Post-exposure prophylaxis of HIV infection in healthcare workers: recommendations for the European setting.

The European Commission funded a project for the standardisation of the management of occupational exposures to HIV/blood-borne infections and antiretroviral post-exposure prophylaxis (PEP) in Europe. Within this project, the following recommendations and rationale were formulated by experts representative of participating countries. Based on assessment of the exposure, material, and source characteristics, PEP should be started as soon as possible with any triple combination of antiretrovirals approved for the treatment of HIV-infected patients; initiation is discouraged after 72 hours Rapid HIV testing of the source could reduce inappropriate PEP. HIV testing should be performed at baseline, 4, 12, and 24 weeks, with additional clinical and laboratory monitoring of adverse reactions and potential toxicity at week 1 and 2. HIV resistance tests in the source and direct virus assays in the exposed HCW are not recommended routinely. These easy-to-use recommendations seek to maximise PEP effect while minimising its toxicity and inappropriate use.

Anti-HIV Agents↗
PubMed2003

Impact of the HIV epidemic in sub-Saharan Africa on the pattern of HIV in the UK.

OBJECTIVE: To describe the epidemiology of HIV infection acquired in Africa and among African communities in the United Kingdom. DESIGN: Descriptive analysis using national HIV and AIDS surveillance data, routine voluntary confidential HIV reporting and unlinked anonymous seroprevalence surveys in the United Kingdom to the end of December 2001. RESULTS: Of all reported HIV infections diagnosed in the United Kingdom by the end of 2001, 21% (9993 of 48,226) were probably acquired in Africa and 90% of these infections were heterosexually acquired. Numbers of diagnoses of HIV infection acquired in Africa have been increasing rapidly, with rises in infections from southeastern and southern Africa predominating recently. Among those living with diagnosed HIV infection in 2000, 23% (4883 of 21,291) were described as black African, 81% of whom lived in London. The proportion living in London has declined over successive prevalence surveys. CONCLUSIONS: Infections acquired in Africa and among Africans are making an increasing contribution to HIV infection in the United Kingdom. Migration, diagnosis of long-standing infection and incident cases are all potential influences, but they are difficult to measure. Improvement in early diagnosis of HIV continues to be an important component of intervention to prevent onward vertical and sexual transmission and to promote access to treatment and care.

Adult↗
PubMed2002

Evaluation of molecular markers in low-grade diffuse astrocytomas: loss of p16 and retinoblastoma protein expression is associated with short survival.

Diffuse astrocytomas have a median survival of 6-8 years. However, in a minority of cases that are histologically low grade, progression is rapid, leading to death within 2 years. Loss of p16, retinoblastoma protein, and deleted-in-colon-carcinoma protein expression, and monosomy of chromosome 10 have been shown to occur in malignant astrocytic tumors. We have investigated the prognostic value of expression of these markers, using techniques applicable in many histopathology laboratories, in diffuse astrocytomas that are histologically low grade. Paraffin sections from 71 diffuse, supratentorial, low-grade astrocytomas, from patients with at least 8-year survival data, were immunostained with antibodies to p16, deleted-in-colon-carcinoma protein, p53, Ki67, and retinoblastoma protein. In situ hybridization with a digoxigenin-labeled probe to chromosome 10 was used to assess chromosomal loss. In most cases there was immunostaining of virtually all tumor cell nuclei with antibodies to p16 and retinoblastoma protein. Three of the 68 tumors in which assessment of p16 was possible included discrete foci with lack of detectable immunoreactivity in tumor cells. The three patients concerned had a significantly shortened median survival (1.1 years vs 4.4 years in those without loss of p16; p <0.01). In six of the 61 cases where assessment of retinoblastoma protein was possible, <70% of tumor cell nuclei showed immunoreactivity. These six patients had a shorter survival (4.0 years) than had the remaining patients (5.4 years), although this difference was not statistically significant. The tumor from one of these patients included areas where only 36% of tumor cells showed retinoblastoma protein immunoreactivity, and this patient survived only 1.5 years. Tumors showing loss of both p16 and retinoblastoma were not seen. p53 and deleted-in-colon-carcinoma protein expression was highly variable and did not correlate with survival. Tumors with monosomy for chromosome 10 were not identified. Both polyploidy and the Ki67 labeling index were significantly associated with the p53 labeling index but not with survival. Focal loss of p16 or retinoblastoma protein is demonstrable in approximately 5% and 10% of diffuse low-grade diffuse astrocytomas, respectively. Tumors with focal loss of immunoreactivity for these proteins are associated with shorter survival than those without, suggesting that immunohistochemistry for p16 and retinoblastoma protein may be a useful adjunct to other methods for assessing the prognosis of astrocytomas.

Astrocytoma↗