Sex: M
Vaccine: HEP
Symptoms: Alanine aminotransferase normal, Hepatitis B, Hepatitis B DNA assay positive, Hepatitis B core antibody negative, Hepatitis B surface antigen negative
Clinical narrative: This case was reported in a literature article and described the occurrence of vaccination failure in a 27-year-old male subject who received Hepatitis B vaccine. Concurrent medical conditions included blood donor and hepatitis B exposure. In 2008, 7 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 7 years after the vaccination, a patient's blood donation was screened and he was found to be positive for hepatitis B DNA but negative for hepatitis surface antigen and hepatitis B core antibodies. Neither immunoglobulin M or total hepatitis B core antibodies, nor hepatitis B surface antigens appeared during the 9-month follow up period, but an increased in the hepatitis B surface antibodies occurred on day 42, when hepatitis B viral DNA became undetectable. 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 43 IU/L and the hepatitis B DNA level was 35 IU/ml. On follow-up, the viraemia was estimated to have lasted from 35 to 42 days at which point an increased in the hepatitis B surface antigen level was observed. The patient did not develop hepatitis B core antibodies or hepatitis B surface antigens during the 9-month follow up. His alanine aminotransferase level was 8-19 U/L during that period. The viral genotype was identified as B2 with 10 clones sequenced and 1xsG112R and 1xsA128T substitutions on S protein. The authors commented that the patient and her 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; and that their full genome sequences were very similar. Diagnostic results (unless otherwise stated, normal values were not provided): In 2008, Alanine aminotransferase result was 8-19 IU/L, Hepatitis B DNA assay result was 35 IU/ml, Hepatitis B core antibody result was Negative absent, Hepatitis B core antibody result was Negative absent, Hepatitis B surface antibody result was 43 IU/L, Hepatitis B surface antigen result was Negative absent and Hepatitis B surface antigen result was Negative absent. Additional information received: This case was reported in literature article and it described the occurrence of a possible vaccination failure in a 27-year-old male patient, who had received unspecified hepatitis B vaccine (manufacturers unknown). The patient as a blood donor whose partner (25-year-old female) was unvaccinated and later found to have a hepatitis B viral DNA level of 1.8 x 108IU/mL and to be negative for hepatitis B surface antibodies. Her viral genotype was B2, wild type, with 9 clones sequenced. Her alanine aminotransferase level was 38 U/L. No further information on the patient's concurrent medical conditions, medical and family history or concomitant medication was provided. On unspecified dates in 2001, 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 an unspecified date in 2008, approximately 7 years after the vaccination, a patient's blood donation was screened and he was found to be positive for hepatitis B DNA but negative for hepatitis surface antigen and hepatitis B core antibodies. Neither immunoglobulin M or total hepatitis B core antibodies, nor hepatitis B surface antigens appeared during the 9-month follow up period, but an increased in the hepatitis B surface antibodies occurred on day 42, when hepatitis B viral DNA became undetectable. The authors believed that the similarity in the patient and his partner's full genome and presurface and surface regions of the hepatitis B surface antigen gene sequences strongly suggested that the patient was infected by his partner who carried high viral load. 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 43 IU/L and the hepatitis B DNA level was 35 IU/ml. On follow-up, the viraemia was estimated to have lasted 35 to 42 days at which point an increased in the hepatitis B surface antigen level was observed. The patient did not develop hepatitis B core antibodies or hepatitis B surface antigens during the 9-month follow up. His alanine aminotransferase level was 8-19 U/L during that period. The viral genotype was identified as B2 with 10 clones sequenced and 1xsG112R and 1xsA128T substitutions on S protein. The authors commented that the patient and her 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; and that their full genome sequences were very similar. 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 case is 1 of the 6 valid cases reported in the same literature article (see case US2015GSK060124).