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AASLD2012:长期随访的HBsAg水平与非活动性HBV携带者的关系 [复制链接]

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发表于 2012-12-6 13:42 |只看该作者 |倒序浏览 |打印
本帖最后由 StephenW 于 2012-12-6 13:44 编辑

The recognition of HBeAg negative CHB has led to a better understanding of the natural history of HBV.  This study by Hansen et al reported on 170 patients deemed inactive carriers with HBV DNA <2000iu/ml.  They followed these patients for 4 years and noted that by 5 years 37% had become active.  Predicting which individuals will become active may be using HBV DNA levels and quantitative HBV DNA at baseline as these two parameters 100% predicted in this study which patients would become active over time.
HBeAg阴性慢性乙肝的认识,更好地了解HBV的自然史的。Hansen等人的这一研究报告的170例患者,被视为非活动,HBV DNA<2000iu/ml的携带者。他们跟着这些患者4年,并指出,5年37%,成为活跃。预测哪些人会变得活跃,在这项研究中基线HBSAg水平和HBV DNA定量100%预测哪些患者会随着时间的推移变得活跃.

Long Term Follow-up of Inactive HBV Carriers and Relation with HBsAg Levels
长期随访的HBsAg水平与非活动性HBV携带者的关系
HBeAg-negative, untreated, normal ALT level patients deemed “inactive carriers” with HBV DNA <2,000 IU/ml (N=170) followed for mean of 4.3 years
HBeAg阴性,未经药物治疗处理的,正常的ALT水平
与HBV DNA<2000 IU /毫升的患者被认为是“非活动性携带者(N = 170),跟随平均4.3年'

1 year 13% became active  1年 13%,成为活跃
2 years 25%  2年 25%
5 years 37%  5年 37%
Baseline HBV DNA <2000 IU/ml and HBsAg level <100 IU/ml predictive of remaining inactive
基线HBV DNA<2000 IU / ml和乙型肝炎表面抗原(HBsAg)水平<100 IU / ml 预测剩余的非活动
Conclusion: Combination of HBV DNA and HBsAg gave 100% prediction of remaining inactive carrier
结论:结合HBV DNA和HBsAg, 100%的预测剩余的非活动性携带者.


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发表于 2012-12-6 13:59 |只看该作者
本帖最后由 StephenW 于 2012-12-6 13:59 编辑


CONTROL ID: 1425030


PRESENTATION TYPE: Oral or Poster
CURRENT CATEGORY: Hepatitis B
CURRENT DESCRIPTORS: I01. Patient-centered, Natural History and Effectiveness Research
TITLE: Longterm follow-up of inactive hepatitis B virus carriers and relation with Hepatitis B surface Antigen levels
AUTHORS (FIRST NAME, LAST NAME): Bettina E. Hansen1, 2, Henry Lik-Yuen Chan3, Pauline Arends1, Beatrice Cherubini4, Markus Cornberg5, Alexander J. Thompson6, Yun -Fan Liaw7, Maurizia R. Brunetto4, Harry L. Janssen1
Institutional Author(s): for the Good Practice in using sAg in Chronic Hepatitis B Study Group (GPs-CHB Study Group)
INSTITUTIONS (ALL): 1. Gastroenterology and Hepatology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands.
2. Public Health, Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands.
3. Department of Medicine & Therapeutics, Chinese University of Hong Kong, Hong Kong , China.
4. Hepatology Unit, University of Pisa, Pisa, Italy.
5. Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
6. Victorian Infectious Diseases Reference Laboratory, North Melbourne, VIC, Australia.
7. Liver Research Unit, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taipei, Taiwan.
ABSTRACT BODY: Introduction  Patients are considered inactive HBV carriers if HBV DNA is <2000IU/mL combined with a normal ALT. Recently a single-point HBsAg<1000IU/mL has been suggested as an additional marker too accurately identify inactive carriers after 1 year of follow-up. The aim was to validate this rule for long-term follow-up of inactive carriers
Methods  This investigator-initiated project studied the follow-up of untreated HBeAg negative HBV patients initially presenting with normal ALT-levels from 8 large centers (GPs-CHB Study Group).
At baseline and during follow-up patients were defined as inactive carriers (IC) (HBV DNA ≤2000IU/mL and normal ALT) or active carries (AC) (HBV DNA>2000IU/mL or abnormal ALT). Survival analyses were used to analyze the transition probability from IC to AC over time.
Results  Repeated measurements of ALT, HBV DNA and quantitative HBsAg were available for 271 consecutive patients during a mean follow-up of 4.3 year. At baseline 170 patients (63%) were identified as IC and these patients were further studied. Total number of visits among IC was 1306. At baseline HBsAg was 675 IU/mL (range 0-49140) and HBV genotypes were: A 7%, B 17%, C 15%, D 44% and other 17%. Two patients had cirrhosis.
At 1 year 87% remained IC, at 2 years 75% and at 5 years 63%. HBsAg<1000IU/mL at baseline was a strong predictor for continued IC (at 1yr 89% vs 83%, 5yr 73% vs 49% in the group with <1000 vs ≥1000, p=0.001), as well as HBV DNA<200IU/mL (p<0.001). There were no differences in reactivation rates between HBV genotypes (p=0.72). HBsAg and HBV DNA were independent predictors of transition to AC (HR=1.4 by 1log increase and HR=2.5 by 1log increase). The combination of HBV DNA<100IU/mL and HBsAg<100IU/mL at baseline (n=17) gave a 100% accurate identification of IC. Overall decline of HBsAg was 0.37log in 5 years (p<0.001). Decline was not dependent on HBV DNA at baseline (p=0.83). In seven patients progression of liver disease was observed (2 HCC (1 with cirrhosis at baseline), 4 decompensation (1 with cirrhosis at baseline) and 1 non-liver related death). Five of those became AC prior to disease progression. The patient with non-liver related death remained IC until end of follow-up (7 years).
Conclusion  IC with a high HBsAg at baseline are at high risk for transition to AC and further progression of liver disease. Our date suggest to revise the definition of IC in CHB patients and to include HBsAg as a marker to accurately identify IC.

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发表于 2012-12-10 00:21 |只看该作者
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南方医院检查结果如下:
1、乙肝病毒表面抗原(自动500倍)3167.88IU/ml
2、乙肝病毒e抗原 0.353s/co
3、乙肝病毒e抗体 0.010s/co
4、乙肝病毒定量(hbv-dna)<1.00E+03 (6月份在本县人民医院检查hbv-dna为2.20E+11,怀疑不准确,因为半年时间从100亿降到<1000,)
5、ALT305、AST150、GGT109, C反应蛋白1.95(参考值0-0.8),类风湿因子81.5(参考值<20),AFP阴性,TBIL正常,B超正常。其他正常。
   本人男,37岁 ,20岁时发现携带大三阳,从未治疗过,有家族CA。母亲肺癌去世,二舅鼻咽癌去世,大哥鼻咽癌治愈,父亲这边的亲属均无肝病和癌症。近两年来由于多应酬,经常饮酒,经常觉得肝区饱帐不适。
   现请教该如何治疗?病毒定量<1.00E+03, 想上派罗欣治疗可行吗?
     医生建议:病毒变异的小三阳肝炎,可以干扰。由于hbv-dna<1.00E+03 ,关键看表面抗原与肝功能。建议不作治疗,先排查肝功异常的原因,观察hbv-dna、表面抗原、肝功能变化情况。
    我的疑问:hbv-dna<1.00E+03 上派罗欣效果好吗?

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发表于 2012-12-10 12:03 |只看该作者
本帖最后由 StephenW 于 2012-12-10 12:04 编辑

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我不是医生。这些只是我的意见。

现在,两个相互矛盾的结果: (hbv-dna)<1.00E+03 和 ALT305
还有C反应蛋白1.95(参考值0-0.8),类风湿因子81.5(参考值<20)不正常.
我同意医生建议暂时不作治疗,先排查肝功异常的原因,观察hbv-dna、表面抗原、肝功能变化情况。
1. C反应蛋白, ALT 不正常极有可能是由于你经常饮酒. 所以,你必须立即停止.
2. 类风湿因子不正常, 如果持续高,可能是由于关节炎. 但也可以反映乙肝疾病的活动.
3. 你是否有小三阳肝炎, 对我来说目前是不明确.
你必须立即停止饮酒, 再次测试hbvdna和 ALT.

hbv-dna<1.00E+03 上派罗欣效果好吗?
如果hbv-dna<1.00E+03, 您没有小三阳肝炎.

在HBeAg阴性肝炎患者中,治疗与聚乙二醇干扰素α-2a单药治疗1年, ,36%的患者
有响应(定义为HBV DNA<20,000拷贝(~4000iu)/ ml和正常的谷丙转氨酶(ALT)水平在停止治疗后6个月).

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发表于 2012-12-10 13:45 |只看该作者
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医生的分析:由于之前dna数量高,而现在dna<1000转胺酶高,极有可能是免疫过激引起,先观察表抗有无降低,转胺酶情况,如果是的话就可上干扰素,增加抗病毒效果。所以建议观察表抗与肝功。

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发表于 2012-12-10 14:39 |只看该作者
本帖最后由 StephenW 于 2012-12-10 14:39 编辑

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我似乎明白你的医生的分析. 在目前,你的免疫系统似乎是
活跃的(因为你的的ALT高). 原理上, 干扰素能降低血清表抗.血清乙肝病毒表面抗原蛋白直接抑制乙型肝炎病毒感染的固有性和适应性免疫应答. 因此上干扰素, 应该增加抗病毒(清除)效果. 但我不知道在这种情况下,使用干扰素的临床研究, 因此,不能告诉你会有什么效果.

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发表于 2012-12-10 15:55 |只看该作者
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谢谢!
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