Huang Zhong-Min, Huang Qi-Wen, Qin Ya-Qin, He Yan-Zhuan, Qin Hou-Ji, Zhou Yiao-Nan, Xu Xiang, Huang Mei-Jin
Department of Infectious Diseases, The Affiliated Hospital of YouJiang Medical College for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China.
World J Gastroenterol. 2005 Feb 14;11(6):867-70. doi: 10.3748/wjg.v11.i6.867.
To polymerase P region (YMDD) mutations of hepatitis B virus gene (HBV DNA) in patients with chronic hepatitis B (CHB) untreated with antiviral medicines and to explore its correlation with pre-c-zone mutations, HBV genotypes and HBV DNA level, and to observe its curative effect.
A total of 104 cases (38 cases in group of familial aggregation and 66 cases in group of non-familial aggregation) were randomly chosen from 226 patients with CHB who did not receive the treatment of lamivudine (LAM) and any other antivirus drugs within the last one year. Their serum YMDD mutations were detected by microcosmic nucleic acid and cross-nucleic acid quantitative determination, HBV genotypes by PCR-microcosmic nucleic acid cross-ELISA, HBV DNA quantitative determination and fluorescence ration PCR analysis, hepatitis B virus markers (HBVM) by ELISA. LAM was taken by 10 patients with YMDD mutations and its curative effect was observed.
Twenty-eight cases (26.9%) had YMDD mutations, of them 11 cases (28.9%) were in familial aggregation group (38 cases) and 17 cases (25.8%) in non-familial aggregation group (66 cases) with no significant difference between the two groups. Twenty-seven point one percent (16/59) cases were positive for HBeAg YMDD mutations, and 26.7% (12/45) cases were negative for HBeAg and positive for anti-HBe. There was also no significant difference between the two groups. Different YMDD incidence rate existed in different HBV genotypes. HBV DNA level did not have a positive correlation with the incidence of YMDD mutations. LAM was effective for all patients with mutations.
Wild mutant strains in HBV and their incidence rate have no significant difference between familial aggregation and non-familial aggregation. It may have no significant relationship between YMDD mutations and pre-c-zone mutations. HBV DNA level may not have a positive correlation with YMDD mutations. LAM is clinically effective for CHB patients with YMDD mutations.
检测未经抗病毒药物治疗的慢性乙型肝炎(CHB)患者乙肝病毒基因(HBV DNA)聚合酶P区(YMDD)突变情况,探讨其与前C区突变、HBV基因型及HBV DNA水平的相关性,并观察其疗效。
从226例过去1年内未接受拉米夫定(LAM)及其他任何抗病毒药物治疗的CHB患者中随机选取104例(家族聚集组38例,非家族聚集组66例)。采用微量核酸及交叉核酸定量测定法检测其血清YMDD突变,采用PCR-微量核酸交叉ELISA法检测HBV基因型,采用荧光定量PCR分析法检测HBV DNA定量,采用ELISA法检测乙肝病毒标志物(HBVM)。对10例YMDD突变患者给予LAM治疗并观察疗效。
28例(26.9%)存在YMDD突变,其中家族聚集组(38例)11例(28.9%),非家族聚集组(66例)17例(25.8%),两组差异无统计学意义。HBeAg阳性患者中YMDD突变率为27.1%(16/59),HBeAg阴性、抗-HBe阳性患者中YMDD突变率为26.7%(12/45),两组差异无统计学意义。不同HBV基因型的YMDD发生率不同。HBV DNA水平与YMDD突变发生率无正相关。LAM对所有突变患者均有效。
HBV野生株及其突变率在家族聚集与非家族聚集患者间差异无统计学意义。YMDD突变与前C区突变可能无明显关系。HBV DNA水平与YMDD突变可能无正相关。LAM对CHB患者YMDD突变临床有效。