The prevalence of hepatitis B virus (HBV) infection in our unit was 45% (86/190): there were 77 (40.5%) and 9 (4.7%) patients with previous and persistent HBV infection, respectively. Recombinant hepatitis B vaccine was given to 118 chronic HD patients with a regimen of 3 double doses administered intramuscularly at 0, 1 and 2 months, obtaining a seroprotection rate of 67% (79/118), 57% (45/79) being high responders. At month 24, 78% (40/51) maintained protective levels of anti-HBs, 45% (18/40) of them being high responders. There was a statistically significant difference between responder and non-responder patients with regard to nutritional parameters such as serum total proteins and mean levels of transferrinemia. The number of diabetic patients was significantly increased in the nonresponder group. Patients with persistent antibodies (‘persistent responders’) were younger and had a shorter duration of HD treatment compared to those responders who rapidly lost anti-HBs (‘transient responders’). Serological positivity for antibodies against hepatitis B core antigen significantly facilitates the decrease of anti-HBs antibodies over time. We detected seven episodes of HBV infection among HD patients at our unit before the beginning of the vaccination program. On the contrary, there were no episodes of HBV infection among responder vaccinees during the 24-month follow-up period. After the initial cost of vaccination, a savings of US$ 3,272 per year was realized by the elimination of frequent serologic screening of vaccine responders.
Patients on maintenance dialysis and kidney transplant recipients are at increased risk of HGV infection; HGV is very frequently associated to hepatitis C co-infection, regardless of HCV genotype. HGV may be transmitted by blood transfusions but transmission routes other than transfusion are possible; 37.5% of HGV RNA-positive patients showed raised serum aminotransferase levels. Further investigations are necessary to clarify the role of HGV infection in the development of liver disease in this clinical setting.
There is little information about the serologic survey for control of hepatitis C by using third-generation assays among chronic haemodialysis (HD) patients, and no analysis of costs has been made to this end. A serologic survey for control of hepatitis C was performed in 190 HD patients attending a single dialysis unit, using second- and third-generation assays. Costs of both serologic surveys were calculated. Anti-HCV prevalence tested by third-generation assays increased from 25% (48/190) to 28% (53/190) compared to second-generation testing; 56% (9/16) of patients showing uncertain findings by second-generation tests gave unequivocal results by third-generation assays; median duration of HD treatment and raised aminotransferase levels were positively associated (P = 0.004 and P = 0.012, respectively) with anti-HCV detected by third-generation assays. The serologic survey for control of hepatitis C in HD patients at our centre was slightly more expensive by third-generation assays compared to second-generation testing (US$18866 vs US$17200 per year). In summary, the use of third-generation tests largely clarified the uncertain results of second-generation tests; new additional positive patients were detected by third-generation assays compared to second-generation testing. Third-generation assays showed the association of duration of HD treatment and raised aminotransferase levels with anti-HCV antibody, as previously found by first- and second-generation assays. To date, third-generation screening and confirmatory assays seem extremely useful in the serologic survey for control of hepatitis C in HD centres without a considerable outlay.
We used first- and second-generation assays such as Ortho 1, Ortho 2 and 4-RIBA to define prevalence and risk factors for anti-HCV antibodies in haemodialysed patients. Forty-nine (24%) subjects were found to be anti-HCV positive. Anti-HCV positivity was related to duration of dialysis and past or current elevations of GOT and GPT; the frequency of transfused patients was greater in HCV-positive than in HCV-negative subjects; there were 31 patients (prevalence of 20%) with anti-HCV antibodies among non-transfused patients. These findings show that, tested by second-generation assays, HCV infection is detected more than twice as commonly in haemodialysis patients and may be responsible for a significant proportion of liver disease in this clinical setting. Acquisition of hepatitis C virus by dialysis patients is not only through blood transfusions but also secondary to hepatitis C virus presence within the unit itself.
HCV subtype 2a was dominant in our cohort of anti-HCV-positive dialysis patients; there was no association between HCV genotypes and demographic or clinical features of patients; the absence of antibody response toward the NS4-related antigens was frequent in genotype 2a carriers and may serve to predict responses to interferon therapy. The relative homogeneity of the viral population in dialysis patients attending our unit suggests a nosocomial transmission of HCV in this clinical setting.
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