In a case-control study, 62 Somali patients with chronic liver disease (CLD) including primary hepatocellular carcinoma (HCC) and the same number of age and sex matched controls were investigated for serological markers of hepatitis C virus (HCV) and hepatitis B virus (HBV) infections. Antibody to HCV (anti-HCV) was detected in 40.3% and 6.5% of cases and controls, respectively. The corresponding prevalences of hepatitis B surface antigen (HBsAg) were 37.1% and 9.7%, respectively. Of the HBsAg-positive cases, 34.6% had antibodies to hepatitis D virus (anti-HD) compared with 14.3% among the HBsAg-positive controls. Anti-HCV was less prevalent in HBsAg-positive cases than among HBsAg-negative patients (p < 0.001), indicating that these agents were independent causes of CLD/HCC. The odds ratios for patients with CLD/HCC associated with the presence of anti-HCV, anti-HD, HBsAg without anti-HD and anti-HCV, were found to be 9.8, 10.4, and 3.3, respectively. When the patients were divided into tumour and non-tumour cases, using the criteria of serum alpha-fetoprotein > 100 ng/ml and/or solid hepatic lesions detected by ultrasonography, they did not differ with regard to frequencies of HBsAg and/or anti-HCV, although they did differ when these markers were taken together (43/49 versus 5/13, respectively). The mean age of the tumour patients with anti-HCV alone was significantly higher than that of tumour patients with HBsAg as the sole marker, 61.7 versus 31.4 years (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Somatic cell hybrids between normal mouse cells and simian virus 40 (SV40)-transformed human cells, which contained a diploid complement of mouse chromosomes and the human chromosome 7 carrying the genome of SV40, were tumorigenic in nude mice. One single copy of human chromosome 7 per hybrid cell appeared to be sufficient for the tumorigenicity of the hybrids.
Chronic liver disease (CLD) is frequent in Somalia. In a case-control study, 116 in-patients with CLD were compared with the same number of age and sex matched controls. Demographic variables, use of drugs, symptoms and signs, serological markers for hepatitis B virus (HBV) and serum alpha-foetoprotein (AFP) were assessed. Hepatitis B surface antigen (HBsAg) was found in 44 cases of which 17 had antibodies to hepatitis D virus (anti-HD) and 7 had hepatitis B e antigen (HBeAg). Twenty-three controls were HBsAg-positive, of whom 3 had anti-HD and one HBeAg. Increased relative risks (95% confidence intervals in parentheses) were 2.5 (1.3-4.5) for HBsAg, 6.5 (1.7-21.5) for anti-HD, and 7.4 (0.9-66.5) for HBeAg. Despite the association between the presence of HBV markers and CLD, 62% of the cases had no markers indicating current HBV infection. This was reflected in the low risk attributable to chronic HBV infection (22.6%), which was lower than that in patients with CLD in other African populations with a high HBsAg carrier rate. The prevalence of HBV markers did not differ between cases with AFP greater than 100 ng/ml and those with AFP less than 100 ng/ml. The former were characterized by male predominance, shorter duration of symptoms, and larger mean liver size, indicative of malignancy. The mean age of HBsAg-positive cases with AFP greater than 100 ng/ml was significantly lower (by 7.7 years) than that of HBsAg-negative cases with AFP greater than 100 ng/ml. Among the CLD patients with AFP less than 100 ng/ml, 48 were HBsAg-negative. These cases differed significantly from the other 68 cases in that more were females (35% against 16%), more originated from an agricultural area (56% against 30%), and more were regular consumers of drugs (48% against 28%). In conclusion, factors as yet undefined play a considerable role in the causation of CLD in Somalia. The possibility of determining the role of hepatitis C virus (HCV) awaits the development of more specific assays for anti-HCV antibodies.
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