Hepatitis C: quick reference guide for primary care (2009 edition) in two sides of A4 provides information and good practice advice about hepatitis C testing and diagnosis for use by doctors and nurses in primary care. It includes a testing and diagnosis flowchart. It supersedes the 2007 version.

For the public there is the leaflet Hepatitis C: Get tested. Get treated.

Meine Frau wird diese Woche ihre zweite Therapie gegen Hepatitis C beginnen. Diesmal wird es länger werden,  der ganze Rest vom Jahr.
Und wir beide hoffen, daß wir es diesmal besser in den Griff bekommen und besser damit umgehen können.
Für meine Frau heisst das Medikamente in Massen, Nebenwirkungen und kaum mehr Teilnahme am Leben. Ich hoffe daß ich diesmal mehr dazu tun kann, das zu ändern.

Ich sellbst habe mir vorgenommen meine beiden Professionen auszubauen und zu verstärken, nämlich Fotografie und Musik.
Ich hoffe, daß ich durch Planung, Disziplin( Gott wo soll ich die herbekommen lol) und eine ruhigere Einstellung das auch schaffe.

My wife will start her second therapy against Hepatitis C. this time it will be much longer, the rest of this year.
And we both hope we will handle it this time in a better way.
For my wife this means medication in mass, side effects and a dull life. I hope i can do much more this time to change this.

I myself want to built up my two professions again, Photography and music.
I hope with planing, discipline ( God how should i get that lol) and a much calmer attitude i will make it.

Hyponatremia and Mortality among Patients on the Liver-Transplant Waiting List

W. Ray Kim, M.D., Scott W. Biggins, M.D., Walter K. Kremers, Ph.D., Russell H. Wiesner, M.D., Patrick S. Kamath, M.D., Joanne T. Benson, B.A., Erick Edwards, Ph.D., and Terry M. Therneau, Ph.D.

ABSTRACT

Background Under the current liver-transplantation policy, donor organs are offered to patients with the highest risk of death.

Methods Using data derived from all adult candidates for primary liver transplantation who were registered with the Organ Procurement and Transplantation Network in 2005 and 2006, we developed and validated a multivariable survival model to predict mortality at 90 days after registration. The predictor variable was the Model for End-Stage Liver Disease (MELD) score with and without the addition of the serum sodium concentration. The MELD score (on a scale of 6 to 40, with higher values indicating more severe disease) is calculated on the basis of the serum bilirubin and creatinine concentrations and the international normalized ratio for the prothrombin time.

Results In 2005, there were 6769 registrants, including 1781 who underwent liver transplantation and 422 who died within 90 days after registration on the waiting list. Both the MELD score and the serum sodium concentration were significantly associated with mortality (hazard ratio for death, 1.21 per MELD point and 1.05 per 1-unit decrease in the serum sodium concentration for values between 125 and 140 mmol per liter; P<0.001 for both variables). Furthermore, a significant interaction was found between the MELD score and the serum sodium concentration, indicating that the effect of the serum sodium concentration was greater in patients with a low MELD score. When applied to the data from 2006, when 477 patients died within 3 months after registration on the waiting list, the combination of the MELD score and the serum sodium concentration was considerably higher than the MELD score alone in 32 patients who died (7%). Thus, assignment of priority according to the MELD score combined with the serum sodium concentration might have resulted in transplantation and prevented death.

Conclusions This population-wide study shows that the MELD score and the serum sodium concentration are important predictors of survival among candidates for liver transplantation.

Prolonged Therapy of Advanced Chronic Hepatitis C with Low-Dose Peginterferon

Adrian M. Di Bisceglie, M.D., Mitchell L. Shiffman, M.D., Gregory T. Everson, M.D., Karen L. Lindsay, M.D., James E. Everhart, M.D., M.P.H., Elizabeth C. Wright, Ph.D., M.P.H., William M. Lee, M.D., Anna S. Lok, M.D., Herbert L. Bonkovsky, M.D., Timothy R. Morgan, M.D., Marc G. Ghany, M.D., Chihiro Morishima, M.D., Kristin K. Snow, Sc.D., Jules L. Dienstag, M.D., for the HALT-C Trial Investigators

ABSTRACT

Background In patients with chronic hepatitis C who do not have a response to antiviral treatment, the disease may progress to cirrhosis, liver failure, hepatocellular carcinoma, and death. Whether long-term antiviral therapy can prevent progressive liver disease in such patients remains uncertain.

Methods We conducted a randomized, controlled trial of peginterferon alfa-2a at a dosage of 90 µg per week for 3.5 years, as compared with no treatment, in 1050 patients with chronic hepatitis C and advanced fibrosis who had not had a response to previous therapy with peginterferon and ribavirin. The patients, who were stratified according to stage of fibrosis (622 with noncirrhotic fibrosis and 428 with cirrhosis), were seen at 3-month intervals and underwent liver biopsy at 1.5 and 3.5 years after randomization. The primary end point was progression of liver disease, as indicated by death, hepatocellular carcinoma, hepatic decompensation, or, for those with bridging fibrosis at baseline, an increase in the Ishak fibrosis score of 2 or more points.

Results We randomly assigned the patients to receive peginterferon (517 patients) or no therapy (533 patients) for 3.5 years. The level of serum aminotransferases, the level of serum hepatitis C virus RNA, and histologic necroinflammatory scores all decreased significantly (P<0.001) with treatment, but there was no significant difference between the groups in the rate of any primary outcome (34.1% in the treatment group and 33.8% in the control group; hazard ratio, 1.01; 95% confidence interval, 0.81 to 1.27; P=0.90). The percentage of patients with at least one serious adverse event was 38.6% in the treatment group and 31.8% in the control group (P=0.07).

Conclusions Long-term therapy with peginterferon did not reduce the rate of disease progression in patients with chronic hepatitis C and advanced fibrosis, with or without cirrhosis, who had not had a response to initial treatment with peginterferon and ribavirin. (ClinicalTrials.gov number, NCT00006164 [ClinicalTrials.gov] .)

Tenofovir Disoproxil Fumarate versus Adefovir Dipivoxil for Chronic Hepatitis B

Patrick Marcellin, M.D., E. Jenny Heathcote, M.D., Maria Buti, M.D., Ed Gane, M.D., Robert A. de Man, M.D., Zahary Krastev, M.D., George Germanidis, M.D., Sam S. Lee, M.D., Robert Flisiak, M.D., Kelly Kaita, M.D., Michael Manns, M.D., Iskren Kotzev, M.D., Konstantin Tchernev, M.D., Peter Buggisch, M.D., Frank Weilert, M.D., Oya Ovung Kurdas, M.D., Mitchell L. Shiffman, M.D., Huy Trinh, M.D., Mary Kay Washington, M.D., Jeff Sorbel, M.S., Jane Anderson, Ph.D., Andrea Snow-Lampart, B.S., Elsa Mondou, M.D., Joe Quinn, M.P.H., and Franck Rousseau, M.D.

ABSTRACT

Background 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.

Methods In two double-blind, phase 3 studies, we randomly assigned patients with hepatitis B e antigen (HBeAg)–negative or HBeAg-positive chronic HBV infection to receive tenofovir DF or adefovir dipivoxil (ratio, 2:1) once daily for 48 weeks. The primary efficacy end point was a plasma HBV DNA level of less than 400 copies per milliliter (69 IU per milliliter) and histologic improvement (i.e., a reduction in the Knodell necroinflammation score of 2 or more points without worsening fibrosis) at week 48. Secondary end points included viral suppression (i.e., an HBV DNA level of <400 copies per milliliter), histologic improvement, serologic response, normalization of alanine aminotransferase levels, and development of resistance mutations.

Results At week 48, in both studies, a significantly higher proportion of patients receiving tenofovir DF than of those receiving adefovir dipivoxil had reached the primary end point (P<0.001). Viral suppression occurred in more HBeAg-negative patients receiving tenofovir DF than patients receiving adefovir dipivoxil (93% vs. 63%, P<0.001) and in more HBeAg-positive patients receiving tenofovir DF than patients receiving adefovir dipivoxil (76% vs. 13%, P<0.001). Significantly more HBeAg-positive patients treated with tenofovir DF than those treated with adefovir dipivoxil had normalized alanine aminotransferase levels (68% vs. 54%, P=0.03) and loss of hepatitis B surface antigen (3% vs. 0%, P=0.02). At week 48, amino acid substitutions within HBV DNA polymerase associated with phenotypic resistance to tenofovir DF or other drugs to treat HBV infection had not developed in any of the patients. Tenofovir DF produced a similar HBV DNA response in patients who had previously received lamivudine and in those who had not. The safety profile was similar for the two treatments in both studies.

Conclusions Among patients with chronic HBV infection, tenofovir DF at a daily dose of 300 mg had superior antiviral efficacy with a similar safety profile as compared with adefovir dipivoxil at a daily dose of 10 mg through week 48. (ClinicalTrials.gov numbers, NCT00116805 [ClinicalTrials.gov] and NCT00117676 [ClinicalTrials.gov] .)