A short course of add-on adefovir dipivoxil treatment in lamivudine-resistant chronic hepatitis B patients


İDİLMAN R., KAYMAKOĞLU S., ÖNDER F. O., Ahishali E., Bektas M., ÇINAR K., ...Daha Fazla

JOURNAL OF VIRAL HEPATITIS, cilt.16, sa.4, ss.279-285, 2009 (SCI-Expanded) identifier identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 16 Sayı: 4
  • Basım Tarihi: 2009
  • Doi Numarası: 10.1111/j.1365-2893.2009.01074.x
  • Dergi Adı: JOURNAL OF VIRAL HEPATITIS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.279-285
  • Anahtar Kelimeler: adefovir, hepatitis B virus, lamivudine, resistance, VIROLOGICAL RESPONSE, NUCLEOSIDE-NAIVE, ENTECAVIR, THERAPY, RECOMMENDATIONS, COMBINATION, HBV
  • Acıbadem Mehmet Ali Aydınlar Üniversitesi Adresli: Hayır

Özet

The aims of the study were to investigate the efficacy of rescue therapy with lamivudine (LAM) and adefovir (ADV) combination for 6 months followed by ADV monotherapy in lamivudine-resistant chronic hepatitis B (LAM-R CHB) patients, and to analyze the frequency of ADV resistance mutant development in such patients. A total of 170 consecutive LAM-R CHB patients (male/female: 130/40, mean age: 42.9 +/- 13.4 years) with viral breakthrough under LAM therapy were analyzed. A total of 68 had HBeAg-positive. Patients received rescue therapy with LAM [100 mg (qd)]+ADV [10 mg (qd)] for 6 months after which LAM was discontinued. HBV-DNA was assessed with the HBV-DNA 3.0 bDNA assay. ADV-resistant mutations were identified by sequencing the reverse transcriptase region. The median duration of rescue therapy was 24 months. Cumulative probability of becoming HBV-DNA undetectable was 33.8%, 59.6% and 68.2% after 24, 48 and 96 weeks of treatment, respectively. These figures were 43.2%, 58.0% and 73.1% for ALT normalization. Among 68 HBeAg-positive CHB patients, 10 patients had an e-antigen seroconversion. Low baseline HBV-DNA level (< 10(7) copies/mL) was a significant predictor of response to ADV treatment (P < 0.01). Cumulative probability of ADV resistance was 1.2%, 15.1% and 37.3% at 12, 24 and 36 months of therapy, respectively. By multivariate analysis, baseline high viral load and primary nonresponse to treatment at week 24 predicted ADV resistance. The data indicate that a time limited add-on strategy does not provide benefit over the switch strategy with respect emergence of ADV resistant mutants in LAM-R CHB patients.