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The Role of Cholesterol On Sustained Virological Response (SVR) in the Treatment of Genotype-1 Infected Hepatitis C (cHC) Patients with Peginterferon Alfa-2a (PEG) and Ribavirin (RBV)
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Reported by Jules Levin
DDW May 17-22, 2008, San Diego
from Jules: As I have suggested recently, a higher cholesterol may be secondary to early HCV disease when liver is functioning better and better synthesizing lipids. In this study as in other recent studies SVR rates were higher when patients had higher cholesterol.
Stefan Mauss1, Elmar Zehnter2, Dietrich Hueppe3, Stephan Kaiser4, Klaus Boeker5, Thomas Lutz6, Renate Heyne7, Christine John8, Gero Moog9, Andreas Schober10, Rainer Pfaff11, Andreas Zipf12, Stefan A Racky13, Jueregn Lohmeyer14, Bernd Bokemeyer15, Birgit Kallinowski16, Thomas Witthoeft17, Ulrich Alshuth18
1. Center for HIV and Hepatogastrenterology, Duesseldorf, Germany, 2. Center of Gastroenterology, Dortmund, Germany, 3. Center of Gastroenterology, Herne, Germany, 4. Klinikum der Eberhard-Karls-Universitat, Tuebingen, Germany, 5. Center of Gastroenterology, Hannover, Germany, 6. Infektiologikum, Frankfurt, Germany, 7. Center of Gastroenterology and Livercenter, Berlin, Germany, 8. Center of Gastroenterology, Berlin, Germany, 9. Center of Gastroenterology, Kassel, Germany, 10. Center of Gastroenterology, Goettingen, Germany, 11. Center of Gastroenterology, Giessen, Germany, 12. Center of Gastroenterology, Mannheim, Germany, 13. Center of Gastroenterology, Bad Schwalbach, Germany, 14. Justus Liebig-Universitat Giessen, Giessen, Germany, 15. Gastroenterology Practice, Minden, Germany, 16. Center of Gastroenterology, Schwetzingen, Germany, 17. Medical Department I, Div. of Gastroenterology, University Hospital Schleswig-Holstein Campus, Luebeck, Germany, 18. Roche Pharma AG, Grenzach-Wyhlen, Germany
ABSTRACT from program book
HCV life cycle is associated with cholesterol metabolism in host cells. Cholesterol lowering drugs as statins are under discussion to inhibit HCV RNA replication. In contrast, higher cholesterol serum levels have been associated recently with SVR. Methods: To assess the standard of medical care for cHC patients, the Association of German Gastroenterologists in Private Practice (bng) conducts, in cooperation with Roche, a German-wide, internet-based noninterventional study. Until May 2007 data of 4058 patients with completed CHC treatment with PegIFN and RBV were documented. Cholesterol levels were available in 2432 patients. Results: HCV-genotype 1 (G1) patients had more frequently elevated serum cholesterol levels (>200 mg/dl, 5 mmol/l) compared to non-genotype 1 patients: 30.1% vs. 21.8% (p<.001). Of 1429 patients infected with G1, 999 (70%) had normal (N) and 430 (30%) elevated cholesterol (E). Demographics (N/E): age 44.4/45.3 y, 61.4%/53.7% male, BMI 25.3/25.3 kg/m2, concomitant diseases 52.7%/56.3%, duration of infection 12.5/12.9 y, source of infection (>1 answer possible): transfusion 22.4%/23.7%, iv drug abuse 34.2%/33.3%, medical action 9.7%/13.5%, unknown 27.6.5%/25.1%. 56.9% of N and 57.8% of E pts had high viral load at baseline (cut-off 400.000 IU/ml). Liver biopsies were available in one third of patients. 49.9% of N and 33.3% of E showed fibrosis stage ≥2 (Desmet-Scheuer). Differences between N and E were seen in cumulative dose of PEG (≥80%: 58.1%/69.4%) and RBV (≥80%: 46.4%/57.4%). Discontinuation rates due to virological non-response were 20.1% and 11.6%. The virologic response rates are shown in the table below: Conclusion: In contrast to the observation that about 60% of adult population has elevated cholesterol levels, in this CHC cohort only 30% had cholesterol >200mg/dl. Differences between N/E were found in liver histology and gender. Virological response to PEG/RBV was better in patients with elevated serum cholesterol indicating, that SVR may not only depend on well-known predictive factors but although on host factors related to cholesterol levels.
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