Hepatitis B virus infection and primary hepatocellular carcinoma.

Ninety-three patients with biopsy-proven primary hepatocellular carcinoma (PHC) from Uganda, Zambia, and the United States were examined for serologic evidence of hepatitis B virus (HBV) infection. Patients were tested for hepatitis B surface antigen (HBsAg) and its antibody (anti-HBs), antibody to the hepatitis B core antigen (anti-HBc), hepatitis B e antigen (HBeAg), and its antibody (anti-HBe). Active HBV infection, as indicated by positive tests for HBsAg (with or without anti-HBs) and anti-HBc (without anti-HBs), was present in 62% of PHC patients (58 of 93), in contrast with 10% of African controls (9 of 90), and less than 1% of most United States adult populations reported in the literature. The presence of HBeAg or anti-HBe was rare among PHC patients and controls.     

乙肝病毒前S1抗原检测在乙型肝炎向肝癌演变中的临床意义

目的探讨前S1抗原与原发性肝癌（PHC）的关系。方法采用ELISA法检测302例PHC患者的血清学乙肝病毒标志物（HBVM）及前S1抗原。结果302例PHC患者，HBVM检出率为99．0％（299／302）。其中单项阳性率HBsAg94．0％（284／302）、AntiHBs5．6％（17／302）、HBeAg20．2％（61／302）、AntiHBe72．8％（220／302）、AntiHBc97．4％（294／302）。61例HBeAg阳性样本中前S1抗原阳性46例（75．4％）；而196例HBeAg阴性AntiHBe阳性标本中前S1抗原阳性98例（50．0％）；而35例HBeAg和AntiHBe均阴性标本中前S1抗原阳性10例（26．3％）。前S1抗原在血清学表达上与HBeAg的阳性符合率高达75．4％。结论血清前S1抗原是乙型肝炎病毒（HBV）在体内复制的可靠标志，通过检测血清前S1抗原有助于提高认识PHC发生的可能性。     

Hepatitis B viral markers in patients with primary hepatocellular carcinoma in Taiwan

The presence of hepatitis B viral markers in patients with primary hepatocellular carcinoma (PHC) was studied retrospectively at the Taiwan Veterans General Hospital in Taipei, Taiwan. Serum samples from 102 PHC patients and from 100 control individuals were tested for hepatitis B surface antigen (HBsAg), antibody to HBsAg (anti-HBs), antibody to hepatitis B core antigen (anti-HBc), hepatitis Be antigen (HBeAg), and antibody to HBeAg (anti-HBe). Of the 102 PHC patients, 72 (71%) were positive for HBsAg. Nine (9%) additional patients were positive for anti-HBc alone in high titer, 19 (19%) had both anti-HBc and anti-HBs, and 9 (9%) had HBsAg, anti-HBc, and anti-HBs. In the 100 controls, 12 (12%) were HBsAg-positive, whereas 22 (22%) had anti-HBc alone and 50 (50%) had both anti-HBc and anti-HBs. Only 4 (4%) controls and no PHC patients had anti-HBs alone. Of the HBsAg-positive patients with PHC, 17 (29%) had HBeAg and 36 (61%) had anti-HBe. The alpha-fetoprotein (AFP) levels above 400 ng/ml were found in 44% of the PHC patients. Values of AFP above 1 x 10(5) ng/ml were more frequently detected in PHC patients who were HBsAg-positive. Categorization of the geographic origins of the families whose members had PHC revealed that most families had originated from southern China. This study confirms that hepatitis B viral markers are frequently present in Chinese patients with PHC.     

Hepatitis B virus markers in Chinese twins

Chinese same-sex twins were recruited in order to study the distribution of different markers of hepatitis B virus (HBV) infection, including HBV surface antigen (HBsAg), antibody to HBV core antigen (anti-HBc), antibody to HBsAg (anti-HBs), HBV e antigen (HBeAg) and antibody to HBeAg (Anti-HBe), as well as to compare the concordance of these markers in pair-wise fashion among monozygotic (MZ) and dizygotic (DZ) twins and singleton controls. A total of 289 pairs of MZ twins, 102 pairs of DZ twins and 375 pairs of age-sex-matched singleton controls were studied. More than 50 percent of the members of each group (64.71% of MZ twins, 51.96% of DZ twins and 62.13% of controls) were found to be infected with HBV. In general, the patterns of the response to HBV infection in the 3 groups were similarly distributed. 20.17% of the members of the 3 groups (21.45% of MZ twins, 14.22% of DZ twins, and 20.80% of controls) were HBsAg carriers. Among the HBsAg carriers, 49.19% (44.35% of MZ twins, 34.48% of DZ twins and 55.77% of controls) were HBeAg carriers. No significant difference in the concordance of HBV infection was observed in the MZ and DZ twins. However, highly significant differences were noted between MZ twins and controls, and between DZ twins and controls. Highly significant differences were also observed in the concordance of carrier status between MZ and DZ twins and between MZ twins and controls, but not between DZ and controls. As for the other HBV markers, no significant differences were observed. It is concluded that the genetic influence in response to HBV infection markers is not well-characterized and requires further study.     

Evidence for clustering of hepatitis B virus infection in families of patients with primary hepatocellular carcinoma.

Family member of 13 patients with hepatitis B surface antigen (HBsAg) positive primary hepatocellular carcinoma (PHC) were tested for the presence of hepatitis B virus-associated antigens and antibodies. Of the 122 members examined, circulating HGsAg was detected in 47 (39%), antibody to HBsAg (anti-HBs) was found in 37 (30%), and antibody to hepatitis B core antigen (anti-HBc) alone was present in 13 (11%). The relatives with the highest frequency of HBsAg positivity were the offspring of the propositus, followed by the nieces and nephews and the grandchildren. Anti-HBs and anti-HBc were detected most often in the spouses and non-blood relatives. Evidence for past and present hepatitis B virus (HBV) infection was more frequently found in the Asian family members when compared to the non-Asians. The e antigen (HBeAg) was present in 38% of the HBsAg positive individuals, including four with PHC; antibody to HBcAg (anti-HBe) was rarely detected. These results indicate that clustering of HBV infection was commonly present in family members of patients with PHC. The HBsAg positive individuals may be major contributors to the endemic pool of the virus, and may themselves be potential cases of chronic active type B hepatitis, cirrhosis, and PHC.     

Association of hepatitis B virus infection with hepatocellular carcinoma in American patients

Thirty-four patients from the Philadelphia area with hepatocellular carcinoma (HCC) were matched with colon cancer patients, lung cancer patients and blood donors according to age and sex. Sera from the four groups were tested to determine the prevalence of hepatitis B surface antigen (HBsAg), antibody to HBsAg (anti-HBs), and antibody to hepatitis B core antigen (anti-HBc). Five of the HCC patients (14.7%) and none of the controls were positive for HBsAg. At least one of the three serologic markers of hepatitis B virus (HBV) infection was found in 51.5% of the HCC patients, 5.3% of the colon cancer patients, 11.1% of the lung cancer patients, and 10.7% of the blood donors. Twelve of the seventeen seropositive HCC patients (70.6%) were positive for anti-HBc alone, while all of the seropositive lung cancer patients and donors were positive for anti-HBs alone. Sera positive for any HBV marker were also tested for e antigen (HBeAg) and its antibody (anti-HBe). Four of the HCC patients (23.5% of the seropositives) had anti-HBe, while none of the sera tested had HBeAg. A history of alcoholism did not appear to influence HBV seropositivity in the HCC patients. This study supports the hypothesis that HBV infection is closely associated with HCC even in areas where both conditions are uncommon. The wide disparity between seropositivity for HBsAg and anti-HBc in the HCC patients is an unusual feature, for which an age effect may be the best explanation.     

A case-control study of primary hepatocellular carcinoma in Taiwan

A case-control study was carried out to explore possible risk factors of primary hepatocellular carcinoma (PHC) in Taiwan. One hundred thirty-one PHC patients and 207 hospital control patients were interviewed and blood samples were collected for blood type and hepatitis B virus (HBV) infection marker tests. Eighty-three percent of the PHC patients were found to be hepatitis B surface antigen (HBsAg) positive as compared with 21.0% of the control patients with an odds ratio (OR) of 21.5. Hepatitis B e antigen (HBeAg) positive status increased the risk of PHC. No significant association was observed between erythrocyte genetic markers and PHC, except c of the Rh system, which was significantly lower in the PHC cases. As compared with the control patients, the PHC patients had a higher proportion with a history of liver diseases and more siblings affected with liver diseases. However, the variables such as cigarette smoking, alcohol drinking, peanut consumption, frequent intake of raw fish, heart diseases, peptic ulcer, malaria, hypertension, diabetes, color blindness, G-6-PD deficiency, surgical operation, blood transfusion, and liver diseases of parents and children were not found to be associated with PHC.     

Hepatitis B virus and primary hepatocellular carcinoma: Family studies in Korea

Chronic infection with hepatitis B virus (HBV) is closely associated with the etio-pathogenesis of primary hepatocellular carcinoma (PHC). It has been proposed that infection with HBV early in life, frequently transmited by an HBV-carrier mother, leads to persistent infection with HBV, which in turn is associated with the development of chronic active hepatitis (CAH), post-necrotic cirrhosis and PHC. If this view is correct, then there should be clustering of chronic carriers of HBV in families of patients with chronic liver disease. We tested this hypothesis in Korea by collecting serum from 132 patients with these chronic liver diseases admitted to the Seoul National University Hospital and 664 of their first-degree relatives. Controls (636) were members of two churches in Seoul and a rural village population; 261 of the controls were between the ages of 30 and 59, the age range that included 95% of the cases of chronic liver disease. Sera were assayed for hepatitis B surface antigen (HBsAg), antibody to HBsAg (anti-HBs) and antibody to hepatitis B core antigen (anti-HBc). Almost all cases showed evidence of present or past infection with HBV; 80% were HBsAg(+) and 14% were anti-HBs(+); 100% of 47 cases of PHC, 100% of 35 cases of cirrhosis, and 94% of 50 cases of CAH were anti-HBc(+); 6% of males and 4% of females in the control population (30–59 years of age) were HBsAg(+), 71% were anti-HBc(+), and 51% were anti-HBs(+), HBsAg(+) patients with chronic liver disease tended to be younger than HBsAg(?) patients with anti-HBs or anti-HBc antibodies. Mothers of patients were more frequently HBsAg(+) (9 of 33) than agematched women in the control population (0 of 34) or wives of patients (5 of 68). Five of 23 fathers were also HBsAg(+) compared with 1 of 25 age-matched controls. As first observed in Africa, there was a deficit of anti-HBs in the fathers of cases compared with the controls. Siblings of patients were frequently HBsAg(+) (45% of 154), with the highest prevalence in brothers (53%). Family history shows that five fathers, two mothers and five brothers of cases have died of PHC. These data are compatible with the hypothesis tested and lend further support to the view that prevention of infection with HBV will lead to a marked decrease in the incidence of CAH, cirrhosis and PHC in areas where these diseases are endemic. Members of the families of patients with these diseases are at high risk of developing persistent infection with HBV and chronic liver disease. It would be appropriate to focus preventive strategies on infants and children in such families.     

乙型肝炎病毒e抗体检测在原发性肝癌中的临床意义

本文报告119例PHC和非肝脏恶性肿瘤和肝良性占位变82例血清HBV感染结果。表明在PH-C和其他疾病的HBV感染标志的阳性率分别是:e抗体60.5％和24.4％,HBsAg63.0％和17.1％,抗HBc为78.2％和24.4％,抗HBs 5％和14.6％,HBeAg11.8％和8.5％,HBV总暴露率91.6％和32.9％,其中e抗体,抗HBc,HBV总暴露率PHC组显著地高于对照组。抗HBs则相反。资料表明e抗体阳性率随病情的进展,肿块的增大而增高。提示e抗体的存在与癌细胞的增殖,肝细胞的癌变有关。它作为HBV感染标志之一应予重视。     

Epidemiologic assessment of interactions of hepatitis-C virus with seromarkers of hepatitis-B and -D viruses, cirrhosis and tobacco smoking in hepatocellular carcinoma.

A recently introduced enzyme immunoassay procedure for antibodies against the hepatitis-C virus (HCV) was used to test samples from 185 cases with hepatocellular carcinoma (HCC) and 432 hospital controls. The anti-HCV results were examined in conjunction with previously reported data from this study concerning hepatitis-B virus (HBV) serology, hepatitis-D virus (HDV) antibodies, presence of cirrhosis and tobacco smoking. There was evidence for interaction between HBV and HCV in the causation of HCC: as previously reported, the rate ratio (RR) linking the presence of anti-HCV to HCC among subjects positive for hepatitis-B surface antigen (HBsAg) was substantially higher than the corresponding RR among those negative for this marker; furthermore, among HCC patients positive for HBsAg, a high proportion (33/61) of those who were positive for hepatitis-Be antigen (HBeAg) or its antibody were positive for anti-HCV, whereas among HBsAg-positive controls who were also positive for HBeAg or its antibody, none was positive for anti-HCV (0/18; p less than 10(-4)). The anti-HCV-related RR for HCC was also higher among HCC patients with cirrhosis than among those without evidence of co-existing cirrhosis (RR 11.4 vs. 4.4; p = 0.06). In addition, there was some evidence of interaction between tobacco smoking and HCV in the origin of HCC; after controlling for age, sex and HBsAg status, the RR for subjects positive for anti-HCV was 6.8 among smokers but only 3.2 among non-smokers (p = 0.26). By contrast, there was no suggestion of an interaction between anti-HCV and anti-HDV, in agreement with the presumed minimal role, if any, of HDV in HCC etiology. These results support the notion that HCV is involved in the etiology of HCC by advancing, through a chronic liver disease process, carcinogenesis initiated by other factors.     

Hepatitis B virus serological markers in Africans with liver cirrhosis and hepatocellular carcinoma

Serum samples were collected at the time of hospitalization from 221 black Africans suffering from cirrhosis and 453 suffering from hepatocellular carcinoma (HCC). These patients came from Senegal, Burundi and Mali, and 6655 adults from different population groups in these countries were used as controls. Hepatitis B virus (HBV) serum markers, including hepatitis B surface antigen (HBsAg), anti-HBs, antibody to hepatitis B core antigen (anti-HBc), HBeAg and anti-HBe, were determined by radioimmunoassay, while alpha-fetoprotein and complexes between HBsAg and IgM were detected by ELISA tests. HBsAg was detected in 11.8-17.6% of controls as opposed to 63.3% of patients suffering from cirrhosis and 62.7% of patients suffering from HCC. There was less evidence for HBV replication in cirrhosis and HCC in older patients. A significant increase in the frequency of HBsAg/IgM complexes was found in passing from the HBsAg chronic carrier state (13.9%) to cirrhosis (29.9%) and finally to HCC (33.7%).     

乙肝病毒相关的肝癌p16异常甲基化

Objective： To investigate the potential linkage between high rate of p16 methylation and hepatitis B virus （HBV） infection, methylation status of p16, HBV infection markers in serum and HBV-DNA replication level in cancerous and non-cancerous tissue of 32 cases of hepatocellular carcinomas （HCC） with HBV infection and 12 HCCs without HBV infection were examined. Methods： p16 methylation was detected with methylation-specific polymerase Chain reaction （PCR）, and HBV markers were examined with real-time PCR and immunologic method. Results： Methylation of p16 promoter was found in 31 （70.5%） of 44 cancerous tissues of HCC, 2 （16.7%） of 12 HCC without HBV infection, 29 （90.6%） of 32 HCCs with HBV infection marker, p16 methylation was detected in 5 （83.3%） of 6 HCCs positive for HBsAg and HBeAg, 17 （94.4%） of 18 HCCs positive for HBsAg and negative for HBeAg, 7/8 （87.5%） of HCCs positive for other HBV infection markers, such as HBsAB, HBcAb, HBeAb. p16 methylation products were also found in non-cancerous tissues of 4 cases of HCCs with HBV infection, not detected in non-cancerous tissues without HBV infection. HBV-DNA was detected in cancerous tissues of 29/32 （90%） HCCs with HBV infection. Surprisingly, Methylation product of p16 promoter was found in all cases （29/29） of HCCs with detectable HBV-DNA in neoplastic tissue. Conclusion： Persistent HBV infection may promote p16 hypermethylation, suggesting that HBV, via enhancing the aberrant methylation of p16, indirectly involved in development of HCC.     

Delta agent and the etiology of hepatocellular carcinoma

Sera from 87 patients with hepatitis B surface antigen (HBsAg)-positive hepatocellular carcinoma (HCC) and from 29 HBsAg-positive hospital controls were tested for delta (delta) antigen with an immunoenzymatic procedure and for anti-delta antibody, hepatitis Be antigen (HBeAg) and antibody to HBeAg (anti-HBe) by radioimmunoassay. All the sera, from both the HCC cases and the control patients, were negative for delta-antigen. Among the HCC cases 9 were positive for serum anti-delta (10%) whereas among the controls none was positive for this antibody (p = 0.067); the anti-delta-positive cases were found only among HCC patients negative for HBeAg. The lower prevalence of anti-delta among HBsAg-positive HCC patients, as compared to the corresponding prevalence among HBsAg-positive patients with chronic active hepatitis or cirrhosis (reported in the literature) indicates that the pathogenesis of HCC is frequently independent of the pathogenesis of the other HBsAg-positive common chronic liver diseases. By contrast, the higher prevalence of anti-delta among HBsAg-positive HCC cases than among HBsAg-positive controls may reflect the longer average duration of the carrier state in HCC patients (until integration is accomplished and the induction period completed). Serum HBeAg was higher among HBsAg-positive HCC patients with cirrhosis (23%) than among HBsAg-positive HCC patients without cirrhosis (6%) or HBsAg-positive controls (3%); thus, the conflicting results in the literature concerning the association of the HBeAg/anti-HBe system with HCC may be accounted for, in part, by the variable association of HCC with an underlying cirrhosis.     

Hepatitis B virus infection status is an independent risk factor for multiple myeloma patients after autologous hematopoietic stem cell transplantation

The purposes of this study were to evaluate the infection by hepatitis B virus (HBV) and its impact on survival and to provide a clinical reference for monitoring and treating HBV during and after autologous hematopoietic stem cell transplantation (ASCT) in patients with multiple myeloma (MM). A retrospective analysis of HBV infections was performed in 70 MM patients who received a sequential bortezomib-containing induction therapy and ASCT in our department from June 2006 to February 2012. Among the 70 patients in our study, 11 cases (15.7 %) were hepatitis B surface antigen positive (HBsAg+), and 23 cases (33.3 %) were hepatitis B core antibody positive (HBcAb+). Eight cases were HBsAg, hepatitis B e antibody (HBeAb), and HBcAb positive, while one case was HBsAg, hepatitis B e antigen (HBeAg), and HBcAb positive. The median follow-up times for the HBsAg+ group and the HBsAg-negative (HBsAg?) group were 27.0 (7.6–85.2) months and 28.7 (7.1–111.0) months, respectively. The 1-year, 2-year, and 3-year overall survival rates of the HBsAg+ group were 90.9, 80.8, and 34.6 %, respectively, and the median survival time was 31.2 months (95 % CI, 24.8–37.6). The 1-year, 2-year, and 3-year overall survival rates of the HBsAg? group were 98.2, 94, and 84.6 %, respectively, while the median survival time was not yet available. There was a statistically significant difference (p?=?0.008) in the overall survival rate between the two groups. By Cox regression analysis, we found that the HBsAg+ status was a prognostic factor, which could independently influence the overall survival rate for ASCT. In conclusion, the HBsAg+ status is an independent risk factor for patients with MM receiving ASCT. The application of standard antiviral treatment might help to overcome this risk factor.     

青少年原发性肝癌与乙型和丙型肝炎病毒感染的相关性分析

目的探讨青少年原发性肝癌(PHC)患者中乙型肝炎病毒(HBV)、丙型肝炎病毒(HCV)及HBV和HCV混合感染率及其相互关系。方法将50例青少年PHC患者纳入观察组,将同期住院的50例其他肝病患者纳入对照组,检测两组患者血清中HBV、HCV、HBV/HCV标志物阳性率等情况。结果观察组患者血清中HBsAg、抗Hbe和HBV-DNA阳性率均显著高于对照组患者,差异有统计学意义(P<0.05)。两组患者血清中HBeAg阳性率比较,差异无统计学意义(P>0.05)。观察组和对照组患者血清中抗HCV和HCV-RNA阳性率比较,差异无统计学意义(P>0.05);HBV(+)HCV(+)和HBV(+)HCV(-)与青少年PHC发病呈正相关性(P<0.05),HBV(-)HCV(+)与青少年PHC发病无相关性(P>0.05),HBV(-)HCV(-)与青少年PHC发病呈负相关性(P<0.05)。结论 HBV感染与青少年PHC发病有着较强的相关性,属高度危险因素。     

ABO血型与PHC患者HBV感染标记相关性研究

研究伴ＨＢＶ感染的ＰＨＣ４４５例乙型肝炎抗原抗体与ＡＢＯ血型的关系，结果表明：１．伴ＨＢＶ感染的ＰＨＣＡ型血者显著高于对照组（Ｐ＜０．０１）。２．ＰＨＣ患者中ＨＢｓＡｇ、抗－ＨＢｃ的阳性率均以Ａ型血显著高于对照组（Ｐ＜０．０５）。３．ＰＨＣ患者中ＨＢｓＡｇ与抗－ＨＢｃ均阳性模式Ａ型血者显著多于对照组，而Ｂ型血者显著少（Ｐ＜０．０５）；抗－ＨＢｅ与抗ＨＢｃ均阳性的ＰＨＣ中，亦为Ａ型血者显著多（Ｐ＜０．０５）。提示有ＨＢＶ感染的Ａ型血者罹患ＰＨＣ的倾向性最高；而有ＨＢＶＭ、ＨＢｓＡｇ、抗－ＨＢｃ的Ａ型血者则为ＰＨＣ的易感人群，其中以ＨＢｓＡｇ和抗－ＨＢｃ同时阳性或抗－ＨＢｅ和抗－ＨＢｃ同时阳性的感染模式更易发生ＰＨＣ；也提示ＰＨＣ、ＨＢＶ、Ａ型血三者之间存在某种密切的、复杂的联系，对ＰＨＣ的发生有协同作用。对上述人群应密切关注，定期复查，以期早诊早治。     

A profile of primary hepatocellular carcinoma patients in the Gizan Area of Saudi Arabia

Clinical, laboratory, and ultrasonographic features of 75 patients of primary hepatocellular carcinoma (PHC) living in the Gizan Area of Saudi Arabia and their follow-up, during a 2-year period, were characterized. Eighty-nine percent of the cases were defined histologically, whereas in the rest, ultrasonographic (US) evidence along with an alphafetoprotein (AFP) level exceeding 480 ng/ml were taken as the positive evidence for PHC. Eighty percent of the cases were male patients, with the peak incidence during the seventh decade. The most common clinical presentations were hepatic enlargement (91%), abdominal pain (76%), splenic enlargement (33%), and acites (33%), followed by bruit, fever, metastases, and varices. Alteration in a liver function test was manifest in 97% of the cases, AFP values greater than 480 ng/ml in 57%, and a hepatitis B virus surface antigen (HBsAg) positivity in 65% of the cases. There was no intersex variation in positivity for HBsAg, antibody to HBsAg (anti-HBs), antibody to hepatitis B virus core antigen (anti-HBc) among the 30 PHC cases studied. Positivity for HBsAg or the overall hepatitis B virus exposure in PHC cases was higher than the normal controls (P less than 0.001). In addition to histologic confirmation of PHC in 67 cases, there was histologic evidence of cirrhosis in 25%, or chronic active hepatitis in 19% of the cases. At the time of diagnosis, the average duration of the presenting illness was less than 2 months, while the mortality in the ensuing 2-month period was 73%. The average span of total illness in the vast majority of cases was 4 to 6 months. Two female patients (one with fibrolamellar carcinoma) however, survived for 2 years. Immunization against hepatitis B virus should be considered for all newborns in such hyperendemic communities. A continuous program should be started in such communities to screen and immunize all those yet unexposed to hepatitis B virus. The established HBsAg carriers should be periodically examined ultrasonographically along with an AFP estimation for initiating the chemotherapeutic and other measures against PHC in fairly early stages of malignancy.     

异基因造血干细胞移植中供受体乙肝病毒感染的意义

 目的 分析白血病患者移植前供、受者感染乙型肝炎病毒（HBV）对异基因造血干细胞移植（allo-HSCT）临床结果的影响。方法 对该院1996年5月至2005年2月间进行的31例合并HBV感染的HSCT患者临床资料进行回顾性分析。结果 31例受者均达到造血干细胞植活,乙型肝炎指标供者阳性、受者阴性8例,其中1例26个月死于肝硬化,2例在免疫抑制剂停用后,发展为慢性活动性肝炎;乙型肝炎指标供者阴性、受者阳性20例,其中2例乙型肝炎指标转阴,5例获得HBsAb（+）,4例移植后HBcAb转阴及HBeAb转阴,仅HBsAb（+）,1例转为"HBsAg（+）、HBeAg（+）、HBcAb（+）";乙型肝炎指标供者、受者均阳性3例,1例患者并发肝静脉闭塞病（VOD）,1例获得一过性HbsAg（+）,1例获得HbsAb（+）。结论 HBV感染对干细胞植活时间无明显影响;供、受者感染乙肝病毒不是HSCT的绝对禁忌证;HBsAg（+）及HBV滴度是影响移植后乙型肝炎复发的重要因素;HBsAg（+）的患者可作为HbsAb（+）受者的供者,但对HbsAb（-）受者则应慎重;拉米夫定及乙肝免疫球蛋白联合应用较乙肝疫苗单独使用更能有效地控制HBsAg（+）的供受者在移植后的乙型肝炎疾病的进展;HSCT有可能通过过继免疫治疗乙型肝炎。     

HBV、HCV在原发性肝癌发生中的相互作用研究

为了解河南省原发性肝癌（PHC）发生中HBV、HCV的相互作用，我们应用ELISA法和PCR法对PHC患者及其1：1对照进行了HBV标志物（HBVM）和HCV标志物（HCVM）检测。结果：PHC患者HBVM阳性率为81．25％，对照组HBVM阳性率为9．60％，P＜0.01，OR=70（25．36，193．23）；PHC患者HCVM阳性率为19．79%，对照组HCVM阳性率为8.33％，P＜0.05，OR＝2．57（1．11，5．95）；PHC患者HBVM、HCVM双重阳性率为18．75％，对照组双重阳性率为1.04％，将HBVM和（或）HCVM阳性看成不同的暴露等级与HBVM和HCVM均阴性组进行比较，得到HBV和HCV双重感染时的OR值为83.65，明显高于两者分别感染的OR值（34．85和1．58）之积。结果提示：HBV、HCV在PHC的发生中有显著的病因协同作用。     

Hepatitis B virus infection in southern African blacks with hepatocellular cancer.

The association between hepatitis B virus (HBV) infection and hepatocellular cancer (HCC) in southern African blacks was investigated by examination of patients' sera for all the currently known markers of HBV. Hepatitis B surface antigen (HBsAg) was present in the sera of 61.6% (178/289) of the patients compared with only 11.3% (24/213) of age-matched, sex-matched, and ethnically matched controls (P less than 0.001). Antibody against HBsAg was found in 17% of the patients and 41.7% of the controls (P less than 0.001). In 74 patients studied in more detail, antibody against the hepatitis B core antigen (anti-HBc) was detected in 89%, almost always in high or moderately high titer. Anti-HBc was found in 37.5% of the controls. Active HBV infection, as indicated by positive tests for HBsAg or anti-HBc, was present in 91% of the patients compared with 39.4% of the controls (P less than 0.001). Hepatitis B e-antigen was detected in 2.3% and its specific antibody in 20.5% of the patients. The corresponding figures in the controls were 0 and 55%. HBs antigenemia was more common in younger patients with HCC. No relationship was demonstrated between alpha-fetoprotein and HBs antigenemia. HBV infection was equally common in patients with and without cirrhosis in the nontumorous liver.