Objective:To explore the correlation between hepatitis B virus e antigen(HBeAg) and hepatocellular carcinoma(HCC) in residents of Qidong — a high-risk area of HCC in Jiangsu Province,China.Methods:This study included 807 hepatitis B virus surface antigen(HBsAg) carriers and 761 age-and gender-matched HBsAg(-) controls enrolled in a prospective cohort in Qidong during 1992.The relationship between the occurrence of HCC and HBsAg was analyzed during the follow-up period from May 1992 to March 2010.Results:A total of 24 715 person-years(PY) was observed.Of 807 cases in HBsAg-positive group,156 cases had developed HCC,and the incidence rate of HCC was 1 288.83/100 000 PY;while in HBsAg-negative group,9 of 761 cases had developed HCC,and the incidence rate of HCC was 71.37/100 000 PY.The relative risks(RRs) of HCC were 13.25(95% confidence interval:6.67-26.33;P0.001) and 28.05(95% confidence interval:13.87-56.73;P0.001) in HBsAg(+) /HBeAg(-) group and HBsAg(+) /HBeAg(+) group,respectively.In the HBsAg(+) group,the RRs for HCC of the four subgroups(HBeAg titer24,1:24-1:27,1:28-1:212,and212) were 2.55(95% confidence interval:1.54-4.22;P0.001),5.02(95% confidence interval:2.89-8.73;P0.001),1.71(95% confidence interval:0.91-3.18;P0.05),and 1.19(95% confidence interval:0.64-2.23;P0.05) folds higher than that of HBeAg(-) subgroup,respectively.Conclusion:HBeAg is an essential predictive factor for the development of HCC.The patients with low titers of HBeAg are at a high-risk of HCC.

Objective:To study the relationship between hepatitis B surface antigen(HBsAg) and the primary liver cancer (PLC).Methods:A 20-year prospective follow-up study was performed continuously in Qidong on a cohort of 515 HBsAg positive male patients aged 20-60 years old.The markers of hepatitis B virus,HBsAg,HBsAb,HBeAg,HBeAb and HBcAb (HBVM 1,2,3,4,5) were detected at the first time of the follow-up.Results:The PLC incidence of the whole cohort was 1 340.90/100 000 person years(PY).The middle age of the PLC diagnosis was 43 with an average survival of 15 months.The PLC incidence was significantly higher in 41-50 age group than that of other age groups(P 0.05).The three major HBVM patterns were 15,135 and 145 in the cohort with percentages of 38.83%(200/515),15.92%(82/515)and 44.08%(227/515) respectively.The PLC incidences of these three patterns were 1 433.69/100 000 PY,2 284.71/100 000 PY,984.10/100 000 PY respectively,showing a significant difference between 135 and 145 (P 0.01).The percentages of 15,135 and 145 were 39.64%(44/111),23.42%(26/111) and 35.14%(39/111) in PLC patients respectively,showing a significant difference between 15 and 135 (P 0.01).The liver cirrhosis mortality of those three patterns were 195.50/100 000 PY,966.61/100 000 PY and 277.57/100 000 PY respectively,showing the significant differences between 135 and other two patterns (P 0.01).Conclusion:HBsAg carriers were high risk population of PLC.The regular following-up is helpful on early diagnosis and treatment of PLC in those people,and can prolong the survival time.It was found that 135 had higher PLC risk than other HBVM patterns,suggesting a relationship between HBV duplication and PLC.The anti-virus treatment may delay or remove the occurring of PLC.

Residents of Qidong, People's Republic of China, are at high risk for development of hepatocellular carcinoma, in part from consumption of foods contaminated with aflatoxins. Chlorophyllin, a mixture of semisynthetic, water-soluble derivatives of chlorophyll that is used as a food colorant and over-the-counter medicine, has been shown to be an effective inhibitor of aflatoxin hepatocarcinogenesis in animal models by blocking carcinogen bioavailability. In a randomized, double-blind, placebo-controlled chemoprevention trial, we tested whether chlorophyllin could alter the disposition of aflatoxin. One hundred and eighty healthy adults from Qidong were randomly assigned to ingest 100 mg of chlorophyllin or a placebo three times a day for 4 months. The primary endpoint was modulation of levels of aflatoxin-N(7)-guanine adducts in urine samples collected 3 months into the intervention measured by using sequential immunoaffinity chromatography and liquid chromatography-electrospray mass spectrometry. This aflatoxin-DNA adduct excretion product serves as a biomarker of the biologically effective dose of aflatoxin, and elevated levels are associated with increased risk of liver cancer. Adherence to the study protocol was outstanding, and no adverse events were reported. Aflatoxin-N(7)-guanine could be detected in 105 of 169 available samples. Chlorophyllin consumption at each meal led to an overall 55% reduction (P = 0.036) in median urinary levels of this aflatoxin biomarker compared with those taking placebo. Thus, prophylactic interventions with chlorophyllin or supplementation of diets with foods rich in chlorophylls may represent practical means to prevent the development of hepatocellular carcinoma or other environmentally induced cancers.

We followed 145 men with chronic hepatitis B virus (HBV) hepatitis for 10 years to determine whether exposure to aflatoxin, or concomitant exposure to hepatitis C virus (HCV), or family history of hepatocellular carcinoma (HCC) increased the risk of developing HCC. We collected 8 monthly urine samples before beginning follow-up and pooled them to detect aflatoxin metabolite M1 (AFM1). AFM1 was detected in 78 (54%) of the subjects. The risk of HCC was increased 3.3-fold (with a 95% confidence interval of 1.2-8.7) in those with detectable AFM1 (above 3.6 ng/L). This relative risk was adjusted for age and for HCV status. The attributable risk from exposure to detectable AFM1 was 0.553 (0.087, 0.94). The relative risk of fatal cirrhosis for those with elevated AFM1 was 2.8 (0.6, 14.3), and the odds of having a persistently elevated alanine transaminase (ALT) were 2.5-fold greater in those with detectable AFM1 (P =.007). Concomitant infection with HCV increased the risk of HCC 5.8-fold (2. 0-17), adjusted for age and AFM1 status. A family history of HCC increased the risk of HCC 5.6-fold, adjusted for age and AFM1. Four men with detectable AFM1 and HCC all had missense mutation in codon 249 of the p53 gene in cancer tissues. This study shows that exposure to AFM1 can account for a substantial part of the risk of HCC in men with chronic HBV hepatitis and adds importantly to the evidence that HCV and family history of HCC increase the risk of HCC in men with chronic HBV hepatitis.

A prospective study on consuming population from selenium-salt (Se-salt) in Qidong jJiangsu high primary liver cancer (PLC) prevalent area was reported The results of 6-year observation showed that there was a rising serum Se level in these people. The incidence of PLC decreased gradually, from 52.84 /105 in 1984 to 34.49/105 in 1990 . in contrast to the stable high incidence rate of PLC in the controlled group. It suggested that ingesting Se in small anount may prevent PLC. In addition, the incidence of hepatits i in foe population consuming Se-salt was significantly less than that in controlled group when viral hepatitis prevailed in Qidong in 1987. It was shown that Se may prevent PLC and viral hepatitis. It is a cheep seasoning with a simple productive technque and can be extensively used in a Se-low area.