Hepatitis: Mauss S

Rockstroh JK, Bhagani S, Benhamou Y, Bruno R, Mauss S, Peters L, Puoti M, Soriano V, Tural C, Anonymous00076. · Department of Medicine I, University of Bonn, Bonn, Germany. · HIV Med. · Pubmed #18257771 No free full text.

Abstract: OBJECTIVES: With the decline in HIV-associated morbidity and mortality following the introduction of highly active antiretroviral therapy (HAART), liver disease has emerged as a major cause of death in HIV/hepatitis B virus (HBV) and HIV/hepatitis C virus (HCV) coinfected persons. Therefore, screening for underlying viral hepatitis coinfection and the provision of management and treatment recommendations for patients with chronic viral hepatitis are of great importance in preventing, as far as possible, the development of liver disease. With the introduction of new agents for the treatment of hepatitis B and increased knowledge of how best to manage hepatitis C, an update of current guidelines for management of HBV and HCV coinfection with HIV is warranted. SUMMARY: Clearly, all HIV-infected patients should be screened for hepatitis A, B and C, taking into account shared pathways of transmission. Patients who are seronegative for hepatitis A and B should be considered for vaccination. In HIV-infected patients with chronic hepatitis B, the first important differentiation is whether HAART is required or not. In the setting of stable HIV infection, with no need for HAART, several treatment options are available, namely treatment with interferon, early initiation of HAART, or selective non-HIV active anti-HBV nucleoside therapy, with the aim of achieving undetectable HBV DNA levels. In most cases, undetectable HBV DNA can only be achieved with combination therapy. With regard to hepatitis C, individualized tailoring of the duration of HCV therapy is advisable, taking into account rapid or delayed virological response. In patients who do not achieve at least a 2 log drop in HCV RNA at week 12, treatment can be terminated because of the low probability of achieving sustained virological response. Overall, with the currently available treatment algorithms, HCV can be eradicated in over 50% of patients. Therefore, HCV therapy should be considered and discussed with the patient if an indication for HCV therapy (elevated liver enzymes, positive HCV RNA and >F1 fibrosis) is present. CONCLUSIONS: Management of underlying hepatitis B and/or C in patients with HIV infection is of great importance in preventing liver disease-associated morbidity and mortality.

Soriano V, Puoti M, Sulkowski M, Mauss S, Cacoub P, Cargnel A, Dieterich D, Hatzakis A, Rockstroh J. · No affiliation provided · AIDS. · Pubmed #15090824 No free full text.

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Soriano V, Sulkowski M, Bergin C, Hatzakis A, Cacoub P, Katlama C, Cargnel A, Mauss S, Dieterich D, Moreno S, Ferrari C, Poynard T, Rockstroh J. · No affiliation provided · AIDS. · Pubmed #11919483 No free full text.

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Zeuzem S, Berg T, Moeller B, Hinrichsen H, Mauss S, Wedemeyer H, Sarrazin C, Hueppe D, Zehnter E, Manns MP. · Zentrum der Inneren Medizin, Klinikum der Johann Wolfgang Goethe-Universität, Frankfurt, Germany. · J Viral Hepat. · Pubmed #18761607 No free full text.

Abstract: The current preferred treatment for patients with hepatitis C virus (HCV) is combination therapy consisting of pegylated interferon alfa and ribavirin (RBV) for 24-48 weeks. Although this approach appears to be highly effective for patients with HCV genotypes 2 or 3, who have a sustained virological response (SVR) of approximately 80%, the treatment algorithm is less effective for patients with HCV genotype 1, as these patients have SVR rates of just 40-50%. In order to improve treatment outcomes, this article explores potential approaches for the optimization of treatment for patients with HCV genotype 1: considering shorter treatment periods for patients with a rapid virological response (RVR), increasing treatment periods for slow responders, and increasing RBV dose are all suggestions. Results from clinical trials suggest that approximately 20% of the HCV genotype 1-infected population are slow responders, and around 15% of all HCV genotype-1 infected patients could benefit from a shorter treatment duration without compromising the SVR rate. Interest has also focused on whether treatment duration could be individualized in some patients with genotype 2 and 3 infection. Here all the findings from recent studies are translated into practical advice, to help practitioners make evidence-based treatment decisions in everyday clinical practice. Although there are areas where currently available data do not provide conclusive evidence to suggest amending treatment approaches, there is clearly potential for individualized treatment in all aspects of hepatitis treatment in the future.

Soriano V, Puoti M, Peters M, Benhamou Y, Sulkowski M, Zoulim F, Mauss S, Rockstroh J. · Department of Infectious Diseases, Hospital Carlos III, Madrid, Spain. · AIDS. · Pubmed #18614862 No free full text.

Abstract: Nearly 10% of the estimated 36 million people having HIV worldwide suffer from chronic hepatitis B virus (HBV) infection. The advent of new antiviral agents against HBV and the recent availability of improved molecular diagnostic tools have revolutioned the management of HIV/HBV coinfected patients. The present study represents an update of the current knowledge about HBV/HIV coinfection and an intent to provide practical advise about how to give the best care to HIV-infected persons with chronic hepatitis B.

Mauss S. · Center for HIV and Gastroenterology, Düsseldorf, Germany. · J HIV Ther. · Pubmed #18391895 No free full text.

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Mauss S, Wedemeyer H. · Center for HIV and Hepatogastroenterology, Grafenberger Allee 128a, 40237 Duesseldorf, Germany. · Expert Rev Anti Infect Ther. · Pubmed #18380601 No free full text.

Abstract: Treatment options for chronic HBV infection have improved considerably in recent years. However, with the increased number of available antiviral drugs, it is also more difficult to select the optimal drug for each individual patient. Antiviral potency, the risk for the development of drug resistance, safety and costs of treatment all need to be considered. In this review, we describe current concepts in the treatment of chronic hepatitis B, with a special focus on the importance of drug resistance and its implications for the long-term management of hepatitis B. Suggestions for avoiding resistance and management of established drug resistance are provided for each individual approved compound.

Mauss S. · Center for HIV and Hepatogastroenterology, Grafenberger Allee 128a, 40237 Duesseldorf, Germany. · J HIV Ther. · Pubmed #17589391 No free full text.

Abstract: Today hepatitis C remains one of the unsolved medical problems and represents a significant proportion of the remaining deaths in the HIV population, particularly in southern Europe and the USA where the prevalence of HCV/HIV-co-infection in the HIV-population ranges from 30% to 50%. Recent trials using pegylated interferon-alfa in combination with low-dose ribavirin have achieved overall sustained response rates of up to 50%. However high discontinuation rates, adverse events associated with mitochondrial toxicities or treatment of patients with advanced cirrhosis may decrease response to treatment and result in serious adverse events. Optimising antiretroviral therapy before the start of interferon-based therapy and active management of adverse events will reduce complications and improve treatment success. As novel agents to treat chronic hepatitis C may not be accessible in the coming years on a broader scale for HIV-co-infected patients the use of higher ribavirin doses and longer treatment periods should be systematically studied to improve hepatitis C therapy in co-infected patients in the near future.

Soriano V, Puoti M, Sulkowski M, Cargnel A, Benhamou Y, Peters M, Mauss S, Bräu N, Hatzakis A, Pol S, Rockstroh J. · Department of Infectious Diseases, Hospital Carlos III, Calle Sinesio Delgado 10, 28029 Madrid, Spain. · AIDS. · Pubmed #17502718 No free full text.

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Mauss S. · Center for HIV and Hepatogastroenterology, Grafenberger Allee 128a, 40237 Duesseldorf, Germany. · J Hepatol. · Pubmed #16356579 No free full text.

Abstract: For the treatment of HBV/HIV-co-infection, study data on interferon-based therapy are very limited and insufficient to draw any specific conclusions. In contrast, data on HBV-polymerase inhibitors (lamivudine, adefovir, tenofovir) are available from controlled trials. Lamivudine is well tolerated and safe, however, development of HBV-resistance is frequent. Adefovir has a nephrotoxic potential and may at least theoretically induce antiretroviral resistance in HBV/HIV-patients treated with adefovir. Tenofovir has gastrointestinal side effects, is associated with hypophospatemia, which has not induced serious osteopenia so far and may have a nephrotoxic potential. For HCV/HIV-co-infection pegylated interferon alpha plus ribavirin is standard of care. Flu-like symptoms, fatigue and depressive mood changes are frequent. In patients with a history of neurotic or minor depression initiation of treatment with antidepressants before the start of interferon-based therapy should be considered. Weight loss may be pronounced in individual cases. A marked decrease in absolute, but not relative CD4 +/- cells is the rule, but no relevant increase in opportunistic infection was observed, and anaemia (<10 g/dl) is reported in up to 30% of patients. Neutropenia (< 1,000 cells/microl) is observed in up to 50% of the patients. Adverse events specific to the HCV/HIV-patient population as compared to HCV-mono-infected patients are the occurrence of hyperlactataemia/lactic acidosis and hepatic decompensation.

Mauss S, Rockstroh JK. · Center for HIV and Hepatogastroenterology, Grafenberger Allee 128a, 40237 Duesseldorf, Germany. · J Antimicrob Chemother. · Pubmed #16115826 links to  free full text

Abstract: Today hepatitis C is one of the unsolved medical problems and results in a significant number of deaths in the HIV population, particularly in southern Europe and the USA, where the prevalence of HCV/HIV-coinfection in the HIV population ranges from 30-50%. Recent trials using pegylated interferon alfa in combination with low dose ribavirin have achieved overall sustained response rates of up to 42%. However, high discontinuation rates, adverse events associated with mitochondrial toxicities or treatment of patients with advanced cirrhosis may decrease response to treatment and result in serious adverse events. Optimizing antiretroviral therapy before the start of interferon-based therapy and active management of adverse events will reduce complications and improve treatment success. The use of higher ribavirin doses and longer treatment periods should be systematically studied to improve hepatitis C therapy in coinfected patients in the near future.

Witthöft T, Möller B, Wiedmann KH, Mauss S, Link R, Lohmeyer J, Lafrenz M, Gelbmann CM, Hüppe D, Niederau C, Alshuth U. · Medical Department I, Division of Gastroenterology, University Hospital Schleswig-Holstein Campus Lübeck, Lübeck, Germany. · J Viral Hepat. · Pubmed #17927615 links to  free full text

Abstract: The combination treatment of peginterferon alpha-2a (PEG-IFN alpha-2a; Pegasys) plus ribavirin (RBV) is recommended as a standard care for HCV infections. Side effects and aspects of efficacy and safety have to be balanced. This study evaluates clinical practice data on safety and efficacy of HCV treatment with PEG-IFN in combination with RBV over 24 and 48 weeks. This study was a phase III, multi-centre, open-label study with two treatment groups: PEG-IFN in combination with RBV for 24 or 48 weeks. The allocation to the treatment groups was at the discretion of the investigator; 309 patients entered active treatment: 90 patients received PEG-IFN plus RBV for 24 weeks and 219 patients PEG-IFN plus RBV for 48 weeks. A sustained virological response (SVR) was achieved in 48.9% of all patients. Genotype 1 patients with a 48-week combination treatment achieved an SVR of 39.9%. In the 48-week group a low baseline viral load was associated with a higher SVR rate (47.0% vs. 32.4%). For genotype 2 or 3 patients, the SVR was 67.9%. For these patients there was no relevant difference between patients with low and high viral loads; 97.7% of the patients experienced at least one adverse event. The incidence of serious adverse events was distinctly lower in the 24-week group (4.4% vs. 10.5%). This investigation confirms the well-known risk-benefit ratio found in controlled studies in a clinical practice setting. The safety profile is similar and shows the highest incidence of adverse events in the first 12 weeks of treatment.

Schmutz G, Nelson M, Lutz T, Sheldon J, Bruno R, von Boemmel F, Hoffmann C, Rockstroh J, Stoehr A, Wolf E, Soriano V, Berger F, Berg T, Carlebach A, Schwarze-Zander C, Schürmann D, Jaeger H, Mauss S. · Center for HIV and Hepatogastroenterology, Grafenberger Allee 128a, 40237 Duesseldorf, Germany. · AIDS. · Pubmed #16988516 No free full text.

Abstract: OBJECTIVE: At present sequential monotherapy for chronic hepatitis B with hepatitis B virus (HBV)-polymerase inhibitors is clinical practice. It is unknown to date whether combination therapy with lamivudine plus tenofovir could be superior to sequential therapy with tenofovir after the occurrence of lamivudine resistance. METHODS: We conducted a multicenter, 1: 2 matched pair analysis comparing patients with HBV/HIV-coinfection starting an antiretroviral regimen including tenofovir plus lamivudine with patients who had highly replicative, lamivudine resistant HBe-antigen positive chronic hepatitis B and started with tenofovir as the only active HBV polymerase inhibitor subsequent to lamivudine. RESULTS: At baseline patients on tenofovir plus lamivudine (n = 25) had a median HBV DNA of 5.9 x 10(7) copies/ml compared to 1.37 x 10(8) copies/ml in the tenofovir arm (n = 50; P = 0.32). A sustained undetectable HBV DNA < 1000 copies/ml was achieved in 19/25 (76%) patients on tenofovir plus lamivudine and in 42/50 (84%) on tenofovir (P = 0.53). A loss of HBe-antigen was observed in 9/25 (36%) patients on tenofovir plus lamivudine and in 12/50 (24%) patients on tenofovir (P = 0.29). HBs-antigen loss was found in 1/25 (4%) and 3/50 (6%) patients. CONCLUSIONS: In this cohort of HBV/HIV-coinfected individuals, full HBV DNA suppression was achieved in the majority of patients independent of treatment allocation. Loss of HBe- and HBs-antigen was not different between the two study arms. Over a median treatment period of 116 weeks tenofovir was as effective as tenofovir plus lamivudine. Longer treatment periods may be needed to evaluate potential benefits of first-line combination therapy for chronic hepatitis B.

Voigt E, Schulz C, Klausen G, Goelz J, Mauss S, Schmutz G, Jessen H, Weitner L, Mutz A, Schranz D, Rockstroh JK, Kaad Study Group. · University of Bonn, Bonn, Germany. · J Infect. · Pubmed #16269184 No free full text.

Abstract: OBJECTIVES: HIV-coinfection accelerates the course of HCV-related liver disease. Since, highly active anti-retroviral therapy significantly improved survival of HIV-patients more coinfected patients develop end stage liver disease. Therefore, treatment options for chronic hepatitis C in HIV-coinfected patients need to be evaluated. METHODS: Efficacy and safety of pegylated interferon alpha-2b (peg IFN) plus ribavirin (RBV) was examined within this prospective, uncontrolled, multicentre trial. Patients received peg IFN (1.5 microg/kg) once weekly plus RBV 800 mg daily for 48 weeks for HCV genotypes (GT) 1/4 and 24 weeks for GT 2/3. RESULTS: One hundred and twenty-two patients were enrolled. Patients were predominantly male (68%) and former i.v. drug users (61%). Baseline characteristics (median) were as follows: age 39 years (range 23-58), CD4 count 494 cells/microl (range 150-1578/microl), HIV-RNA 2.3log copies/ml (range <1.7-5.4log copies/ml). 61% currently received anti-retroviral treatment. Fifty-six percent had HCV GT 1. EOT response was achieved by 52%. However, only 25% achieved sustained response (SR) due to a high relapse rate. SR rates were significantly higher among patients with GT 2/3 compared to those with GT 1/4 (44 vs. 18%). SR was observed in only one patient without early response (ER). Discontinuation rate was 30%, 21% discontinued due to adverse events. CONCLUSION: Peg IFN/RBV appears safe and effective in HIV/HCV-coinfected patients. GT 2/3 is associated with better SR. Lack of ER strongly predicts non-response. High relapse rates substantially reduce treatment success. In terms of toxicity neuro-psychiatric side effects frequently required treatment discontinuation.

Sheldon J, Camino N, Rodés B, Bartholomeusz A, Kuiper M, Tacke F, Núñez M, Mauss S, Lutz T, Klausen G, Locarnini S, Soriano V. · Hospital Carlos ill, Madrid, Spain. · Antivir Ther. · Pubmed #16218172 No free full text.

Abstract: BACKGROUND: Tenofovir (TDF) is an adenosine nucleotide analogue that has been approved for the treatment of HIV-1 infection. It also shows activity against hepatitis B virus (HBV) in patients with or without lamivudine (LAM)-associated mutations. Development of clinical or virological HBV breakthrough during TDF therapy has not been reported so far. The aim of this study was to analyse the HBV polymerase (pol) from HIV/HBV-coinfected patients with detectable serum levels of HBV DNA during treatment with TDF for longer than 6 months. METHODS: The HBV pol was sequenced from 43 patient's serum before and during TDF therapy. Phenotypic analyses were performed using HBV replication-competent plasmids carrying unique mutations selected under TDF therapy. RESULTS: Mean exposure to LAM was 35.3 +/- 27.5 months and to TDF 11.2 +/- 6.7 months. Genotypic analyses from 21 of the patients revealed LAM-associated mutations, and a further two patients developed a novel mutation, rtA194T, along with LAM-resistance-associated mutations. Phenotypic analyses revealed that constructs harbouring rtA194T combined with rtL180M and rtM204V displayed an over 10-fold increase in the IC50 for TDF compared with the wild type. CONCLUSION: The selection of HBV mutations in HBV/HIV-coinfected patients failing TDF therapy is an unlikely event within the first 12 months of treatment. However, HBV from two of the 43 patients treated with TDF for more than 12 months was found to contain one novel mutation located distal to the catalytic site of the HBV pol. In vitro, rtA194T conferred a reduced susceptibility to TDF in the presence of LAM-associated mutations.

van Bömmel F, Wünsche T, Mauss S, Reinke P, Bergk A, Schürmann D, Wiedenmann B, Berg T. · Medizinische Klinik mit Schwerpunkt Hepatologie und Gastroenterologie, Charité, Universitätsmedizin Berlin, Campus Virchow, Berlin, Germany. · Hepatology. · Pubmed #15565615 No free full text.

Abstract: Adefovir dipivoxil was recently approved for the treatment of wild-type and lamivudine-resistant hepatitis B virus (HBV) infection. Tenofovir disoproxil fumarate, a congender of adefovir that is used in the treatment of HIV infected patients, has recently been shown to also be effective in patients with lamivudine-resistant HBV infection. We therefore compared the two substances in a study of 53 patients defined by high HBV DNA (>6 log10 copies/mL) levels and genotypic evidence of lamivudine resistance. Thirty-five patients received tenofovir for 72 to 130 weeks, and 18 received adefovir for 60 to 80 weeks. Changes in HBV DNA levels were followed for the complete period of 48 weeks. Early viral kinetics were compared on matched subgroups of 5 patients each. Individually, all tenofovir-treated patients showed a strong and early suppression of HBV DNA within a few weeks whether they were coinfected with HIV or were without comorbidity. In contrast, considerable individual variations in HBV DNA decline were observed in the adefovir group. Thus at week 48, only 44% of these patients had HBV DNA levels below 10(5) copies/mL in contrast to 100% of the tenofovir-treated patients (P = .001). No severe side effects were noticed in either group. No evidence of phenotypic viral resistance could be demonstrated in the tenofovir-treated patients in the long term (up to 130 weeks). In conclusion, tenofovir may become an effective alternative for the treatment of patients with lamivudine-resistant HBV infection.

Mauss S, Valenti W, DePamphilis J, Duff F, Cupelli L, Passe S, Solsky J, Torriani FJ, Dieterich D, Larrey D. · Center for HIV and Hepatogastroenterology, Düsseldorf, Germany. · AIDS. · Pubmed #15316334 No free full text.

Abstract: OBJECTIVE: Hepatic decompensation was reported from two recent trials (APRICOT and RIBAVIC) assessing interferon (IFN)-based treatment of hepatitis C virus (HCV) in HIV/HCV-coinfected patients. This paper identifies risk factors associated with hepatic decompensation in APRICOT. METHODS: APRICOT is a randomized, partially-blinded, controlled trial comparing treatment with peg-IFN alpha-2a 180 microg once weekly plus ribavirin/placebo 400 mg twice daily with IFN alpha-2a 3 million units three times weekly plus ribavirin 400 mg twice daily for 48 weeks in a total of 859 patients. Multiple logistic regression analysis was performed comparing the baseline characteristics of those cirrhotic patients who experienced decompensation with those of the other cirrhotic patients enrolled. RESULTS: Fourteen patients, all cirrhotic, experienced hepatic decompensation during the study. The incidence in the cirrhotic subgroup of the study was 10.4% (14/134). Six of the 14 patients died as a result of hepatic decompensation. The risk factors associated with hepatic decompensation were increased bilirubin, decreased haemoglobin, increased alkaline phosphatase or decreased platelets, and treatment with didanosine. Markers of viral replication, histological activity, cellular immune status or HCV-therapy, treatment with ribavirin and pegylated versus non-pegylated IFN were not associated with hepatic decompensation. CONCLUSIONS: The results from APRICOT indicate that the overall risk of hepatic decompensation in HIV/HCV-coinfected patients without cirrhosis receiving IFN-based treatment is low. In contrast, patients with markers of advanced cirrhosis, despite the absence of a history of hepatic decompensation, should be monitored closely during IFN-based therapy, because they are at risk of hepatic decompensation. Treatment with antiretrovirals such as didanosine may increase the risk further.

Mauss S, Berger F, Goelz J, Jacob B, Schmutz G. · Center for HIV and Hepatogastroenterology, Dusseldorf, Germany. · Hepatology. · Pubmed #15239094 No free full text.

Abstract: We examined the feasibility of hepatitis C treatment in patients on opioid maintenance. One hundred patients with chronic hepatitis C, 50 on methadone maintenance, and 50 with no intravenous drug use or opioid maintenance for at least 5 years were prospectively matched for sex, age, hepatitis C virus (HCV) genotype and HCV RNA. The primary end point was undetectable HCV RNA at 24 weeks posttreatment. Treatment with peginterferon alfa-2b (1.5 microg/kg per week) and ribavirin (1000-1200 mg /day) was initiated for 24 weeks (HCV genotype 2, 3) or 48 weeks (HCV genotype 1, 4). Within the first 8 weeks of therapy, discontinuation due to noncompliance or patient request was observed in 22% (11/50) in the methadone group versus 4% (2/50) in the control group (P =.02). After 8 weeks, there was no significant difference in discontinuation due to noncompliance or patient request (4/39 [10%] vs. 4/48 [8%]). There was no difference in discontinuation of therapy because of viral failure or adverse events (10/50 methadone vs. 6/50 control, P =.41). At the end of treatment, 50% (25/50) in the methadone group and 76% (38/50) in the control group had undetectable HCV RNA (P =.01). Sustained viral response was 42% (21/50) in the methadone group and 56% (28/50) in the control group (P =.16). No serious psychiatric event occurred in either group. In conclusion, peginterferon and ribavirin seem reasonably safe and sufficiently effective in patients on methadone maintenance. Patients discontinuing therapy due to noncompliance or request did so early, thereby limiting the cost of an unsuccessful approach to treatment.

Körner C, Krämer B, Schulte D, Coenen M, Mauss S, Fätkenheuer G, Oldenburg J, Nattermann J, Rockstroh JK, Spengler U. · Department of Internal Medicine I, University of Bonn, Germany, Sigmund-Freud-Str. 25, Bonn 53127, Germany. · Clin Sci (Lond). · Pubmed #19128241 No free full text.

Abstract: Apoptosis importantly contributes to loss of CD4+ T-cells in HIV infection, and modification of their apoptosis may explain why HIV/HCV (hepatitis C virus)-co-infected patients are more likely to die from liver-related causes, although the effects of HCV on HIV infection remain unclear. In the present study, we studied in a cross-sectional and serial analysis spontaneous ex vivo CD4+ T-cell apoptosis in HIV/HCV-co-infected and HIV-mono-infected patients before and after HAART (highly active antiretroviral therapy). Apoptosis of peripheral blood CD4+ T-cells was measured by both a PARP [poly(ADP-ribose) polymerase] and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling) assay to detect cells with irreversible apoptosis. Although hepatitis C alone did not increase CD4+ T-cell apoptosis, HCV co-infection disproportionately increased elevated rates of apoptosis in CD4+ T-cells from untreated HIV-positive patients. Increased CD4+ T-cell apoptosis was closely correlated with HIV, but not HCV, viral loads. Under HAART, increased rates of CD4+ T-cell apoptosis rapidly decreased both in HIV-mono-infected and HIV/HCV-co-infected patients, without any significant difference in apoptosis rates between the two patient groups after 4 weeks of therapy. Nevertheless residual CD4+ T-cell apoptosis did not reach the normal levels seen in healthy controls and remained higher in HIV patients receiving protease inhibitors than in patients with other antiretroviral regimens. The results of the present study suggest that HCV co-infection sensitizes CD4+ T-cells towards apoptosis in untreated HIV-positive patients. However, this effect is rapidly lost under effective antiretroviral therapy.

Mauss S. · Zentrum für HIV und Hepatogastroenterologie, Düsseldorf. · MMW Fortschr Med. · Pubmed #19031564 No free full text.

This publication has no abstract.

Hüppe D, Zehnter E, Mauss S, Böker K, Lutz T, Racky S, Schmidt W, Ullrich J, Sbrijer I, Heyne R, Schober A, John C, Hey KH, Bokemeyer B, Kallinowski B, Möller B, Pape S, Gutmann M, Alshuth U, Niederau C. · Gastroenterologische Gemeinschaftspraxis Herne, Herne. · Z Gastroenterol. · Pubmed #18188814 No free full text.

Abstract: Little is known about the epidemiology of chronic hepatitis C (CHC) in Germany and especially about the importance of transmission, duration of infection, genotypes, symptoms and quality of life of the patients. The current study prospectively evaluates epidemiological and clinical data of patients infected with the hepatitis C virus (HCV). Using online data entry, various characteristics of 10,326 untreated patients with CHC were documented from March 2003 until May 2006 in 352 centres all over Germany. Mean age of patients was 43.4 years. Patients infected by i.v. drug abuse were considerably younger (36.5 years) than the remaining patients (49.2 years). As indicated by their native language, 64.4% of the patients came from Germany and 19.2% from Russia. 61.7% were infected with genotype 1 and 34.9% with genotype 2 or 3. 45.5% of the patients had been infected by i.v. drug abuse. In at least 5.4% of the patients liver cirrhosis had been proved by biopsy. 63.5% of the patients felt an impairment of quality of life caused by CHC. In many patients infected with hepatitis C socio-economic issues are existent. This is reflected, i.e., in very high rates of unemployment in special subpopulations. Coinfections with hepatitis B and HIV occurred in 1.5% and 4.7%, respectively. Nearly 80% of patients were managed near their homes. The data of the 10 326 patients represent about 2% of all German patients with CHC. This database is up to now the largest of its kind and gives a representative insight into the epidemiological situation of CHC in Germany.

Sheldon JA, Corral A, Rodés B, Mauss S, Rockstroh J, Berger F, Schwarze-Zander C, Soriano V. · Department of Infectious Diseases, Hospital Carlos III, Madrid, Spain. · AIDS. · Pubmed #16260913 No free full text.

Abstract: Seven antiretroviral-naive HIV-infected individuals with chronic hepatitis B treated with adefovir for longer than 6 months were assessed. Using bulk population sequencing and a sensitive limiting dilution analysis, the selection of K65R or other resistance mutations did not occur in HIV, suggesting that adefovir can be confidently used as hepatitis B virus (HBV) therapy in HIV/HBV-co-infected patients who do not require antiretroviral therapy.

Bäuerle J, Laguno M, Mauss S, Mallolas J, Murillas J, Miquel R, Schmutz G, Setzer B, Gatell JM, Walker UA. · Department of Clinical Immunology, Medizinische Universitätsklinik, Freiburg, Germany. · HIV Med. · Pubmed #15807720 No free full text.

Abstract: OBJECTIVES: It has been suggested that chronic hepatitis C virus (HCV) infection depletes mitochondrial DNA (mtDNA) in the liver. Because decreased mtDNA levels were also found in humans infected with HIV, we investigated whether HIV may have aggravated hepatic mtDNA depletion in individuals with HCV infection. METHODS: In this cross-sectional study, liver biopsies were performed in a total of 40 individuals prior to any antiviral therapy. The individuals were recruited from the Hospital Clinic, Barcelona and the HIV Centre, Dusseldorf. Seventeen patients were negative for HIV and HCV and were biopsied for liver enzyme elevation of unknown cause (controls), 14 individuals had chronic HCV but no HIV infection, and nine subjects were coinfected with both viruses. mtDNA and liver histology were centrally assessed. RESULTS: The groups did not differ with respect to age, gender, liver function tests and HCV viral load, where applicable. mtDNA levels were decreased by 19% in the HCV-monoinfected group (P=0.03) and by 27% in the HIV/HCV-coinfected subjects (P=0.02) compared to controls. The mtDNA content, however, did not differ between individuals with HCV monoinfection and HCV/HIV coinfection (P=0.75). The degrees of liver fibrosis, inflammatory activity or steatosis did not correlate with mtDNA content. CONCLUSIONS: Liver mtDNA content is reduced in both HCV-monoinfected and HIV/HCV-coinfected patients. Under the limitations of our study, we could demonstrate only a slight trend towards more pronounced mtDNA depletion in HIV/HCV-coinfected subjects.

Mauss S. · Zentrum für HIV und Hepatogastroenterologie, Düsseldorf. · MMW Fortschr Med. · Pubmed #15373041 No free full text.

Abstract: HIV patients co-infected with hepatitis B can be successfully treated with lamivudine, adefovir and tenofovir. However, in a variable portion of patients resistance against these agents may occur. The application of pegylated interferon alfa in combination with ribavirin represents an advance in the treatment of hepatitis C and HIV co-infected patients. In patients with markers of advanced liver cirrhosis a substantial risk for the development of hepatic decompensation under interferon-based therapy was observed. Antiretroviral therapy with didanosine may further enhance this risk.

Mauss S. · Zentrum Für HIV und Hepatogastroenterologie, Düsseldorf. · MMW Fortschr Med. · Pubmed #15011579 No free full text.

Abstract: In patients with HIV coinfection, chronic hepatitis B was initially treated with interferon alpha, but the long-term results were disappointing. Currently, pegylated interferon is being investigated in an ongoing study. The nucleoside analogues lamivudine and adefovir may well become established as alternatives to interferon alpha. Treatment of hepatitis C in HIV coinfection with interferon alpha plus ribavirin also proved less efficacious compared to HCV-monoinfection. Initial preliminary results of studies on pegylated interferon alpha indicate an advantage over conventional interferon. Under treatment for hepatitis metabolic acidosis and hepatic decompensation may occur--in particular with didanosine and/or stavudine--and these substances may therefore be avoided as antiretroviral therapy in dual infection with hepatitis and HIV.