Zhonghua yi xue za zhi · 1998
[Hepatitis B virus infection and aflatoxin exposure in the development of primary liver cancer].
Аннотация на английскомСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Lu P, Kuang S, Wang J
Аннотация
OBJECTIVE: To investigate the role of hepatitis B Virus (HBV) infection and aflatoxin (AF) exposure in the development of primary liver cancer (PLC).
METHODS: A 10-year prospective case-control study was carried out in 737 HBsAg carriers and 699 HBsAg negative cases, and the aflatoxin B1 albumin adducts (AFB1-Alb) were detected in the serum of the cohort including 30 HBsAg postive cases and 150 control individuals according to the case-control study model (ratio 1:5) at random in the high prevalance area of PLC.
RESULTS: The average year-incidence rate was significantly higher in the HBsAg postive group (824.13/100,000) than in the control group (70.97/100,000, RR = 11.61). There was no significant difference in the incidence rate of other tumors between the two groups (P > 0.05). The serum positive rate of AFB1-Alb was significantly higher in the PLC group (76.67%) than in the control group (48.67%, OR = 3.47), and the serum concentration of AFB1-Alb was also significantly higher in the PLC group than in the control group (P < 0.01).
CONCLUSION: HBV infection and AF exposure are important etiological factors in the development of PLC and both result in carcinogenic synergy.
METHODS: A 10-year prospective case-control study was carried out in 737 HBsAg carriers and 699 HBsAg negative cases, and the aflatoxin B1 albumin adducts (AFB1-Alb) were detected in the serum of the cohort including 30 HBsAg postive cases and 150 control individuals according to the case-control study model (ratio 1:5) at random in the high prevalance area of PLC.
RESULTS: The average year-incidence rate was significantly higher in the HBsAg postive group (824.13/100,000) than in the control group (70.97/100,000, RR = 11.61). There was no significant difference in the incidence rate of other tumors between the two groups (P > 0.05). The serum positive rate of AFB1-Alb was significantly higher in the PLC group (76.67%) than in the control group (48.67%, OR = 3.47), and the serum concentration of AFB1-Alb was also significantly higher in the PLC group than in the control group (P < 0.01).
CONCLUSION: HBV infection and AF exposure are important etiological factors in the development of PLC and both result in carcinogenic synergy.