Hepatitis: Sönnerborg A

Lindh M, Uhnoo I, Bläckberg J, Duberg AS, Friman S, Fischler B, Karlström O, Norkrans G, Reichard O, Sangfeldt P, Söderström A, Sönnerborg A, Weiland O, Wejstål R, Wiström J. · Department of Infectious Diseases, Sahlgrenska University Hospital, Göteborg, Sweden. · Scand J Infect Dis. · Pubmed #18584530 No free full text.

Abstract: The main goal for treatment of chronic hepatitis B is to prevent complications such as liver cirrhosis or hepatocellular carcinoma. Knowledge from population studies of the long-term risk of chronic HBV infection, as well as the recent introduction of pegylated interferon and additional nucleoside analogues has changed the therapeutic situation. Recently, a Swedish expert panel convened to update the national recommendations for treatment. The panel recommends treatment for patients with active HBV infection causing protracted liver inflammation or significant liver fibrosis, verified by liver histology. In general, pegylated interferon alpha-2a is recommended as first-line treatment, in particular for HBeAg-positive patients with HBV genotypes A or B. Among nucleoside analogues, entecavir is the first choice and adefovir or tenofovir can be used as alternatives. Lamivudine monotherapy is not recommended due to the high risk of resistance development. Combinations of nucleoside analogues such as tenofovir and lamivudine or emtricitabine are alternatives for patients with non-response or infection with resistant variants, or as first choice for patients with advanced liver disease. Nucleoside analogue treatment should be monitored to detect primary non-response and virological breakthrough. Special recommendations are given for HBV/HIV coinfected patients, immunosuppressed patients, children, and for treatment before and after liver transplantation. The present guideline is translated from Swedish, where it is published on the MPA and RAV websites (www.mpa.se and www.rav.nu.se) including 7 separate papers based on thorough literature search. The complete reference list can be received from the Medical Products Agency upon request.

Karlström O, Sönnerborg A, Weiland O. · Division of Infectious Diseases, Department of Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden. · AIDS. · Pubmed #18427210 No free full text.

Abstract: We prospectively studied early hepatitis C virus kinetics and sustained virological response rates in HIV/HCV coinfected (n = 13) and HCV monoinfected matched controls (n = 26) with HCV genotype 2/3 treated with pegylated interferon (peg-IFN) alpha-2a 135 microg/week plus ribavirin 11 mg/kg daily during 24 weeks. No significant difference in HCV-RNA decay was seen at any time point during the initial 12 weeks of therapy. Sustained virological response was achieved in 9/13 (69%) versus 20/26 (77%) patients (intent-to-treat), respectively. The lower-than-standard peg-IFN dose offered high compliance and reasonable sustained virological response rates.

Pembrey L, Newell ML, Tovo PA, van Drimmelen H, Quinti I, Furlini G, Galli S, Meliconi MG, Burns S, Hallam N, Sönnerborg A, Cilla G, Serrano E, Laccetti P, Portella G, Polywka S, Icardi G, Bruzzone B, Balbo L, Alfarano A, Anonymous00307. · Centre for Paediatric Epidemiology and Biostatistics, Institute of Child Health, London, United Kingdom. · J Med Virol. · Pubmed #12683407 No free full text.

Abstract: To investigate whether it is appropriate to assume comparability of hepatitis virus C (HCV)-RNA results across laboratories in multi-centre studies, nine laboratories of the European Paediatric HCV Network participated in an international proficiency study of HCV-RNA assays. A panel of 12 samples of different dilutions and genotypes was sent to each laboratory and tested with qualitative and/or quantitative HCV-RNA assays according to local procedures. Commercial assays were used in seven laboratories and in-house assays in two. All six laboratories in which a commercial qualitative assay was used were proficient, as were four of six runs (in five laboratories) in which a commercial quantitative assay was used. The proficiency of the laboratories where in-house assays were used could not be assessed according to the VQC definition because of differences in the methods used. Overall, there were several false-negative results, but only one false-positive result with a quantitative assay and none with a qualitative assay. The false-negative results may have implications for the diagnosis of infection, and highlight the need for an antibody test to be performed at 18 months to confirm the absence of infection. The results of qualitative assays were generally consistent across laboratories but it was difficult to evaluate and compare the results of quantitative assays. Multivariate analysis of data collected in multi-centre studies should therefore allow for centre and/or assay used.

Nowak P, Schvarcz R, Ericzon BG, Flamholc L, Sönnerborg A. · Division of Clinical Virology, Huddinge University Hospital, Karolinska Institutet, SE-171 77 Stockholm, Sweden. · AIDS Res Hum Retroviruses. · Pubmed #12581512 No free full text.

Abstract: The prognosis of HIV-1-infected patients has dramatically improved but progression to liver failure occurs now frequently in subjects coinfected with hepatitis C virus (HCV). This has raised the issue of organ transplantation, but the knowledge about the effect of concomitant antiretroviral and immunosuppressive therapy is limited. The objective of the study was to describe viral and immunological events in antiretroviral-treated orthotopic liver transplant (OLT) recipients with primary (PHI) or chronic HIV-1 infection. Three HIV-1-infected patients with liver cirrhosis due to chronic HCV infection underwent OLT. A fourth patient developed PHI at OLT. Immunosuppressive drugs and combination antiretroviral therapy were given. The effects on HIV-1 load, viral diversity and divergence, and CD4(+) T cell counts, were studied. One patient died after 3 months. Three subjects were alive after 9 months, 14 months, and 3 years, respectively. In the PHI patient, viral load decreased during the second week of illness despite immunosuppression. During the third week the viremia increased until antiretroviral treatment was initiated. In all four patients, the HIV-1 replication was effectively inhibited during follow-up by the treatment, as determined by undetectable plasma viremia, lack of viral sequence changes, and increase in CD4(+) T cells. The pattern of viral dynamics may suggest that the innate immunity causes the earliest decline of viral load in PHI patients. A lack of adaptive immunity may thereafter lead to an increase in viremia in heavily immunosuppressed individuals. However, a specific HIV-1 immunity is not necessary to efficiently inhibit the viral replication when potent antiretroviral therapy is given in liver transplant recipients with primary or chronic HIV-1 infection.

Wejstål R, Fischler B, Glaumann H, Norkrans G, Reichard O, Sönnerborg A, Uhnoo I, Weiland O. · Infektionskliniken, Sahlgrenska Universitetssjukhuset/Ostra, Göteborg. · Lakartidningen. · Pubmed #10584541 No free full text.

This publication has no abstract.

Carlsson T, Struve J, Sönnerborg A, Weiland O. · Division of Infectious Diseases, Karolinska Institutet, Danderyd Hospital, Sweden. · Scand J Infect Dis. · Pubmed #10381226 No free full text.

Abstract: To study early seroconversion rates after hepatitis B vaccination intramuscular (i.m.) and low-dose intradermal (i.d.) vaccination was compared when given either according to the registered 0, 4, 8 weeks scheme (scheme A), or to an accelerated 0, 2, 6 weeks scheme (scheme B). Medical staff received either 2 microg i.d. or 20 microg i.m. of a recombinant hepatitis B vaccine, in a non-randomized open trial. Two weeks after the third dose i.m. vaccinees overall had significantly higher rates of protective anti-HBs levels (anti-HBs > or = 10 IU/I), (23/30, 77%) compared with i.d. vaccinees (75/166, 45%) (p < 0.001). We conclude that when rapid protection against hepatitis B virus (HBV) infection is desirable, such as for post-exposure prophylaxis, an accelerated low-dose i.d. vaccination schedule cannot be used.

Halasz R, Barkholt L, Lara C, Hultgren C, Ando Y, Broomé U, Fischler B, Nemeth A, Ericzon BG, Sönnerborg A, Sällberg M. · Division of Clinical Virology, F68, Department of Immunology, Microbiology, Pathology, and Infectious Diseases, Karolinska Institutet, Huddinge University Hospital, S-141 86 Huddinge, Sweden. · Gut. · Pubmed #9895390 links to  free full text

Abstract: BACKGROUND: The role of the recently discovered GB virus C (GBV-C)/hepatitis G virus in fulminant hepatic failure (FHF) has been debated. Although GBV-C RNA has been detected in many cases of FHF, recent data suggest that the relation between GBV-C and FHF may be accidental. AIMS: To retrospectively investigate the possible relation between the presence of GBV-C markers (RNA or antibodies to the GBV-C envelope 2 (E2) glycoprotein) and FHF. METHODS: The presence of GBV-C RNA was determined in serum samples from 58 patients diagnosed with FHF using a reverse transcriptase polymerase chain reaction. Amplified genetic fragments were directly sequenced by the dideoxy chain termination method. Antibodies to GBV-C in serum samples were detected by enzyme immunoassay based on a recombinant GBV-C E2 protein. RESULTS: Nine (16%) patients with FHF had GBV-C RNA and 13 (22%) [corrected] had GBV-C E2 antibodies, which are higher frequencies than in healthy subjects (p<0.01 and p<0.05 respectively). Six of nine [corrected] patients with GBV-C markers during FHF tested negative for these markers before therapy with blood and/or blood products. Sequence analysis of the GBV-C NS3 region fragments of six FHF patients showed no common sequence pattern or motif. CONCLUSIONS: The frequencies of both GBV-C RNA and antibodies are higher in patients with FHF than in healthy subjects. However, these increased frequencies may in many cases be explained by the use of contaminated blood and/or blood products given as therapy.