小兒科NI, YEN-HSUANYEN-HSUANNICHANG, MEI-HWEIMEI-HWEICHANGCHEN, PEI -JERPEI -JERCHENTSAI, KEH-SUNGKEH-SUNGTSAIHSU, HONG-YUANHONG-YUANHSUCHEN, HUEY-LINGHUEY-LINGCHENTSUEI, DAW-JENDAW-JENTSUEICHEN, DING-SHINNDING-SHINNCHEN蔡克嵩2008-12-052018-07-112008-12-052018-07-112007http://ntur.lib.ntu.edu.tw//handle/246246/88629Background & Aims: This study investigated the viremia profiles in children with chronic hepatitis B virus (HBV) infection and spontaneous heptitis B e antigen (HBeAg) seroconversion. Methods: Fifty-eight children with chronic HBV infection met the following criteria: normal alanine aminotransferase (ALT) level at enrollment, followed up for more than 10 years, no antiviral treatment, and having under -gone spontaneous HBeAg seroconversion during fol-low-up evaluation. They were grouped according to the post-HBeAg seroconversion HBV-DNA levels: (1) low viremia: transient or never 10 4 copies/mL or greater (n=35) (2) fluctuating high viremia: 104 copies/mL or greater at least twice at intrervals more than 1 year apart (n=23). Abdominal sonography, ALT, and HBV-DNA levels were assessed annually. Another 14 nonseroconverted children served as controls . The precore mutant (nt1896) and genotypes were examined. Results: The initial HBV-DNA level of the 58 serovonverters was 108.4±1.0 copies/mL and decreased to 102.9±2.0 copies/ mL at the end of fol-low-up period. Their mean ages at enrollment, at peak HBV-DNA, at peak ALT, at HBeAg serovonversion, and at final follow-up were 7.0±3.7, 13.4±5.8, 16.3±6.0 , 17.2±5.8, and 23.7±4.1 years, respedtively. The precore mutant appeared more often in the fluctuating- high-viremia group than in the low -viremia group (60.9% vs 22.9%, p=0.004). HBV genotypes had no effect on the viremia profiles. AfterHBeAg seroconverters had decreased viral loads, normal ALT levels, and uneventful coruses after HBeAg seroconversion. A longer follow-up period is necessary to elucidate the significance of HBeAg seroconversion occurring in childhood and young adulthood.en-USNATURAL-HISTORYHEPATOCELLULAR-CARCINOMACORE PROMOTERGENOTYPEMUTANTSUPDATE[SDGs]SDG3journal article