我的乙肝病史，请GZ，0411和各位病友帮我分析解惑

亥猪

1991-1998一直是4，5阳
1998-2003未查
2003-现在一直是2，5阳，2003年hbsab滴度是30.9mIU/ml,2009年是53.88mIU/ml

liver411

可能处在产生免疫的阶段。过一阵检查看看抗体滴度是否增高，DNA是否逐渐少于100-200copies/ml...先之后评估。

就是产生免疫，体内仍然带有病毒。只不过免疫系统可以识别抗拒过去。也需要日后定期随访排除癌变等等。

亥猪

gz老师快过来帮我看看呀

亥猪

gz老师，您在哪呀，请帮我看看吧

亥猪

有人和我情况类似吗

liver_GZ

Gastroenterology. 2008 Oct;135(4):1192-9. Epub 2008 Jul 16.

HBsAg Seroclearance in chronic hepatitis B in Asian patients: replicative level and risk of hepatocellular carcinoma.
Yuen MF, Wong DK, Fung J, Ip P, But D, Hung I, Lau K, Yuen JC, Lai CL.

Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong. [email protected]

Comment in:

Gastroenterology. 2009 Apr;136(4):1459-60; author reply 1460-1.
Gastroenterology. 2009 May;136(5):1842-3; author reply 1843-4.

BACKGROUND & AIMS: Our aims were to study the virologic, histologic, and clinical outcome in chronic hepatitis B (CHB) patients with hepatitis B surface antigen (HBsAg) seroclearance. METHODS: We determined the age of HBsAg seroclearance that is associated with a lower risk for hepatocellular carcinoma (HCC) in 298 CHB patients (median follow-up, 108 months). The following virologic and histologic features were also determined: liver stiffness (n = 229), liver histology, serum HBV DNA levels over time (n = 265), intrahepatic HBV DNA with covalently closed circular DNA (cccDNA) levels, and messenger RNA (mRNA) expression. RESULTS: The median age of HBsAg seroclearance was 49.6 years. Seven (2.4%) patients developed HCC. Cumulative risk for HCC was higher in patients with HBsAg seroclearance at ages >or=50 years compared with those with HBsAg seroclearance at ages <50 (P = .004) years. Of these 2 groups of patients, 29.5% and 7.9%, respectively, had significant fibrosis by liver stiffness measurement (P = .001), and 15.4% of patients had mild histologic fibrosis. Intrahepatic total HBV DNA and cccDNA were detected in 100% and 79.3% of patients, respectively. All patients had undetectable surface and precore/pregenomic RNA transcripts. One (9.1%) patient had X mRNA expression. Serum HBV DNA were detectable in 13.4%, 6.1%, and 3.7% of patients within 1 year and 5-10 and >10 years after HBsAg seroclearance, respectively, and 82.1% patients had persistently normal alanine aminotransferase levels. CONCLUSIONS: HBV persisted at low replicative and transcriptional levels after HBsAg seroclearance. HBsAg seroclearance at age <50 years was associated with a lower risk for the development of HCC.


HBsAg Seroclearance: The More and Earlier, the Better , 19 March 2009
Tai–Chung Tseng, Jia–Horng Kao
Gastroenterology
May 2009 (Vol. 136, Issue 5, Pages 1842-1843)

Dear Sir:
We read with great interest the article entitled “HBsAg Seroclearance in Chronic Hepatitis B in Asian Patients: Replicative Level and Risk of Hepatocellular Carcinoma”by Yuen et al in the October 2008 issue of GASTROENTEROLOGY. 1 Although effective vaccines have been available for >2 decades,2 chronic hepatitis B virus (HBV) infection remains a leading cause of end-stage liver disease and hepatocellular carcinoma (HCC) worldwide. In clinical practice, seroclearance of hepatitis B surface antigen (HBsAg) has been recognized as an important endpoint in both natural history of HBV infection and treatment of chronic hepatitis B.3,4 However, because of the rarity of spontaneous or treatment-induced HBsAg seroclearance, the incidence and long-term outcomes of HBV carriers experiencing this event remain disputed.5,6 Yuen et al analyzed 298 patients who achieved HBsAg seroclearance between 1980 and 2006. Among them, the risks of significant hepatic fibrosis and HCC were significantly lower in patients with HBsAg seroconversion at ages <50 years than at >50.1 Their findings suggested that earlier HBsAg seroconversion with sustained suppression
of HBV DNA and remission of liver damage can bring out a better prognosis over time. Although these data are important to practicing gastroenterologists and hepatologists, some of their results deserve further discussion.
In a long-term follow-up cohort in Taiwan, a total 245 patients achieving spontaneous HBsAg seroclearance were identified.7 The annual HBsAg seroclearance was estimated to be 1.15% on the basis of 21,267 person-years follow-up (1965 anti-HBe–positive HBsAg carriers with 10.8 +- 5.4 years of follow-up). In the current study, the number of patients achieving HBsAg seroclearance was even greater than that in the Taiwanese study. Unfortunately, the number of HBV carriers and total person-years of the entire cohort were not offered. If the authors would provide relevant data, we could understand more about the annual incidence of  spontaneous HBsAg seroclearance in Asian HBV carriers.
Two possible flaws were also noted in this study. First, the surveillance for HCC was to perform ultrasound of the liver in patients with elevated
-fetoprotein levels. This measure is misleading and obviously violates the recommendations of current guidelines of HCC management, 3 and may lead to a later diagnosis of HCC in their  patients. Second, intrahepatic HBV-related mRNAs were analyzed and none but X-mRNA was identified in 1 of the 11 HBsAg seroconverters. This observation is contradictory to our understanding of HBV lifecycle. It is known that all 4 HBV-related mRNAs overlapped at the open reading frame of X gene8; therefore, only X-mRNA could be found by using region-specific primers seems unusual. One possibility is that the visible band on the gel might not be X-mRNA alone, but the summation of all m-RNAs. Further studies are needed to clarify this interesting observation.
In summary, existing lines of evidence indicate that spontaneous or treatment-induced HBsAg seroclearance, albeit rare, does occur in chronic hepatitis B patients. The better prognosis of earlier HBsAg seroclearance is likely caused by less HBV replication as well as less liver damage. To provoke more and earlier HBsAg seroclearance in HBV carriers, a better understanding of the mechanisms involved in HBsAg seroclearance is required.
TAI–CHUNG TSENG
Division of Hepatogastroenterology
Department of Internal Medicine
Buddhist Tzu Chi General Hospital Taipei Branch
Taipei, Taiwan
JIA–HORNG KAO
Division of Gastroenterology
Department of Internal Medicine and
Graduate Institute of Clinical Medicine and
Hepatitis Research Center, and
Department of Medical Research
National Taiwan University College of Medicine and
National Taiwan University Hospital
Taipei, Taiwan
1. Yuen MF, Wong DK, Fung J, et al. HBsAg Seroclearance in chronic hepatitis B in Asian patients: replicative level and risk of hepatocellular carcinoma. Gastroenterology 2008;135:1192–1199.
2. Kao JH, Chen DS. Universal hepatitis B vaccination: killing 2 birds with 1 stone. Am J Med 2008;121:1029–1031.
3. Lok AS, McMahon BJ. Chronic hepatitis B. Hepatology 2007;45:507–539.
4. Kao JH, Chen DS. Global control of hepatitis B virus infection. Lancet Infect Dis 2002;2:395–403.
5. Liaw YF, Sheen IS, Chen TJ, et al. Incidence, determinants and significance of delayed clearance of serum HBsAg in chronic hepatitis B virus infection: a prospective study. Hepatology 1991;13: 627–631.
6. Hsu HY, Chang MH, Lee CY, et al. Spontaneous loss of HBsAg in children with chronic hepatitis B virus infection. Hepatology 1992; 15:382–386.
7. Chu CM, Liaw YF. HBsAg seroclearance in asymptomatic carriers of high endemic areas: appreciably high rates during a long-term follow-up. Hepatology 2007;45:1187–1192.
8. Block TM, Guo H, Guo JT. Molecular virology of hepatitis B virus for clinicians. Clin Liver Dis 2007;11:685–706.


Reply. We would like to thank Tseng and Kao for their interest in our study.1 The following are our responses to their comments. Our study was primarily aimed at examining various virologic and histologic aspects as well as clinical events for chronic hepatitis B patients with hepatitis B surface antigen (HBsAg) seroclearance. Therefore, we did not mention the size of the study population to estimate the incidence of this event. This supplementary information was mentioned in our reply to another letter to editor submitted by Chu and Liaw.2 In brief, the total number of patients followed during the study period of 26 years is 8690. The estimated annual incidence for HBsAg seroclearance is 0.13%. This is comparable with previous published data.3,4

[ 本帖最后由 liver_GZ 于 2010-2-3 23:14 编辑 ]

liver_GZ

不好意思,回复晚了.
答案应该在上面的文章里了.

HBsAg血清转阴率,年发生率0.13%-1.15%.
发生越早越好(HBsAg Seroclearance: The More and Earlier, the Better ).50岁以后,获益相对受限.

楼上已经HBsAg转阴，发生时间应该是20岁左右；发生时已存在一定的慢性肝损改变。

今后如何进展：
存在的肝损，或许会有缓慢进展，因为cccDNA可能无法彻底清除；但不需有太大顾虑，HCC发生风险已经大为降低。定期复查即可：AFP和影像学检查。

至于“血管瘤”的怀疑，如有顾虑，可行MRI检查。

亥猪

原帖由 liver_GZ 于 2010-2-3 23:27 发表
不好意思,回复晚了.
答案应该在上面的文章里了.

HBsAg血清转阴率,年发生率0.13%-1.15%.
发生越早越好(HBsAg Seroclearance: The More and Earlier, the Better ).50岁以后,获益相对受限.

楼上已经HBsAg转阴，发生时 ...

谢谢GZ老师的分析，
我这样理解：母婴传播，20岁发病时，清除了大部分的病毒，但没有完全清除病毒，HBSAG转阴，但HBSAB10年以后才出现，在这10年里持续造成肝损害，最终形成肝硬化（早期），HBSAB出现以后，血液中病毒可能不存在复制的可能，但肝硬化一启动就无法停止，所以现在出现肝硬化结节；由于肝细胞中存在HBV的CCCDNA，并且出现了大的肝硬化结节，所以无法阻止日后可能出现肝癌的可能。
GZ老师，我这样的理解对吗？
另外，通过我乙肝五项进口酶标定量和DNA检查，能排除HBV没有发生S区变异吗？我很担心变异，这会对我的家人造成危害

王震宇

我的看法
1.你没什么病，别整天倒腾你那肝了
2.不像是肝癌，也没肝硬化
3.别纠结了，干活---挣钱去！

亥猪

原帖由 王震宇 于 2010-2-18 00:08 发表 我的看法1.你没什么病，别整天倒腾你那肝了2.不像是肝癌，也没肝硬化3.别纠结了，干活---挣钱去！

谢谢王大夫，也谢谢每个给我看过大夫！我可能还得纠结，我要每三月检查一次，如果结节大过1cm，我就作手术