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Version 8 er udarbejdet af en arbejdsgruppe nedsat af Dansk Selskab for Infektionsmedicin samt Dansk Selskab for Gastroenterologi og Hepatologi
Medlemmer: Nina Weis (formand), Mette Rye Clausen, Peer Brehm Christensen, Henrik Krarup, Alex Lund Laursen, Lone Galmstrup Madsen
Forfattere: Jan Gerstoft, Nina Weis, Terese L. Katzenstein (Dansk Selskab for Infektionsmedicin), Anders Nyboe Andersen og Jens Fedder (Dansk Fertilitetsselskab).
Anbefaling for profylakse og opfølgning af stikuheld og anden blodeksposition.
Revideret februar 2016. Arbejdsgruppen bestod af
Suzanne Lunding (formand), Peer Brehm Christensen, Christian Erikstrup, Terese L. Katzenstein, Henrik Krarup, Alex Lund Laursen, Birgitte Mørn og Nina Weis
Sundhedsstyrelsen har udarbejdet en fælles vejledning for forebyggelse af blodbåren smitte, diagnostik og håndtering af personer der har HIV eller hepatitis B og C. Vejledningen afspejler, at behandlingsmulighederne for disse sygdomme er væsentligt forbedrede.
EASL Clinical Practice Guidelines
Medicin.dk om behandling af hepatitis B
Medicin.dk om behandling af hepatitis C
Medicinrådets lægemiddelrekommandation for behandling af kronisk hepatitis C infektion
Dansk standard for rapportering af kronisk hepatitis B og C
Klik her for flere resultater
Dore G, Cowie B.
Nayagam S, Chan P, Zhao K, et al.
AbstractBackgroundIn 2016, the first global viral hepatitis elimination targets were endorsed. An estimated one-third of the world’s population of individuals with chronic hepatitis B virus (HBV) infection live in China and liver cancer is the sixth leading cause of mortality, but coverage of first-line antiviral treatment was low. In 2015, China was one of the first countries to initiate a consultative process for a renewed approach to viral hepatitis. We present the investment case for the scale-up of a comprehensive package of HBV interventions.MethodsA dynamic simulation model of HBV was developed and used to simulate the Chinese HBV epidemic. We evaluated the impact, costs, and return on investment of a comprehensive package of prevention and treatment interventions from a societal perspective, incorporating costs of management of end-stage liver disease and lost productivity costs.ResultsDespite the successes of historical vaccination scale-up since 1992, there will be a projected 60 million people still living with HBV in 2030 and 10 million HBV-related deaths, including 5.7 million HBV-related cancer deaths between 2015 and 2030. This could be reduced by 2.1 million by highly active case-finding and optimal antiviral treatment regimens. The package of interventions is likely to have a positive return on investment to society of US$1.57 per US dollar invested.ConclusionsIncreases in HBV-related deaths for the next few decades pose a major public health threat in China. Active case-finding and access to optimal antiviral treatment are required to mitigate this risk. This investment case approach provides a real-world example of how applied modeling can support national dialog and inform policy planning.
Fan R, Peng J, Xie Q, et al.
AbstractBackgroundSafe nucleos(t)ide analogue discontinuation in chronic hepatitis B (CHB) is an unmet need. We aimed to investigate whether combining HBV RNA and hepatitis B core-related antigen (HBcrAg) could perform satisfactorily in predicting off-treatment outcomes.MethodsThe evaluation cohort included 127 HBeAg-positive patients from a multi-centre prospective trial who stopped telbivudine-based therapy after achieving HBeAg seroconversion and HBV DNA48 weeks. As validation, 59 patients treated with entecavir or tenofovir before discontinuation were analysed.ResultsAt the end of treatment (EOT), HBV RNA and HBcrAg were significant independent predictors of the clinical relapse risk. In the evaluation cohort, no clinical relapse occurred among patients with negative HBV RNA and HBcrAg
Juan Yin, Peifeng Liang, Gang Chen, Fuzhen Wang, Fuqiang Cui, Xiaofeng Liang, Guihua Zhuang
Journal of Medical Virology, Accepted Article.
Hepatitis B virus disease is a potentially life-threatening liver infection and a major global health problem. It causes chronic infection and puts people at high risk of death from cirrhosis and liver cancer. WHO estimated 257 million people are living with hepatitis B virus (HBV) infection and in 2015 alone HBV resulted in to 887,000 deaths globally. We determined the prevalence and associated factors of hepatitis B virus infection among Antenatal Care (ANC) attendees in Gamawa Local Government Area, Bauchi State.
We conducted a descriptive cross-sectional, health facility-based study between March and April 2018. We used systematic random sampling technique to recruit 210 pregnant women aged 15–49 years. With a structured questionnaire, we interviewed the respondents and collected blood sample to test for hepatitis B surface antigen. We calculated frequencies, means, proportions, and tested for associations using Epi Info 7.2 and Microsoft Excel.
The mean age of respondents was 24.5 ± 6.0 years; 112 (53%) of whom were younger than 25 years. All were married, 183 (87%) had no formal education and up to 190 (90%) were employed. Overall, 14 (6.7%) tested positive for HBsAg; women aged ≥35 years had the highest prevalence (10%). None with tertiary education tested positive and women married before 18 years had 13 (6.2%) prevalence.
The prevalence of HBsAg among pregnant women in Gamawa LGA was 6.7% which is quite lower than the national prevalence reported. We recommended improved surveillance of HBV infection and screening of women attending ANC.
Wonderful T. Choga,
Jason T. Blackard
Journal of Medical Virology, Volume 0, Issue ja, -Not available-.
Worldwide, there is limited epidemiologic evidence on the seroprevalence of undiagnosed chronic viral infections including HIV, hepatitis B virus (HBV) and hepatitis C virus (HCV) infections among patients with severe psychiatric disorders. To our knowledge, this is the first study to explore and compare undiagnosed seroprevalence rates of HIV, HBV, and HCV infections among patients with severe psychiatric disorders.
In this study, we included a random sample of 309 patients with severe psychiatric disorders selected by systematic sampling technique. We used a structured clinical interview for DSM-IV (SCID) to confirm the diagnosis of severe psychiatric disorders among the participants. Binary and multivariable logistic regression models, adjusting for the potential confounding factors was used to explore the potential determinants of chronic viral infections.
The prevalence estimates of HIV infection among patients with severe psychiatric disorders in this study (3.24%) was roughly 3 times the estimated population prevalence of HIV infection in Ethiopia (1.1%). This study showed that the prevalence rates of HBV and HCV infections among patients with severe psychiatric disorders were 4.85 and 1.29%, respectively. Our results also showed that among patients with chronic viral infections, HIV, HBV and HCV, 76.92, 60, 80, and 75% respectively were undiagnosed. Regarding associated factors, the presence of chronic viral infection was found to be significantly associated with the age of the participants (ranging between 30 and 40 years) after adjusting for the possible confounding factors [AOR = 3.95 (95%CI.18–13.17)].
Even though the prevalence estimates of HIV (3.24%), HBV (4.85%), and HCV (1.29%) infections were high among patients with severe psychiatric disorders, the majority of them remained undiagnosed. HBV was found to be the commonly undiagnosed infection (4 out of 5) followed by HCV (3 out of 4) and HIV (6 out of 10). The present study provided evidence of a significant association between the age of the participant (between 30 and 40 years) and chronic viral infections in patients with severe psychiatric disorders. Increasing the awareness of psychiatry professionals and early screening, as well as interventions of chronic viral infections among patients with severe psychiatric disorders are imperative.
Nguyen, M. H., Wong, G., Gane, E., Kao, J.-H., Dusheiko, G.
Currently, despite the use of a preventive vaccine for several decades as well as the use of effective and well-tolerated viral suppressive medications since 1998, approximately 250 million people remain infected with the virus that causes hepatitis B worldwide. Hepatitis C virus (HCV) and hepatitis B virus (HBV) are the leading causes of liver cancer and overall mortality globally, surpassing malaria and tuberculosis. Linkage to care is estimated to be very poor both in developing countries and in high-income countries, such as the United States, countries in Western Europe, and Japan. In the United States, by CDC estimates, only one-third of HBV-infected patients or less are aware of their infection. Some reasons for these low rates of surveillance, diagnosis, and treatment include the asymptomatic nature of chronic hepatitis B until the very late stages, a lack of curative therapy with a finite treatment duration, a complex natural history, and a lack of knowledge about the disease by both care providers and patients. In the last 5 years, more attention has been focused on the important topics of HBV screening, diagnosis of HBV infection, and appropriate linkage to care. There have also been rapid clinical developments toward a functional cure of HBV infection, with novel compounds currently being in various phases of progress. Despite this knowledge, many of the professional organizations provide guidelines focused only on specific questions related to the treatment of HBV infection. This focus leaves a gap for care providers on the other HBV-related issues, which include HBV’s epidemiological profile, its natural history, how it interacts with other viral hepatitis diseases, treatments, and the areas that still need to be addressed in order to achieve HBV elimination by 2030. Thus, to fill these gaps and provide a more comprehensive and relevant document to regions worldwide, we have taken a global approach by using the findings of global experts on HBV as well as citing major guidelines and their various approaches to addressing HBV and its disease burden.
Berke, J. M., Dehertogh, P., Vergauwen, K., Mostmans, W., Vandyck, K., Raboisson, P., Pauwels, F.
Capsid assembly is a critical step in the hepatitis B virus (HBV) life cycle, mediated by the core protein. Core is a potential target for new antiviral therapies, the capsid assembly modulators (CAMs). JNJ-56136379 (JNJ-6379) is a novel and potent CAM currently in phase II trials. We evaluated the mechanism of action (MOA) and antiviral properties of JNJ-6379 in vitro. Size exclusion chromatography and electron microscopy studies demonstrated that JNJ-6379 induced formation of morphologically intact viral capsids devoid of genomic material (‘primary' MOA). JNJ-6379 accelerated the rate and extent of HBV capsid assembly in vitro. JNJ-6379 specifically and potently inhibited HBV replication; median 50% effective concentration (EC50) 54 nM (HepG2.117 cells). In HBV-infected primary human hepatocytes (PHHs), JNJ-6379, when added with the viral inoculum, dose-dependently reduced extracellular HBV DNA levels (median EC50 93 nM) and prevented covalently closed circular DNA (cccDNA) formation, leading to a dose-dependent reduction of intracellular HBV RNA levels (median EC50 876 nM) and reduced antigen levels (‘secondary' MOA). Adding JNJ-6379 to PHHs 4/5 days post infection reduced extracellular HBV DNA and did not prevent cccDNA formation. Time-of-addition PHH studies revealed that JNJ-6379 most likely interfered with post-entry processes. Collectively, these data demonstrate that JNJ-6379 has a dual MOA on the early and late steps of the HBV life cycle, which is different to the MOA of nucleos(t)ide analogues. JNJ-6379 is in development for chronic hepatitis B treatment, and may translate into higher HBV functional cure rates.
Lisa Hefele, Souphaphone Vannachone, Vilaysone Khounvisith, Nouanthong Phonethipsavanh, Somphou Sayasone, Sengchang Kounnavong, Phetsavanh Chantavilay, Claude P. Muller, Antony P. Black
Maravelia P, Frelin L, Ni Y, et al.
AbstractBackgroundChronic hepatitis B and D virus (HBV/HDV) infections can cause cancer. Current HBV therapy using nucleoside analogues (NAs) is life-long and reduces but does not eliminate the risk of cancer. A hallmark of chronic hepatitis B is a dysfunctional HBV-specific T cell response. We therefore designed an immunotherapy driven by naïve healthy T cells specific for the HDV antigen (HDAg) to bypass the need for HBV-specific T cells in order to prime PreS1-specific T cells and PreS1 antibodies blocking HBV entry.MethodsTen combinations of PreS1 and/or HDAg sequences were evaluated for induction of PreS1 antibodies and HBV- and HDV- specific T cells in vitro and in vivo. Neutralization of HBV by PreS1-specific murine and rabbit antibodies was evaluated in cell culture, and rabbit anti-PreS1 were tested for neutralization of HBV in mice repopulated with human hepatocytes.ResultsThe best vaccine candidate induced T cells to PreS1 and HDAg, and PreS1 antibodies blocking HBV entry in vitro. Importantly, adoptive transfer of PreS1 antibodies prevented, or modulated, HBV infection after a subsequent challenge in humanized mice.ConclusionWe here describe a novel immunotherapy for chronic HBV/HDV that targets viral entry to complement NAs and coming therapies inhibiting viral maturation.
Hepatitis B virus (HBV) infection is a global health problem and interferon-alpha (IFN-α) is one of the effective therapies. However, little is known about the genetic background of the HBV infection or the genetic determinants of the IFN-α treatment response. Thus, we aim to explore the possible molecular mechanisms of HBV infection and its response to the IFN-α therapy with a comprehensive bioinformatics analysis.
The Gene Expression Omnibus datasets (GSE83148, GSE84044 and GSE66698) were collected and the differentially expressed genes (DEGs), key biological processes and intersecting pathways were analyzed. The expression of the co-expressed DEGs in the clinical samples was verified by quantitative real time polymerase chain reaction (qRT-PCR).
Analysis of all the 3 datasets revealed that there were eight up-regulated and one down-regulated co-expressed DEGs following the HBV infection and after IFN-α treatment. In clinical samples, the mRNA level of HKDC1, EPCAM, GSN, ZWINT and PLD3 were significantly increased, while, the mRNA level of PLEKHA2 was significantly decreased in HBV infected liver tissues compared to normal liver tissues. PI3K-Akt signaling pathway, focal adhesion, HTLV-I infection, cytokine-cytokine receptor interaction, metabolic pathways, NF-κB signaling pathway were important pathways associated with the HBV infection and the response of IFN-α treatment.
The co-expressed genes, common biological processes and intersecting pathways identified in the study might play an important role in HBV infection and response of IFN-α treatment. The dysregulated genes may act as novel biomarkers and therapeutic targets for HBV.
Marijn Thijssen, Nídia Sequeira Trovão, Thomas Mina, Piet Maes, Mahmoud Reza Pourkarim
Yu-Liang Zhao, Lu-Lu Pan, Zhi-Yong Hao, Fei Jin, Yan-Hong Zhang, Min-Jie Li, Xin-Jiang Zhang, Bi-Hua Han, Hai-Song Zhou, Tian-Li Ma, Feng Wang, Jing-Chen Ma, Li-Peng Shen, Qi Li
Adeel A. Butt, Peng Yan, Samia Aslam, Kenneth E. Sherman, Dawd Siraj, Nasia Safdar, Bilal Hameed
Dezanet L, Maylin S, Gabassi A, et al.
AbstractBackgroundTo describe the kinetics of hepatitis B core-related antigen (qHBcrAg) and anti-hepatitis B core antibody (qAnti-HBc) during tenofovir (TDF)-treatment and assess their ability to predict HBeAg-seroclearance in patients co-infected with HIV and hepatitis B virus (HBV).MethodsSerum qHBcrAg, qAnti-HBc and HBV-DNA were obtained at TDF-initiation and every 6-12 months. On-treatment kinetics of qHBcrAg (ΔqHBcrAg) and qAnti-HBc (ΔqAnti-HBc) were estimated using mixed-effect linear regression. Hazard ratios (HR) assessing the association between markers and HBeAg-seroclearance were calculated using proportional hazards regression and sensitivity (Se) and specificity (Sp) of marker levels in predicting HBeAg-seroclearance were assessed using time-dependent ROC curves.ResultsDuring a median 4.6 years, cumulative incidence of HBsAg-seroclearance and HBeAg-seroclearance were 3.2% (n=5/158) and 27.4% (n=26/95), respectively. ΔqHBcrAg was biphasic in HBeAg-positive (-0.051 and -0.011 log10U/mL/month during 18 months, respectively) and monophasic in HBeAg-negative patients. ΔqAnti-HBc was monophasic regardless of HBeAg-status. In HBeAg-positive patients, baseline qHBcrAg and qAnti-HBc levels were associated with HBeAg-seroclearance (adjusted-HR=0.48/log10U/mL; 95%CI=0.33-0.70 and unadjusted-HR=1.49/log10PEIU/mL; 95%CI=1.08-2.07, respectively). Cutoffs with the highest accuracy in predicting HBeAg-seroclearance at 36 months were qHBcrAg4.1 log10PEIU/mL (Se=0.42/Sp=0.81).ConclusionsIn co-infected patients undergoing TDF, qHBcrAg/qAnti-HBc could be of use in monitoring HBeAg-seroclearance.
A major hurdle in the long-term treatment of chronic hepatitis B (CHB) patients is to maintain viral suppression in the absence of drug resistance. To date, no evidence of resistance to tenofovir disoproxil fumarate (TDF) has been observed. A cumulative evaluation of CHB patients who qualified for resistance surveillance over 8 years of TDF treatment was conducted. Patients in studies GS-US-174-0102 (HBeAg-) and GS-US-174-0103 (HBeAg+) were randomized 2:1 to receive TDF or adefovir dipivoxil (ADV) for 48 weeks followed by open-label TDF through year 8. Population sequencing of HBV pol/RT was attempted for all TDF-treated patients at baseline and, annually if viremic, at discontinuation, or with addition of emtricitabine. Overall, 88/641 (13.7%) patients qualified for sequence analysis at one or more time points. The percentage of patients qualifying for sequence analysis declined over time, from 9 to 11% in years 1-2 to <4% over years 3-8. Forty-one episodes of virologic breakthrough (VB) occurred throughout the study, with most (n=29, 70%) associated with nonadherence to study medication. Fifty-nine per cent of VB patients with an opportunity to resuppress HBV achieved HBV DNA resuppression. A minority of patients who qualified for sequencing had polymorphic (41/165, 24.8%) or conserved (17/165, 10.3%) site changes in pol/RT, with six patients developing lamivudine and/or ADV resistance-associated mutations. No accumulation of conserved site changes was detected. The long-term treatment of CHB with TDF monotherapy maintains effective suppression of HBV DNA through 8 years, with no evidence of TDF resistance or accumulation of conserved site changes.
In phase 2 trials, treatment with the combination of the nucleotide polymerase inhibitor sofosbuvir and the NS5A inhibitor velpatasvir resulted in high rates of sustained virologic response in patients chronically infected with hepatitis C virus (HCV) genotype 2 or 3.
A simple treatment regimen that is effective in a broad range of patients who are chronically infected with the hepatitis C virus (HCV) remains an unmet medical need.
Chronic hepatitis C virus (HCV) infection is associated with several extrahepatic manifestations. Patients with HCV may develop mixed cryoglobulinemia and its sequelae, ranging from cutaneous and visceral vasculitis to glomerulonephritis and B-cell non-Hodgkin lymphoma. HCV-infected patients have increased rates of insulin resistance, diabetes, and atherosclerosis, which may lead to increased cardiovascular morbidity and mortality. Neurological manifestations of HCV infection include fatigue and cognitive impairment. The mechanisms causing the extrahepatic effects of HCV infection are likely multifactorial and may include endocrine effects, HCV replication in extrahepatic cells, or a heightened immune reaction with systemic effects. Successful eradication of HCV with interferon alfa and ribavirin was shown to improve some of these extrahepatic effects; sustained virological response is associated with resolution of complications of cryoglobulinemia, reduced levels of insulin resistance, reduced incidence of diabetes and stroke, and improved fatigue and cognitive functioning. The availability of new interferon-free, well-tolerated anti-HCV treatment regimens is broadening the spectrum of patients available for therapy, including those in whom interferon was contraindicated, and will likely result in greater improvements in the extrahepatic manifestations of HCV. If these regimens are shown to confer significant benefit in the metabolic, cardiovascular, or neuropsychiatric conditions associated with HCV infection, extrahepatic manifestations of HCV may become a major indication for treatment even in the absence of liver disease.
Worldwide, although predominantly in low-income countries in the Middle East and Africa, up to 13% of hepatitis C virus (HCV) infections are caused by HCV genotype 4. For patients with HCV genotype 1, the combination of ledipasvir and sofosbuvir has been shown to cure high proportions of patients with excellent tolerability, but this regimen has not been assessed for the treatment of HCV genotype 4. We assessed the efficacy, safety, and tolerability of 12 weeks of combination therapy with ledipasvir and sofosbuvir for patients with chronic HCV genotype 4 infections.
Novel interferon- and ribavirin-free regimens are needed to treat hepatitis C virus (HCV) infection.
The Phase-2 C-SALVAGE study evaluated an investigational interferon-free combination of grazoprevir (a NS3/4A protease inhibitor) and elbasvir (a NS5A inhibitor) with ribavirin for patients with chronic HCV genotype-1 infection who had failed licensed DAA-containing therapy.
Hepatitis C virus (HCV) genotype 4 accounts for about 13% of global HCV infections. Because interferon-containing treatments for genotype 4 infection have low efficacy and poor tolerability, an unmet need exists for effective all-oral regimens. We examined the efficacy and safety of an all-oral interferon-free regimen of ombitasvir, an NS5A inhibitor, and paritaprevir (ABT-450), an NS3/4A protease inhibitor dosed with ritonavir (ombitasvir plus paritaprevir plus ritonavir), given with or without ribavirin.
Patients with cirrhosis resulting from chronic hepatitis C virus (HCV) infection are at risk of life-threatening complications, but consistently achieve lower sustained virological response (SVR) than patients without cirrhosis, especially if treatment has previously failed. We assessed the efficacy and safety of the NS5A inhibitor ledipasvir and the nucleotide polymerase inhibitor sofosbuvir, with and without ribavirin.
Interferon-free regimens are needed to treat hepatitis C virus (HCV) infections. We investigated the efficacy of combined simeprevir and sofosbuvir.
Effective treatment for hepatitis C virus (HCV) genotype 1 infection in patients who have not had a sustained virologic response to prior interferon-based therapy represents an unmet medical need.
In this phase 3 trial we evaluated the efficacy and safety of the interferon-free combination of ABT-450 with ritonavir (ABT-450/r), ombitasvir (also known as ABT-267), dasabuvir (also known as ABT-333), and ribavirin for the retreatment of HCV in patients who were previously treated with peginterferon-ribavirin.
No data are available about the prediction of long-term survival using repeated noninvasive tests of liver fibrosis in chronic hepatitis C (CHC). We aimed to assess the prognostic value of 3-year liver stiffness measurement (LSM), aspartate aminotransferase to platelet ratio index (APRI), and fibrosis 4 (FIB-4) evolution in CHC. CHC patients with two LSM (1,000-1,500 days interval) were prospectively included. Blood fibrosis tests APRI and FIB-4 were calculated the day of baseline (bLSM) and follow-up (fLSM) LSM. Evolution of fibrosis tests was expressed as delta: (follow-up-baseline results)/duration. Date and cause of death were recorded during follow-up that started the day of fLSM. In all, 1,025 patients were included. Median follow-up after fLSM was 38.0 months (interquartile range [IQR]: 27.7-46.1) during which 35 patients died (14 liver-related death) and seven had liver transplantation. Prognostic accuracy (Harrell C-index) of multivariate models including baseline and delta results was not significantly different between LSM and FIB-4 (P ≥ 0.24), whereas FIB-4 provided more accurate prognostic models than APRI (P = 0.03). By multivariate analysis including LSM variables, overall survival was independently predicted by bLSM, delta (dLSM), and sustained virological response (SVR). Prognosis was excellent in patients having bLSM <7 kPa, SVR, or no increase (<1 kPa/year) in 7-14 kPa bLSM. Prognosis was significantly impaired in patients with an increase (≥ 1 kPa/year) in 7-14 kPa bLSM, or decrease (≤ 0 kPa/year) in ≥ 14 kPa bLSM (P = 0.949 between these two groups). Patients with an increase (>0 kPa/year) in ≥ 14 kPa bLSM had the worst prognosis. Baseline and delta FIB-4 also identified patient subgroups with significantly different prognosis.
All-oral combination therapy is desirable for patients with chronic hepatitis C virus (HCV) infection. We evaluated daclatasvir (an HCV NS5A replication complex inhibitor) plus sofosbuvir (a nucleotide analogue HCV NS5B polymerase inhibitor) in patients infected with HCV genotype 1, 2, or 3.
Early treatment of acute hepatitis C virus (HCV) infection with interferon alfa monotherapy is very effective, with cure rates of greater than 85%. However, spontaneous clearance of HCV occurs in 10-50% of cases. We aimed to assess an alternative treatment strategy of delayed antiviral therapy in patients who do not eliminate the virus spontaneously compared with immediate treatment.
Earlier studies have suggested neurocognitive impairment in patients with chronic hepatitis C virus (HCV) infection even before liver cirrhosis has developed. Since these deficits might be reversible after successful antiviral therapy, we analyzed the long-term course of neurocognitive parameters in HCV patients with and without successful virus elimination by an interferon-based antiviral treatment. In a multicenter study including 168 HCV patients receiving antiviral therapy (peginterferon alpha-2b and ribavirin) we performed a long-term follow-up of neurocognitive performance before and after treatment. Neurocognitive function was psychometrically assessed using the computer-aided TAP (Test Battery of Attentional Performance). When tested at least 12 months after termination of antiviral treatment, patients with sustained virologic response (SVR) had improved significantly as compared to their pretreatment performance in three of five TAP subtasks (vigilance, P < 0.001; shared attention: optical task, P < 0.001; working memory, P < 0.001). Patients who failed to eradicate the virus, however, showed no significant long-term changes in neurocognitive performance in all five subtasks assessed (0.194 < P < 0.804). In the posttreatment evaluation, neurocognitive function was significantly better in responders to the antiviral therapy as compared to nonresponders.
A national survey for chronic hepatitis C has not been performed in Denmark and the prevalence is unknown. Our aim was to estimate the prevalence of chronic hepatitis C from public registers and the proportion of these patients who received specialized healthcare.
Since 2000 outbreaks of acute hepatitis C virus (HCV) among HIV-positive men who have sex with men (MSM) who denied injecting drug use have been reported from Europe, the United States, Canada and Australia. Given the burden of liver disease, in particular HCV, on the morbidity and mortality in HIV patients in the era of combination antiretroviral therapy, the rapid and significant rise in the incidence of HCV in the HIV-infected MSM population in high-income countries is alarming. This relates to a significant change in the epidemiology of HCV that has occurred, with HCV emerging as a sexually transmitted infection within this population. Work to date suggests that this permucosal HCV transmission results from high-risk sexual and noninjecting drug use behaviours, reopening the discussion on the importance of sexual transmission. Given this occurs almost exclusively in HIV-infected MSM, HIV probably has a critical role mediated either through behavioural and/or biological factors. Finally, the management of acute HCV in HIV infection is complicated by concomitant HIV infection and combination antiretroviral therapy. This review will synthesize the most recent epidemiological, immunological and management issues that have emerged as a result of the epidemic of acute HCV among HIV-infected MSM.
Tenofovir disoproxil fumarate (DF) is a nucleotide analogue and a potent inhibitor of human immunodeficiency virus type 1 reverse transcriptase and hepatitis B virus (HBV) polymerase.
The diagnosis and treatment of hepatocellular carcinoma (HCC) have witnessed major changes over the past decade. Until the early 1990s, HCC was a relatively rare malignancy, typically diagnosed at an advanced stage in a symptomatic patient, and there were no known effective palliative or therapeutic options. However, the rising incidence of HCC in several regions around the world coupled with emerging evidence for efficacy of screening in high-risk patients, liver transplantation as a curative option in select patients, ability to make definitive diagnosis using high-resolution imaging of the liver, less dependency on obtaining tissue diagnosis, and proven efficacy of transarterial chemoembolization and sorafenib as palliative therapy have improved the outlook for HCC patients. In this article, we present a summary of the most recent information on screening, diagnosis, staging, and different treatment modalities of HCC, as well as our recommended management approach.
Entecavir, a drug approved by the Food and Drug Administration for the treatment of chronic hepatitis B virus (HBV) infection, is not believed to inhibit replication of human immunodeficiency virus type 1 (HIV-1) at clinically relevant doses. We observed that entecavir led to a consistent 1-log(10) decrease in HIV-1 RNA in three persons with HIV-1 and HBV coinfection, and we obtained supportive in vitro evidence that entecavir is a potent partial inhibitor of HIV-1 replication. Detailed analysis showed that in one of these patients, entecavir monotherapy led to an accumulation of HIV-1 variants with the lamivudine-resistant mutation, M184V. In vitro experiments showed that M184V confers resistance to entecavir. Until more is known about HIV-1-resistance patterns and their selection by entecavir, caution is needed with the use of entecavir in persons with HIV-1 and HBV coinfection who are not receiving fully suppressive antiretroviral regimens.
Entecavir is a potent and selective guanosine analogue with significant activity against hepatitis B virus (HBV).
The natural history of hepatitis C virus (HCV) infection in human immunodeficiency virus (HIV)-infected patients has never been studied according to the concept of liver fibrosis progression. The aim of this work was to assess the fibrosis progression rate in HIV-HCV coinfected patients and in patients infected by HCV only. A cohort of 122 HIV-HCV coinfected patients was compared with a control group of 122 HIV-negative HCV-infected patients. Groups were matched according to age, sex, daily alcohol consumption, age at HCV infection, and duration and route of HCV infection. The fibrosis progression rate was defined as the ratio between fibrosis stage (METAVIR scoring system) and the HCV duration. The prevalence of extensive liver fibrosis (METAVIR fibrosis scores 2, 3, and 4) and moderate or severe activity were higher in HIV-infected patients (60% and 54%, respectively) than in control patients (47% and 30%, respectively; P <.05 and P <.001, respectively). The median fibrosis progression rate in coinfected patients and in control patients was 0.153 (95% confidence interval [CI], 0.117-0.181) and 0.106 (95% CI, 0.084-0.125) fibrosis units per year, respectively (P <.0001). HIV seropositivity (P <.0001), alcohol consumption (>50 g/d, P =.0002), age at HCV infection (<25 years old, P <.0001), and severe immunosuppression (CD4 count =200 cells/microL, P <.0001) were associated with an increase in the fibrosis progression rate. In coinfected patients, alcohol consumption (>50 g/d), CD4 count (=200 cells/microL), and age at HCV infection (<25 years old) (P <. 0001, respectively) were associated with a higher fibrosis progression rate. HIV seropositivity accelerates HCV-related liver fibrosis progression. In coinfected patients, a low CD4 count, alcohol consumption rate, and age at HCV infection are associated with a higher liver fibrosis progression rate.
Our aim was to assess the natural history of liver fibrosis progression in hepatitis C and the factors associated with this progression.
Few data are available concerning the long-term prognosis of chronic liver disease associated with hepatitis C virus infection. This study examined the morbidity and survival of patients with compensated cirrhosis type C.
We measured antibody (anti-HCV) to hepatitis C virus, which causes non-A, non-B hepatitis, by radioimmunoassay in prospectively followed transfusion recipients and their donors. Of 15 patients with chronic non-A, non-B hepatitis documented by liver biopsy, all seroconverted for the antibody; of 5 with acute resolving non-A, non-B hepatitis, 3 (60 percent) seroconverted. The development of anti-HCV was delayed (mean delay, 21.9 weeks after transfusion, or 15 weeks after the onset of clinical hepatitis) and took approximately one year in one patient. Antibody has persisted in 14 of the 15 patients with chronic disease (mean follow-up, greater than or equal to 6.9 years; maximum, greater than or equal to 12), but has disappeared in the 3 with acute resolving disease after a mean of 4.1 years. Anti-HCV was detected in samples of donor serum given to 14 (88 percent) of the 16 anti-HCV-positive patients for whom all donor samples were available. Only 33 percent of the anti-HCV-positive donors tested had an elevated serum concentration of alanine aminotransferase; 54 percent were positive for antibody to the hepatitis B core antigen (anti-HBc). We conclude that hepatitis C virus is the predominant agent of transfusion-associated non-A, non-B hepatitis and that screening of donors for anti-HCV could prevent the majority of cases of the disease. "Surrogate" assays for anti-HBc and alanine aminotransferase would have detected approximately half the anti-HCV-positive donors involved in the transmission of hepatitis that we identified.
International Liver Congress (ILC) 2020
15.04.2020 - 19.04.2020
European Congress of Clinical Microbiology and Infectious Diseases (ECCMID) 2020
18.04.2020 - 21.04.2020
DSI årsmøde 2020 (aflyst)
Hindsgavl Slot, Middelfart
1.05.2020 - 2.05.2020
Kursus i rejsemedicin 2020
Statens Serum Institut
4.05.2020 - 6.05.2020
5.05.2020 - 7.05.2020
COVID-19 retningslinje (2020)
National handlingsplan for antibiotika til mennesker (2017)
Retningslinjer til sundhedsprofessionelle vedr. håndtering af infektion med zikavirus (2019)
Antiviral behandling af hiv smittede personer (2019)
A sub-group of patients with hospital-acquired pneumonia do not require broad-spectrum gram-negative antimicrobial coverage
8.04.2020Clinical Infectious Diseases Advance Access
Potential of chloroquine and hydroxychloroquine to treat COVID-19 causes fears of shortages among people with systemic lupus erythematosus
Invisible spread of SARS-CoV-2
8.04.2020The Lancet Infectious Diseases
Correction to Lancet Infect Dis 2020; published online March 30. https://doi.org/10.1016/S1473-3099(20)30150-X
8.04.2020The Lancet Infectious Diseases
Making decisions to mitigate COVID-19 with limited knowledge
8.04.2020The Lancet Infectious Diseases
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Hvorfor synes Professor Thomas Benfield, at du bør læse"Oral versus Intravenous Antibiotics for Bone and Joint Infection."?
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