RESUMO
The prevalence of end-stage renal disease has increased dramatically in developing countries. Hepatitis B virus [HBV] infection is a global health problem that represents a significant co-morbidity event that has led to outbreaks of hepatitis B. There are inadequate data concerning occult HBV infection among Egyptian chronic hemodialysis patients. This study aimed to detect occult HBV infection among chronic hemodialysis patients in Alexandria, Egypt. A cross-sectional study was performed on 100 patients with end-stage renal disease that received maintenance hemodialysis and had tested negative for HBV surface antigen. Blood samples were collected before the initiation of hemodialysis. Sera were tested for hepatitis C virus [HCV] and hepatitis B core [HBc] antibodies using ELISA, and HBV DNA was detected by SYBR Green real-time PCR using specific primers for the s and c genes and by nested PCR using pol gene-specific primers. The serum activity of alanine and aspartate aminotransferase [ALT and AST] were also measured. Anti-HCV and anti-HBc antibodies were detected in 34% and 48% of patients, respectively, and 70.6% of anti-HCV positive patients were also positive for anti-HBc antibodies. This association was statistically significant [p = 0.001]. HBV DNA was detected in 32% of the hemodialysis patients. A significant association was determined between the presence of HBV DNA and anti-HCV positivity [p = 0.021]. Aminotransferases were elevated in 21% of the studied patients, more often in patients with positive anti-HCV profiles than in patients negative for anti-HCV [p < 0.05]. In conclusion, the serological markers of HBV infection should be verified with molecular tests to investigate possible occult infections, especially among anti-HBc-positive hemodialysis patients, to improve our understanding of their clinical, laboratory, and epidemiological characteristics
RESUMO
Hepatitis C virus [HCV] infection is one of the most common infectious diseases leading to high morbidity and mortality due to the development of liver fibrosis/cirrhosis and hepatocellular carcinoma [HCC]. Transforming growth factor-beta 1 [TGF-beta 1] is the most relevant growth factor that plays a role in induction of hepatic fibrogenesis through stellate cell activation, with a decrease in vitamin A storage in these cells. However, the impact of TGF-beta 1 and vitamin A depletion on initiation of liver neoplasia is controversial. In this study, we intended to evaluate hepatitis C viremia in association with serum levels of TGF-beta 1 and retinol binding protein [RBP], which has been considered to be a good and sensitive index of vitamin A depletion, to assess if there is a potential link between serum titer of HCV and those markers and their importance as risk factors for the development of HCC. Serum levels of TGF-beta 1 and RBP were assayed using commercial ELISA and radial immunodiffusion kits in 30 patients [15 with HCV infection and 15 with HCV infection associated with HCC] along with 10 healthy controls. Quantification of circulating HCV RNA by Real-time polymerase chain reaction was done using TaqMan probe technology. Alpha fetoprotein [AFP] levels and serum aminotransferases' activities were also measured. Serum levels of TGF-beta 1 were considerably higher in HCC and HCV groups compared to healthy controls [23.88 +/- 12.73 and 13.63 +/- 7.58 vs. 8.08 +/- 2.51, p<0.001, p<0.05 respectively]. Furthermore, patients having HCV infection associated with HCC showed significantly higher values of TGF-beta 1 than HCV group [23.88 +/- 12.73 vs. 13.63 +/- 7.58, p<0.01]. Serum RBP levels were 55.32 +/- 16.87, 51.30 +/- 20.10 and 35.11 +/- 16.21 in the controls, HCV and HCC patients respectively. There was a significant decrease in serum RBP levels in HCC group compared to HCV and control groups [p<0.05, p<0.01 respectively]. A positive correlation was found between hepatitis C viremia and serum TGF-beta 1 levels in all patients [p<0.05]. A negative correlation was observed between TGF-beta 1 and RBP, in particular, more evident in HCC group also between RBP and AFP but did not reach statistical significance. Neither Serum TGF-beta 1 nor RBP levels were correlated with aminotransferases' activities in HCV and HCC patients. The progressive increase in serum TGF-beta 1 associated with progressive reduction in serum RBP levels from controls to HCC patients suggest their tumor-promoting effect through facilitating TGF-beta 1-mediated liver fibrogenesis with progressive loss of vitamin A storage giving the chance for the tumor to grow. Correlation of hepatitis C viremia with serum TGF-beta 1 levels signifies that HCV proteins could induce expression of TGF-beta 1 and may contribute to liver carcinogenesis. Therefore, increased serum TGF-beta 1 associated with reduced RBP levels could be considered as risk factors for the evolution of HCC in HCV-infected patients