We assessed the genetic polymorphism of mannose-binding lectin (MBL) in 93 patients with chronic hepatitis C (45 responders and 48 nonresponders to interferon) and 218 healthy controls. Mutant allele was identified only at codon 54 (Gly-->Asp), leading to three genotypes (54 m/m, 54 W/m, and 54 W/W). Frequency of 54 m/m was significantly lower in interferon-responders (2.2%), compared to those in nonresponders (14.6%) and controls (10.6%): p < 0.05. Our results suggest that homozygous carriage of the variant allele of codon 54 of MBL may predict poor response to interferon in chronic hepatitis C patients.
Background and aim: Recent studies indicated that hepatic stem cells in the bone marrow could differentiate into mature hepatocytes, suggesting that bone marrow cells could be used for replacement of damaged hepatocytes in a variety of liver diseases. Hepatocellular carcinoma (HCC) is thought to arise from hepatic stem cells. In this study, we investigated the malignant potential of hepatic stem cells derived from the bone marrow in a mouse model of chemical hepatocarcinogenesis. Methods: Bone marrow cells were obtained from the male b-galactosidase (b-gal) transgenic mouse and transplanted into female recipient mice. Hepatocarcinogenesis was induced by a year of treatment with diethylnitrosamine and phenobarbital (NDEA/PB). One year later, the liver was removed from each treated mouse and evaluated by x-gal staining, immunohistochemistry, and fluorescence in situ hybridisation (FISH). Results: Forty per cent of recipient mice survived and developed multiple HCC. Clusters of b-gal positive mature hepatocytes were detected sporadically in the entire liver of NDEA/PB treated mice who underwent bone marrow transplantation (BMT) with while no such hepatocytes were identified in the liver of BMT mice that were not treated with NDEA/PB. The Y chromosome was detected with the same frequency as the donor male liver in clusters of b-gal positive mature hepatocytes by FISH. However, no HCC was positive for b-gal or the Y chromosome. Immunohistochemically, b-gal positive mature hepatocytes did not express CD34 or a-fetoprotein. Conclusions: Our results suggest that hepatic stem cells derived from the bone marrow have low malignant potential, at least in our model.
TT virus (TTV) lacks obvious pathogenicity; almost all of the infected hosts are symptom-free. A possibility remains, however, that certain strains can cause liver disease while most others are non-pathogenic. Genotypes 1 a and 1 b have been proposed to contain such pathogenic strains. To test this possibility, we constructed a PCR system capable of detecting TTV of the 1 a and 1 b genotypes differentially from the other genotypes, and compared the frequencies of these genotypes between patients with liver disease of unknown etiology (n=42) and healthy individuals (n=50). The assay comprised 3 steps: i) PCR to amplify a 3.2-kb fragment using universal primers; ii) 2nd-round PCR, starting from the 3.2-kb amplicon, for a approximately 280-nt fragment by use of genotype 1-specific primers; and iii) digestion of the approximately 280-nt amplicon with MboI and BanI to discriminate between 1 a and 1 b. Eventually, 40 (95%) of the patients and 47 (94%) of the controls were positive for the 3.2-kb amplicon, and the 1 a, 1 b, 1 a+1 b, and non-1 genotypes of TTV were found in 2 (5%) vs 4 (9 percent), 5 (13%) vs 4 (9%), 1 (3%) vs 1 (2%) and 32 (80%) vs 38 (81%) of the 40 patients and 47 controls, respectively: the distribution was almost identical between the two groups. The hypothesis that the genotype 1 of TTV may be more closely associated with liver disease than other genotypes was not supported by this study.
Demographic, etiological, clinical characteristics and treatment of hepatocellular carcinoma (HCC) were surveyed in 414 patients in Asia, including 107 from China, 15 from India, 101 from Indonesia and 191 from Japan. Males predominated in all countries, accounting for up to 75%. The mean +/- SD age at the development of HCC was about 10 years older for the patients from Japan (63.8 +/- 9.5, P < 0.001) and India (63.1 +/- 11.2, P < 0.05) than those from China (54.0 +/- 13.7) and Indonesia (53.7 +/- 14.2). Hepatitis B surface antigen (HBsAg) in serum was detected in 67% of patients from China who were tested, 27% from India, 21% from Indonesia and 18% from Japan, whereas antibody to hepatitis C virus was detected in 4%, 53%, 40% and 70%, respectively; co-occurrence of hepatitis B and C infections was seen only in 7%, 0%, 2%, and 1%, leaving an etiology other than hepatitis viruses in 22%, 20%, 36% and 11%. HCC was diagnosed primarily by ultrasonography in China (43%) and Japan (52%), and on physical examination in India (60%) and Indonesia (52%). The size of the largest tumor exceeded 5.0 cm in diameter only in 24% of the patients from Japan, much less often than in 67%, 87%, and 71%, respectively, of those from China, India and Indonesia (P < 0.001). The most favored treatment was chemolipidolization in China (81%) and Japan (81%), whereas it was transarterial embolization in India (13%) and Indonesia (26%). These results highlight common as well as distinct characteristics of HCC in Asia, and warrant the need for close cooperation toward early diagnosis and effective treatment of HCC.
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