ABSTRACT
PURPOSE: The aim of this study was to compare patients with hepatocellular carcinoma (HCC) associated with hepatitis C virus (HCV) infection with patients with liver cirrhosis associated with HCV virus infection. METHODS: Forty-five patients were prospectively analyzed, all with HCV infection. Patients were divided into 2 groups. The first group consisted of 21 patients with histologically proven HCC and the second one consisted of 24 patients with liver cirrhosis without HCC. PCR was carried out in order to diagnose active HCV infection and HCV genotyping. RESULTS: There was no statistically significant difference in the structure of the compared groups of patients in relation to sex and age. In 76.19% of the patients with HCC cirrhosis preceded HCC, while 23.81% of the patients had chronic hepatitis. The prevalence of genotypes in the HCC group was 1a in 4.76%, 1b in 80.95% and 2a in 14.29%. In the group with liver cirrhosis 1a was detected in 20.83%, 1b in 45.83%, 2a in 12.50%, 2b in 4.17% and 3a in 16.67% of the patients. The prevalence of genotype 1b was significantly higher among HCV RNA positive patients with HCC compared to the group with liver cirrhosis and HCV RNA positive patients (x(2)=4.48; p=0.034). In the group where cirrhosis preceded HCC, genotype 1b was found in 75% of the cases, genotype 2a in 18.75%, and genotype 1a in 6.25%. Genotype 1b was detected in 100% of patients with chronic hepatitis and HCC. CONCLUSION: The role of HCV infection in the development of HCC has not been fully clarified. Most authors evaluate the role of individual genotypes in the pathogenesis of HCC. This study has shown that the dominant genotype found in patients with HCC is 1b.
Subject(s)
Carcinoma, Hepatocellular/virology , Hepacivirus/pathogenicity , Hepatitis C/virology , Liver Cirrhosis/virology , Liver Neoplasms/virology , Adult , Aged , Carcinoma, Hepatocellular/blood , Carcinoma, Hepatocellular/genetics , DNA, Viral/genetics , Enzyme-Linked Immunosorbent Assay , Female , Hepacivirus/genetics , Hepatitis B Surface Antigens/metabolism , Hepatitis C/blood , Hepatitis C/genetics , Humans , Liver Cirrhosis/blood , Liver Cirrhosis/genetics , Liver Neoplasms/blood , Liver Neoplasms/genetics , Male , Middle Aged , Polymerase Chain Reaction , Prognosis , Prospective Studies , Risk FactorsABSTRACT
The aim of this study was to establish the existence of mGluR7 in normal B lymphocytes and analyse the effect of monosodium glutamate (MSG) on B cell apoptosis in vitro. B cells were purified by magnetic cell sorting using anti-CD19-coupled magnetic beads. Cells (10(6)/ml) were cultured with increasing MSG concentrations (1-100 mM). Detection of apoptosis by flow cytometry was performed using the Annexin V-FITC/Propidium iodide (PI) apoptosis detection kit. Naïve and memory B cell population were identified by CD27 staining. Expression of GluRs was determined using PCR. Exposure to increasing MSG concentrations displayed dose dependent effect on B cell viability altogether, ranging from 35% with 100 mM up to 80% with 1 mM MSG. Moreover, the number of late apoptotic cells as well as necrotic cells was dose dependant. Both CD27- as well as CD27+ B cells were affected by MSG. Basal expression of GluRs7 was detected in unstimulated B cells. Glutamate induced apoptosis can be seen in memory as well as naive B cell population and is probably mediated through mGluR7, whose expression in B cells we also confirmed. Our study suggests a new possible mechanism of crosstalk between the nervous and the immune system through glutamate as a potential key mediator (Fig. 4, Ref. 27). Full Text (Free, PDF) www.bmj.sk.
