Thalassemic patients are considered to be one of the high risk groups suffering from post-transfusion viral infection such as HBV.
Several studies with controversial results regarding immunity level and duration of acquired immunity from hepatitis B vaccination have been performed in different countries. In a study on children in China, serum anti-HBs was 75% within 2 years of vaccination and decreased to 48.2%, 7 years post vaccination[10
]. In Taiwan, 15 years after the vaccination of neonates, 75% were anti-HBs positive, but the level was not determined. The rate of seropositivity of anti-HBc was 2.9%[11
]. In a study on 150 vaccinated children between 1-4.5 years of age in our country, 136 children were anti-HBs positive and 14 cases were anti-HBs negative. In a study in Iran, there was no difference between the immune response of the two sexes, but in others, the immune response in females was more than that in males. The reason could be related to differences in average weight of girls and boys.
In Kerman, Iran, from 215 children with major thalassemia, 34.8% were no responders and the remaining were either low or good responders[12
]. In a study in South Khorasan province, of 38 children with major beta-thalassemia, 16 patients (42.1%) were anti-HBs positive and 22 patients (57.9%) anti-HBs negative[13
In our study, 89.9% of these children were HBs anti-body positive (responders) and 10.1% negative (non-responders). Our results showed that HBV vaccine is immunogenic and safe in multitransfused thalassemic patients. This study is in close agreement with the study which has reported on 150 vaccinated children between 1-4.5 years of age. In the same group, decrease in serum anti-HBs level with age was observed. When the anti-HBs titer falls to less than 10MIU/l HBV infection may occur but this is always subclinical and usually without detectable serum HBsAg. The suspected poor response to hepatitis B vaccine in these children, is due to their immunological abnormalities and frequent transfusion therapy (such as iron overloading)[5
]. Anti-HBc alone may be present in relatively high titers after the disappearance of anti-HBs and indicating recent infection. Anti-HBc is the only anti-body detected after self limited infections in 10% of patients, who never acquire detectable anti-HBs. In addition, anti-HBc is produced in person exposed to HBV and may be a good marker of past HBV infection[14
]. In one study in India, from 70 children with thalassemia, 75.7% had titers exceeding 10IU/l (responders) and 24.3% were non-responders. The seroprevalence of HBV marker (HBsAg and anti-HBc) was 5.7 % and 20%. HBV DNA was detected in 22 of 70 (31.4%) of these thalassemic children [15
In a study in South Khorasan province, none of these patients were positive for HBsAg and anti-HBc anti-body [13
]. In our study, 3.03% of our samples were anti-HBc positive and 1 (1.01%) was HBsAg positive (carrier of HBV) but none of them was HBV DNA positive. These results showed that in Iran the prevalence of HBV infection in beta thalassemic patients is lower than in general population[4
In our study in a region with intermediate HBV prevalence, we have shown frequency of anti-body response to HBV vaccine in a cohort of thalassemic children. 89.9% of these children were HBs anti-body positive and 10.1% negative. A recent study on 416 vaccinated thalassemic patients (mean age 25.6 yr) who had low titer of HBsAb and received a booster dose showed that the numbers of positive vicinal patients have been increased from 46.9 % to 69.4%[16
]. Also, in close agreement with our study, this report revealed that response rate to vaccination was more than 95% after complete course (3 doses) in healthy individuals but failure to fulfill vaccination seems a problem in chronic transfused patients[16
]. Therefore, additional studies such as screening of thalassemic pediatric patients should be strictly followed to determine the efficacy of vaccination to protect these patients from HBV infection. To challenge with HBV, it is necessary to measure anti-HBs antibody level and according to their need, booster dose vaccination should be given especially in a high-risk group like thalassemic children.
In our study, there are a few limitations. The sample size was limited to patients who were referred to our lab and all sickle thalassemia and alpha-thalassemia patients were excluded from this study. There was little information about ferritin level and liver enzymes which indicated an iron load in thalassemic patients. In addition, many factors such as genetic features, HLA structure and T cell subgroups may influence response to the hepatitis B vaccination.