Hepatitis: London, EN

Gilson R, Brook MG. · Centre for Sexual Health And HIV Research, Royal Free and University College Medical School, The Mortimer Market Centre, London WC1E 6AU, UK. · Sex Transm Infect. · Pubmed #17151052 No free full text.

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Hawkins D, Blott M, Clayden P, de Ruiter A, Foster G, Gilling-Smith C, Gosrani B, Lyall H, Mercey D, Newell ML, O'Shea S, Smith R, Sunderland J, Wood C, Taylor G, Anonymous00122. · Chelsea and Westimnster Hospital, London, UK. · HIV Med. · Pubmed #16033339 No free full text.

This publication has no abstract.

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

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Nelson M, Matthews G, Brook MG, Main J, Anonymous00327, Anonymous00328. · Patrick Clements Clinic, Central Middlesex Hospital, London, UK. · HIV Med. · Pubmed #16011539 No free full text.

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Brook MG, Gilson R, Wilkins E, Anonymous00325, Anonymous00326. · Central Middlesex Hospital, London, UK. · HIV Med. · Pubmed #16011538 No free full text.

This publication has no abstract.

Gazzard B, Anonymous00323. · Chelsea and Westimnster Hospital, London, UK. · HIV Med. · Pubmed #16011536 No free full text.

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Vergani D, Alvarez F, Bianchi FB, Cançado EL, Mackay IR, Manns MP, Nishioka M, Penner E, Anonymous00232. · Institute of Liver Studies, King's College Hospital, Denmark Hill, London SE5 9RS, UK. · J Hepatol. · Pubmed #15464251 No free full text.

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Nelson MR, Matthews G, Brook MG, Main J, Anonymous00076. · Chelsea and Westminster Hospital, London, UK. · HIV Med. · Pubmed #14511248 No free full text.

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Brook MG, Gilson R, Wilkins EL, Anonymous00075. · Central Middlesex Hospital, London, UK. · HIV Med. · Pubmed #14511247 No free full text.

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Gilling-Smith C, Almeida P, Anonymous00076. · Assisted Conception Unit, Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH, UK. · Hum Fertil (Camb). · Pubmed #12960441 No free full text.

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Booth JC, O'Grady J, Neuberger J, Anonymous00102. · Department of Gastroenterology, Royal Berkshire Hospital, London Road, Reading RG5 5AN, UK. · Gut. · Pubmed #11413125 links to  free full text

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Alvarez F, Berg PA, Bianchi FB, Bianchi L, Burroughs AK, Cancado EL, Chapman RW, Cooksley WG, Czaja AJ, Desmet VJ, Donaldson PT, Eddleston AL, Fainboim L, Heathcote J, Homberg JC, Hoofnagle JH, Kakumu S, Krawitt EL, Mackay IR, MacSween RN, Maddrey WC, Manns MP, McFarlane IG, Meyer zum Büschenfelde KH, Zeniya M. · Institute of Liver Studies, King's College Hospital, London, UK. · J Hepatol. · Pubmed #10580593 No free full text.

This publication has no abstract.

Gomaa AI, Khan SA, Leen EL, Waked I, Taylor-Robinson SD. · Department of Hepatology and Gastroenterology, Division of Medicine, Imperial College London, St Mary's Hospital Campus, South Wharf Road, London W2 1NY, United Kingdom. · World J Gastroenterol. · Pubmed #19294759 links to  free full text

Abstract: Hepatocellular carcinoma (HCC) is one of the commonest cancers worldwide, particularly in parts of the developing world, and is increasing in incidence. This article reviews the current modalities employed for the diagnosis of HCC, including serum markers, radiological techniques and histological evaluation, and summarises international guidelines for the diagnostic approach to HCC.

Gurusamy KS, Osmani B, Xirouchakis E, Burroughs AK, Davidson BR. · University Department of Surgery, Royal Free Hospital and University College School of Medicine, 9th Floor, Royal Free Hospital, Pond Street, London, UK, NW3 2QG. · Cochrane Database Syst Rev. · Pubmed #19160303 No free full text.

Abstract: BACKGROUND: Antiviral therapy to treat recurrent hepatitis C infection after liver transplantation is controversial. OBJECTIVES: To compare the therapeutic efficacy and side effects of different antiviral regimens in patients with hepatitis C re-infected grafts after liver transplantation. SEARCH STRATEGY: We searched The Cochrane Hepato-Biliary Group Controlled Trials Register, the Cochrane Central Register of Controlled Trials (CENTRAL) in The Cochrane Library, MEDLINE, EMBASE, and Science Citation Index Expanded until September 2007. SELECTION CRITERIA: Only randomised clinical trials (irrespective of language, blinding, or publication status) comparing various antiviral therapies (alone or in combination) in the treatment of hepatitis C virus recurrence in liver transplantation were considered for the review. DATA COLLECTION AND ANALYSIS: Two authors collected the data independently. We calculated the relative risk (RR) or weighted mean difference (WMD) with 95% confidence intervals (CI) using the fixed-effect and the random-effects models based on available case-analysis. MAIN RESULTS: A total of 389 liver transplant recipients with proven hepatitis C recurrence were randomised in eleven trials to various interventions and controls. The mean proportion of genotype I was 77.8% in the seven trials that reported the genotype. Only one or two trials were included under each comparison. All the trials were of high risk of bias. There was no difference in the mortality, graft rejection, or in re-transplantation between intervention and control in any of the comparisons that reported these outcomes. None of the trials reported liver decompensation or quality of life. Life-threatening adverse effects were not reported in either group in any of the comparisons. Up to 87.5% of patients required reduction in dose and up to 42.9% of patients required cessation of treatment in the various comparisons because of adverse effects or because of patient's choice to stop treatment. AUTHORS' CONCLUSIONS: 1. Considering the lack of clinical benefit and the frequent adverse effects, there is currently no evidence to recommend antiviral treatment for recurrent liver graft infection with HCV. 2. Further randomised clinical trials with adequate trial methodology and adequate duration of follow-up are necessary.

Low E, Vogel M, Rockstroh J, Nelson M. · Department of Sexual Health and HIV, Chelsea and Westminster Hospital, London, UK. · AIDS Rev. · Pubmed #19092980 No free full text.

Abstract: Due to the asymptomatic nature of acute hepatitis C it can be difficult to diagnose in the early stage of infection, but with the higher treatment success rates and reduced treatment duration at this stage, it is imperative that diagnoses are made. Therefore, physicians should routinely screen at-risk individuals and investigate abnormal liver function tests. Serum HCV RNA should be considered in any HCV-antibody-negative individual in whom acute HCV is clinically suspected, or annually in those high-risk individuals with previous infection. Acute hepatitis C transmission may be facilitated by the presence of an erosive genital lesion, such as syphilis or lymphogranuloma venereum, and thus testing at this time should be encouraged. Reinfection with HCV does occur and patients need to be informed of the sexual and other high-risk behaviors that put them at risk of reinfection. Public awareness of the possibility of HCV infection, and subsequent reinfection, in high-risk groups should be increased. The question of the optimal treatment regimen is still disputed. However, ongoing trials and the proposed randomized controlled trial from the European AIDS Treatment Network should answer many of our questions. In the meantime, units faced with HIV/acute hepatitis C coinfection should follow recommendations from the HCV-HIV International Panel.

O'Grady JG. · King's College Hospital, Denmark Hill, London, United Kingdom. john.o' · Liver Transpl. · Pubmed #18825687 No free full text.

Abstract: 1. Establishing the cause of fulminant hepatitis is an important determinant in outcomes after liver transplantation. 2. Liver transplantation is an integral part of the management of ALF. 3. In addition to generic posttransplant care, neurologic, septic, and hematologic issues need to be addressed. 4. Outcomes after liver transplantation are poorer than those for elective transplantation but superior to those found for comparably ill patients being transplanted for chronic liver disease. 5. Multiple factors have an influence on outcome, and risk stratification is beginning to emerge.

Dhawan A. · Paediatric Liver Centre, King's College London School of Medicine, King's College Hospital, London, United Kingdom. · Liver Transpl. · Pubmed #18825678 No free full text.

Abstract: 1. The etiology of acute liver failure in children differs from that in adults, with metabolic conditions being commoner in Europe and North America and hepatitis A being the commonest cause in Asia and South America. 2. Encephalopathy usually is a late feature and is not essential for the diagnosis. 3. Unlike adults, there are no good prognostic criteria that can predict survival without liver transplantation. 4. It is important to exclude genetic multisystem disorders before liver transplantation is considered.

Rhodes T, Treloar C. · Centre for Research on Drugs and Health Behaviour, London School of Hygiene and Tropical Medicine, University of London, London, UK. · Addiction. · Pubmed #18821870 No free full text.

Abstract: BACKGROUND: Intervention impact on reductions in hepatitis C virus (HCV) incidence among injecting drug users (IDUs) are modest. There is a need to explore how drug injectors' interpret HCV risk. AIMS: To review English-language qualitative empirical studies of HCV risk among IDUs. METHODS: Qualitative synthesis using a meta-ethnographic approach. Searching of eight electronic databases and reference lists identified manually papers in peer-reviewed journals since 2000. Only studies investigating IDU perspectives on HCV risk were included. Themes across studies were identified systematically and compared, leading to a synthesis of second- and third-order constructs. FINDINGS: We included 31 papers, representing 24 studies among over 1000 IDUs. Seven themes were generated: risk ubiquity; relative viral risk; knowledge uncertainty; hygiene and the body; trust and intimacy; risk environment; and the individualization of risk responsibility. Evidence supports a perception of HCV as a risk accepted rather than avoided. HCV was perceived largely as socially accommodated and expected, and in relative terms to human immunodeficiency virus (HIV) as the 'master status' of viral dangers. Symbolic knowledge systems, rather than biomedical risk calculus, and especially narratives of hygiene and trust, played a primary role in shaping interpretations of HCV risk. Critical factors in the risk environment included policing, homelessness and gendered risk. CONCLUSIONS: Appealing to risk calculus alone is insufficient. Interventions should build upon the salience of hygiene and trust narratives in HCV risk rationality, and foster community changes towards the perceived preventability of HCV. Structural interventions in harm reduction should target policing, homelessness and gendered risk.

Bogdanos DP, Dalekos GN. · Liver Immunopathology, Institute of Liver Studies, Division of Gene and Cell Based Therapy, King's College London School of Medicine at King's College Hospital, UK. · Curr Med Chem. · Pubmed #18781950 No free full text.

Abstract: Characterization of liver-specific autoantigens has given a fresh impetus to research in the pathogenesis of autoimmune liver diseases, viral-triggered and drug-induced autoimmunity affecting the liver. Intriguing is the fact that most of the liver-specific autoantigens are enzymes of key importance for cell's homeostasis. Detection of autoantibodies against the respective antigens is carried out for diagnostic and research purposes using indirect immunofluorescence, immunoblotting, enzyme-linked immunosorbent assays, radioimmunoassay, immunoprecipitation or assays determining inhibition of enzyme activity. In patients with autoimmune hepatitis, a liver disorder of unknown etiology and pathogenesis, disease-specific autoantibodies are frequently directed against drug metabolizing enzymes of phase 1, namely cytochrome P450 2D6 (CYP2D6). The same and other members of these families of enzymes (CYPs) have also been described as targets of liver-specific autoimmunity in chronic hepatitis C virus (HCV)-infected patients, patients with autoimmune hepatitis as part of the autoimmune polyglandular syndrome type-1 (APS-1) and drug-induced autoimmunity. How these enzymes become 'self targets' is not yet established. An antigen release following hepatocyte injury could provide the stimulus for an immune response towards epitopes on these enzymes but the highly-specific, antigen-restricted initiation of the observed autoimmune response is against such an explanation. Accordingly, in this review we will focus on the pathogenic role -if any- of autoimmune responses against liver-related CYPs in autoimmune hepatitis, HCV infection, APS-1 and drug-induced autoimmunity. Learning more about the specificity of antibody responses against these enzymes may help us better understand the mechanisms underlying liver autoimmunity and may facilitate the development of therapeutic and preventive interventions.

Alazawi W, Foster GR. · The Liver Unit, Barts and The London School of Medicine, London, UK. · Curr Opin Infect Dis. · Pubmed #18725801 No free full text.

Abstract: PURPOSE OF REVIEW: Hepatitis B virus is responsible for much morbidity and mortality worldwide. Although the armament of drugs licensed for its treatment grows, it is increasingly apparent that the efficacy of these drugs is dependent upon much more that their pharmacology. RECENT FINDINGS: A better understanding of the natural history of chronic hepatitis B infection together with recent advances in the molecular biology of antiviral resistance have given added dimensions to physicians' decision-making thought processes. SUMMARY: The present review outlines the recent advances in diagnostic testing that enable a better understanding of an individual patient's phase of illness and also how such information can update treatment choices better. In the second part of this review, the licensed therapies and their relative merits are discussed, as is their role in managing resistance to antiviral therapy.

Xirouchakis E, Triantos C, Manousou P, Sigalas A, Calvaruso V, Corbani A, Leandro G, Patch D, Burroughs A. · The Royal Free Sheila Sherlock Liver Centre, Royal Free Hospital, London, UK. · J Viral Hepat. · Pubmed #18673428 No free full text.

Abstract: SUMMARY: Pegylated interferon with ribavirin (Peg/R) is the most effective therapy for chronic hepatitis C virus (HCV) but its utility and effectiveness after liver transplantation has been difficult to assess. We evaluated efficacy, tolerability, and safety of Peg/R in liver transplant candidates and recipients with HCV cirrhosis. We searched medical databases and conference proceedings between January 1999 and January 2008 selecting randomized and nonrandomized studies. Primary end points meta-analytically were: (1) sustained viral response (SVR) and (2) histological response. Secondary end points were: (1) treatment discontinuation, (2) mortality, and (3) rejection episodes. Pegylated interferons using either 1-1.5 mcg/kg of pegylated interferon alpha-2b or 180 microg (pegylated interferon alpha-2a combined with ribavirin 800-1200 mg/day were the most effective compared to any other regimen or no therapy. In three pretransplant studies the median SVR was 19.6% (19.6-50%). In six postransplant studies where a meta-analysis was done the cumulative risk difference in SVR was 0.31% (95% CI, 0.18-0.44, p < 0.001). However histological response was not significantly better compared to no therapy or other antiviral regimens. There were no significant differences in discontinuation of therapy, acute or chronic rejection or mortality between optimal Peg/R vs no treatment or other regimens. Hence pegylated interferon plus ribavirin in full doses is effective pre and post transplant but has a low SVR rate. To date no significant histological improvement has been reported.

Ferri S, Muratori L, Lenzi M, Granito A, Bianchi FB, Vergani D. · Institute of Liver Studies, King's College School of Medicine at King's College Hospital, Denmark Hill, London, UK. · Curr Pharm Des. · Pubmed #18673191 No free full text.

Abstract: Hepatitis C virus (HCV) infection is characterized by a number of autoreactive manifestations, such as autoantibody production, cryoglobulinemia and thyroid disorders. We will analyse critically the mechanisms invoked, and partially documented, to explain such manifestations arising in genetically predisposed individuals exposed to HCV. In particular we will examine the available evidence implicating the virus in lowering the B cell activation threshold, in directly infecting lymphocytes and in inducing self-reactivity through a mechanism of molecular mimicry. We will then move to the HCV related clinical immunopathological manifestations, with a specific attention to the effects of antiviral treatment.

Gomaa AI, Khan SA, Toledano MB, Waked I, Taylor-Robinson SD. · Department of Hepatology and Gastroenterology, Imperial College London, St Mary's Hospital Campus, Praed Street, London W2 1NY, United Kingdom. · World J Gastroenterol. · Pubmed #18666317 links to  free full text

Abstract: Hepatocellular carcinoma (HCC) is the commonest primary malignant cancer of the liver in the world. Given that the burden of chronic liver disease is expected to rise owing to increasing rates of alcoholism, hepatitis B and C prevalence and obesity-related fatty liver disease, it is expected that the incidence of HCC will also increase in the foreseeable future. This article summarizes the international epidemiology, the risk factors and the pathogenesis of HCC, including the roles of viral hepatitis, toxins, such as alcohol and aflatoxin, and insulin resistance.

James WH. · The Galton Laboratory, University College London, Wolfson House, 4 Stephenson Way, London NW 1 2 HE, UK. · J Endocrinol. · Pubmed #18577567 links to  free full text

Abstract: An attempt is made to summarize the evidence that the offspring sex ratios (proportions male at birth) of mammals (including man) are causally related to the hormone levels of both parents around the time of conception. Almost all of the cited studies were reported by non-endocrinologists. This being so, it would seem desirable to have comments of endocrinologists on this topic. The purpose of this article is to elicit such comment. Readers are requested to read the accompanying editorial (Clark & Davis 2008) to gain a better perspective of this hypothesis article.

Bogdanos DP, Invernizzi P, Mackay IR, Vergani D. · Institute of Liver Studies, King's College London School of Medicine, London SE5 9RS, UK. · World J Gastroenterol. · Pubmed #18528935 links to  free full text

Abstract: Liver-related autoantibodies are crucial for the correct diagnosis and classification of autoimmune liver diseases (AiLD), namely autoimmune hepatitis types 1 and 2 (AIH-1 and 2), primary biliary cirrhosis (PBC), and the sclerosing cholangitis variants in adults and children. AIH-1 is specified by anti-nuclear antibody (ANA) and smooth muscle antibody (SMA). AIH-2 is specified by antibody to liver kidney microsomal antigen type-1 (anti-LKM1) and anti-liver cytosol type 1 (anti-LC1). SMA, ANA and anti-LKM antibodies can be present in de-novo AIH following liver transplantation. PBC is specified by antimitochondrial antibodies (AMA) reacting with enzymes of the 2-oxo-acid dehydrogenase complexes (chiefly pyruvate dehydrogenase complex E2 subunit) and disease-specific ANA mainly reacting with nuclear pore gp210 and nuclear body sp100. Sclerosing cholangitis presents as at least two variants, first the classical primary sclerosing cholangitis (PSC) mostly affecting adult men wherein the only (and non-specific) reactivity is an atypical perinuclear antineutrophil cytoplasmic antibody (p-ANCA), also termed perinuclear anti-neutrophil nuclear antibodies (p-ANNA) and second the childhood disease called autoimmune sclerosing cholangitis (ASC) with serological features resembling those of type 1 AIH. Liver diagnostic serology is a fast-expanding area of investigation as new purified and recombinant autoantigens, and automated technologies such as ELISAs and bead assays, become available to complement (or even compete with) traditional immunofluorescence procedures. We survey for the first time global trends in quality assurance impacting as it does on (1) manufacturers/purveyors of kits and reagents, (2) diagnostic service laboratories that fulfill clinicians' requirements, and (3) the end-user, the physician providing patient care, who must properly interpret test results in the overall clinical context.