Age: 17.0
Sex: F
Vaccine: HEP
Symptoms: Alanine aminotransferase normal, Hepatitis B, Hepatitis B DNA assay negative, Hepatitis B surface antibody positive, Hepatitis B surface antigen negative
Clinical narrative: This case was reported in a literature article and described the occurrence of vaccination failure in a 17-year-old female subject who received Hepatitis B vaccine. Concurrent medical conditions included blood donor and hepatitis B exposure. In 2008, 10 years after receiving Hepatitis B vaccine, the subject developed vaccination failure. Serious criteria included GSK medically significant. Additional event(s) included hepatitis B in 2008 with serious criteria of GSK medically significant. The outcome of vaccination failure was unknown. The outcome(s) of the additional event(s) included hepatitis B (recovered/resolved). It was unknown if the investigator considered the vaccination failure and hepatitis B to be related to Hepatitis B vaccine. Relevant Tests: On an unspecified date in 2008, approximately 10 years after the vaccination, the patient's blood donation was screened and she was found to be positive for hepatitis B DNA but negative for hepatitis surface antigen and hepatitis B core antibodies. According to the authors this indicated that a subclinical infection had developed and resolved. Further follow-up showed transiently low levels of hepatitis B surface antigens whereas hepatitis B surface antibodies remained reactive; as well as an increase in hepatitis B surface antibodies that corresponded to the disappearance of hepatitis B surface antigens. The patient's initial blood screening was negative for hepatitis B surface antigen and hepatitis B core antibodies; hepatitis B surface antibodies level at this point was 11 IU/L and the hepatitis B DNA level was 13 IU/ml. On follow-up, the viraemia was estimated to have lasted from 137 to 168 days and the patient was found to have developed hepatitis B core antibodies after 168 days. Hepatitis B surface antigen level during the follow-up period was 108 and the alanine aminotransferase level was 4-7 U/L. The viral genotype was identified as F1, wild type, with 12 clones sequenced. The authors commented that the patient and his partner's sequences of the presurface and surface regions of the hepatitis B surface antigen gene were nearly identical at nucleotide and amino acid level. Diagnostic results (unless otherwise stated, normal values were not provided): In 2008, Alanine aminotransferase result was 4-7 IU/L, Hepatitis B DNA assay result was 13 IU/ml, Hepatitis B core antibody result was Negative absent, Hepatitis B core antibody result was Positive absent, Hepatitis B surface antibody result was 11 IU/L, Hepatitis B surface antigen result was Negative absent and Hepatis B surface antigen result was Low level absent. Additional information received: This case was reported in a literature article and it described the occurrence of a possible vaccination failure in a 17-year-old female patient, who had received an unspecified hepatitis B vaccine (manufacturer unknown). The patient was a blood donor whose partner (19-year-old male) was unvaccinated and later found to have a hepatitis B viral DNA level of 2.6 x 108IU/mL and to be negative for hepatitis B surface antibodies. His viral genotype was F1 with 11 clones sequenced and a 4xsY72 stop substitution on S protein. His alanine aminotransferase level was 36U/L. No further information on the patient's concurrent medical conditions, medical and family history or concomitant medication was provided. On unspecified dates in 1998, the patient received an unknown number of doses of an unspecified hepatitis B vaccine (dosages unknown; administration routes and sites unspecified; batch numbers not provided). On unspecified date in 2008, approximately 10 years after the vaccination, the patient's blood donation was screened and she was found to be positive for hepatitis B DNA but negative for hepatitis surface antigen and hepatitis B core antibodies. According to the authors this indicated that a subclinical infection had developed and resolved. Further follow-up showed transiently low levels of hepatitis B surface antigens whereas hepatitis B surfaced antibodies remained reactive; as well as an increase in hepatitis B surface antibodies that corresponded to the disappearance of hepatitis B surface antigens. The authors believed that the patient had been infected via sexual transmission from his partner as their sequences of the presurface and surface regions of the hepatitis B surface antigen gene were nearly identical at nucleotide and amino acid level. Please note that this case was classified as a possible vaccine failure as the number of vaccine doses received by the patient was not specified and no clinical symptoms were reported. The patient's initial blood screening was negative for hepatitis B surface antigen and hepatitis B core antibodies; hepatitis B surface antibodies level at this point was 11 IU/L and the hepatitis B DNA level was 13 IU/ml. On follow-up, the viraemia was estimated to have lasted from 137 to 168 days and the patient was found to have developed hepatitis B core antibodies after 168 days. Hepatitis B surface antigen level during the follow-up period was 108 and the alanine aminotransferase level was 4-7 U/L. The viral genotype was identified as F1, wild type, with 12 clones sequenced. The authors commented that the patient and his partner's sequences of the presurface and surface regions of the hepatitis B surface antigen gene were nearly identical at nucleotide and amino acid level. Treatment was unknown. Outcome of the acute viral infection was resolution. Outcome of the rest of the events was unspecified at the time of reporting. The authors did not comment on any causal relationship between the vaccines and the events. The authors concluded that "this study showed a higher than expected rate of hepatitis B infection with the use of triplex nucleic acid testing, mainly in donors who had been vaccinated against hepatitis B virus and who would not have been identified by routine screening for hepatitis B surface antigen or hepatitis B core antibodies. However, these acute hepatitis B viral infections rapidly resolved and are of inconsequential clinical significance, but their potential for transmission remains unresolved. Our findings show the efficacy of the hepatitis B vaccine for the prevention of clinical disease but not infection, and the cost of interdicting donations that contain hepatitis B virus DNA from seronegative donors is high in the face of unknown benefit. Because of the high cost of introducing new screening assays for blood donors and the inability to document cost-effectiveness similar to that of other medical interventions, the continued development of new tests either to replace older tests or to detect newly identified agents is in question." This is 1 of the 6 valid cases reported in the same literature article (see case US2015GSK060124).