Evaluation of Hepatitis A and B Vaccine Antibody Response in Pediatric Patients with Type 1 Diabetes Mellitus

Aim:  Type 1 Diabetes; in addition to blood glucose dysregulation, it also progresses with secondary immune dysregulation. Hepatitis A and hepatitis B viruses can therefore cause severe infection in children with type 1 diabetes.

Material and Methods: In this cross-sectional study, pediatric patients with type 1 diabetes mellitus (T1D), aged 3-18, with completed vaccination schedules were involved. Hepatitis B (hepB) vaccine protection was evaluated by measuring anti hepatitis B surface antigen (anti-HBS), and hepatit A (hepA) immunity is measured by anti-hepatitis A virus immunoglobulin G (Anti-HAV IgG) level.

Results: Three hundred and forty-five patients and 250 controls, totally 595 cases were included. The age of diabetic cases was 12.7±4.0 years and the age of control group was 11.9±4.7 years (p=0.027). While anti-HBS positivity was 51.3% (177 patients) in T1D children, it was higher with 59.4% (149 patients) in the control group (p=0.047). The number of participants who received HepA vaccine was 230 (38.6%). Anti-HAV IgG positivity was similar in T1D and control groups (173 (50.2%) and 136 (54.4%), respectively, p=0.378). Anti-HAV IgG positivity was 29.4% (n:107) in 365 participants who were not vaccinated against hepA, while this rate was 90.8% (n:209) in 230 children who were vaccinated (p<0.001).

Conclusion: In T1D patient group, while adequate immune response was achieved against hepA virus after vaccination, insufficient immune response was observed against hepB virus despite vaccination. Anti-HAV IgG testing in this risky group of chronic patients who have not been vaccinated with hepA vaccine at the time of diagnosis may be taken into account. In all patients, regardless of vaccination status, we recommend routine monitoring of anti-HBS levels, this screening should be included in the guidelines, and a booster dose of vaccine for patients with inadequate antibody response should be applied.