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Hepatology. 2005 Dec;42(6):1414-9.

Adefovir rapidly suppresses hepatitis B in HBeAg-negative patients

developing genotypic resistance to lamivudine.

Lampertico P, Vigano M, Manenti E, Iavarone M, Lunghi G, Colombo M.

Department of Gastroenterology and Endocrinology, A. M. and A. Migliavacca

Center for Liver Disease, IRCCS Maggiore Hospital, Fondazione Policlinico,

Mangiagalli e Regina Elena, University of Milan, Milan, Italy.

Progression of hepatitis B in patients with lamivudine-resistant strains is

slowed down by adefovir dipivoxil (ADV). Whether the time point of ADV

administration (genotypic vs. phenotypic resistance) influences the outcome

of therapy is unknown. We compared the outcome of ADV therapy in hepatitis B

e antigen (HBeAg)-negative chronic hepatitis B patients with genotypic and

phenotypic resistance to lamivudine. Ten milligrams of ADV was administered

daily for 2 years to 46 HBeAg-negative patients at the time of phenotypic

resistance (group A, >6 log(10) copies/mL of hepatitis B virus [HBV] DNA and

high alanine aminotransferase [ALT] levels) and 28 patients at the time of

genotypic resistance (group B, 3-6 log(10) copies/mL of HBV-DNA and normal

ALT). HBV DNA was assessed every 2 months using Versant 3.0 assay, and

lamivudine resistance was confirmed via INNO-LiPA assay in all patients. By

month 3, HBV DNA tested negative in all patients from group B compared with

only 20 (46%) in group A (P < .0001). The 2-year rates of virological

response were 100% in the former patients and 78% in the latter ones (P <

..0001). ALT levels remained persistently normal in all group B patients,

whereas in group A patients they normalized at rates of 50% at month 6 (P <

..0001), 72% at month 12 (P < .01), and 93% at month 24. None of the patients

developed ADV resistance or ADV-related side effects. In conclusion, to

optimize antiviral treatment in HBeAg-negative patients selecting resistant

strains to lamivudine, ADV should be added to lamivudine as soon as

genotypic resistance is detected. (HEPATOLOGY 2005.).

PMID: 16317671 [PubMed - in process]

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Hepatology. 2005 Dec;42(6):1414-9.

Adefovir rapidly suppresses hepatitis B in HBeAg-negative patients

developing genotypic resistance to lamivudine.

Lampertico P, Vigano M, Manenti E, Iavarone M, Lunghi G, Colombo M.

Department of Gastroenterology and Endocrinology, A. M. and A. Migliavacca

Center for Liver Disease, IRCCS Maggiore Hospital, Fondazione Policlinico,

Mangiagalli e Regina Elena, University of Milan, Milan, Italy.

Progression of hepatitis B in patients with lamivudine-resistant strains is

slowed down by adefovir dipivoxil (ADV). Whether the time point of ADV

administration (genotypic vs. phenotypic resistance) influences the outcome

of therapy is unknown. We compared the outcome of ADV therapy in hepatitis B

e antigen (HBeAg)-negative chronic hepatitis B patients with genotypic and

phenotypic resistance to lamivudine. Ten milligrams of ADV was administered

daily for 2 years to 46 HBeAg-negative patients at the time of phenotypic

resistance (group A, >6 log(10) copies/mL of hepatitis B virus [HBV] DNA and

high alanine aminotransferase [ALT] levels) and 28 patients at the time of

genotypic resistance (group B, 3-6 log(10) copies/mL of HBV-DNA and normal

ALT). HBV DNA was assessed every 2 months using Versant 3.0 assay, and

lamivudine resistance was confirmed via INNO-LiPA assay in all patients. By

month 3, HBV DNA tested negative in all patients from group B compared with

only 20 (46%) in group A (P < .0001). The 2-year rates of virological

response were 100% in the former patients and 78% in the latter ones (P <

..0001). ALT levels remained persistently normal in all group B patients,

whereas in group A patients they normalized at rates of 50% at month 6 (P <

..0001), 72% at month 12 (P < .01), and 93% at month 24. None of the patients

developed ADV resistance or ADV-related side effects. In conclusion, to

optimize antiviral treatment in HBeAg-negative patients selecting resistant

strains to lamivudine, ADV should be added to lamivudine as soon as

genotypic resistance is detected. (HEPATOLOGY 2005.).

PMID: 16317671 [PubMed - in process]

_________________________________________________________________

Don’t just search. Find. Check out the new MSN Search!

http://search.msn.click-url.com/go/onm00200636ave/direct/01/

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