Hepatitis B Reactivation in a Renal Transplant Patient Due to a Surface Antigen Mutant Strain: A Case Report
Autor: | V. Papanikolaou, A. Fylaktou, I. Mavrovouniotis, D. Papaventsis, I. Fouzas, E. Sianou, M. Daoudaki, V. Dimou |
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Rok vydání: | 2012 |
Předmět: |
Male
Hepatitis B virus Prednisolone medicine.medical_treatment DNA Mutational Analysis Molecular Sequence Data Immunoglobulins medicine.disease_cause Antibodies Monoclonal Murine-Derived Hepatitis B Chronic medicine Humans Kidney transplantation Hepatitis Transplantation Hepatitis B Surface Antigens Base Sequence business.industry Immunization Passive Immunosuppression Middle Aged Mycophenolic Acid Viral Load Hepatitis B medicine.disease Kidney Transplantation Virology Treatment Outcome DNA Viral Mutation Immunology Cyclosporine Drug Therapy Combination Virus Activation Surgery Rituximab business Viral load Biomarkers Immunosuppressive Agents medicine.drug |
Zdroj: | Transplantation Proceedings. 44:2773-2775 |
ISSN: | 0041-1345 |
DOI: | 10.1016/j.transproceed.2012.09.011 |
Popis: | Introduction Reactivation of hepatitis B virus (HBV) is a complication of immunosuppressive treatment in patients with a history of HBV exposure. Case presentation Herein we have reported a case of reactivation after renal transplantation in a 52-year-old male chronic HBV carrier who was treated with hepatitis B immunoglobulin (HBIg) prophylaxis immediately after transplantation in addition to cyclosporine, mycophenolate mofetil and prednisolone for maintenance immunosuppression. After application of rituximab, the patient developed clinical hepatitis with a high load of HBV DNA. Sequence analysis of the surface (S) antigen corresponding to the amino acid residues 101–186 (including the a-determinant region) revealed a genotype D mutant strain, subtype ayw3 with a single amino acid substitution D144E within the S gene. Conclusion This case suggested that immunosuppressive treatment enhanced with rituximab promoted the emergence of an HBV mutant within the determinant region of the S antigen, which escaped HBIg immunoprophylaxis causing HBV reactivation in a kidney transplant recipient. |
Databáze: | OpenAIRE |
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