title: [Can HBsAg levels guide to differentiate inactive HBsAg carriers from HBeAg negative chronic B hepatitis?].
abstract: It is valuable to differentiate the inactive HBsAg carrier state from HBeAg negative chronic B hepatitis (CBH) which develops due to precore or core promoter region mutations in hepatitis B virus (HBV). The aim of this study was to investigate the role of HBsAg S/N (sample rate/index calibrator mean rate) levels in the differentiation of inactive HBsAg carriers from HBeAg negative CBH cases. A total of 134 HBsAg positive patients followed-up in Kocaeli University Medical Faculty hospital between June 2004-September 2005, were included to the study. The patients were classified into four groups according to their serological patterns (Group 1: HBeAg and HBV-DNA negative 34 cases with normal ALT levels; Group 2: HBeAg negative, anti-HBe positive, HBV-DNA >10(5) copies/ml, 36 cases with increased ALT levels; Group 3: HBeAg negative, anti-HBe positive, HBV-DNA 102-10(5) copies/ml, 32 cases with normal ALT levels; Group 4: HBeAg positive, HBV-DNA >10(5) copies/ml, 32 cases with increased ALT levels). The age and gender distributions of the groups were similar. HBV markers have been detected by microparticle enzyme immunoassay (AxSYM System, v3.0, Abbott Laboratories, USA), and viral load were investigated by real-time polymerase chain reaction (iCycler IQ, v3.0a, Bio Rad Laboratories, USA). As a result, the mean HBsAg S/N level in group 2 who were HBeAg negative with a viral load of >10(5) copies/ml, was found significantly higher than group 1 who were inactive HBsAg carriers (285.9+/-78.8 and 214.4+/-108.6, respectively; p<0.05). In contrast there was no statistically significant difference between group 1 (HBV-DNA negative) and group 3 (HBV-DNA <10(5) copies/mL) by means of mean HBsAg S/N levels (214.4+/-108.6 and 216.3+/-57.2, respectively; p>0.05). Although HBsAg levels seem to guide the differentiation of inactive HBsAg carriers from HBeAg negative CBH cases with high viral loads (>10(5) copies/ml), advanced studies are needed to clarify this relationship with the use of quantitative HBsAg measurements (IU/ml) in large patient groups and by performing mutation analysis.
authors.affiliation: Kocaeli Universitesi Tip Fakültesi, Merkez Laboratuvan PCR Unitesi, Kocaeli. sayanmurat@hotmail.com
authors.forename: Murat
authors.initials: M
authors.lastname: Sayan
authors.forename: Birsen
authors.initials: B
authors.lastname: Mutlu
authors.forename: Sarper
authors.initials: S
authors.lastname: Erdoğan
authors.forename: Meliha
authors.initials: M
authors.lastname: Meriç
authors.forename: Ayşe
authors.initials: A
authors.lastname: Willke
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D002353:Carrier State / Q000175:diagnosis*; D004279:DNA, Viral / Q000097:blood; D003937:Diagnosis, Differential; D005260:Female; D006510:Hepatitis B Antibodies / Q000097:blood; D006514:Hepatitis B Surface Antigens / Q000097:blood*; D006513:Hepatitis B e Antigens / Q000097:blood* / Q000276:immunology; D006515:Hepatitis B virus / Q000235:genetics* / Q000276:immunology; D019694:Hepatitis B, Chronic / Q000175:diagnosis*; D006801:Humans; D008297:Male; D008875:Middle Aged
chemical_list: D004279:DNA, Viral; D006510:Hepatitis B Antibodies; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens; D000410:Alanine Transaminase