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DOI: 10.1055/s-0042-1757489
Letter: Parvovirus B19 Related Severe Aplastic Anaemia following Liver Transplantation
A 58-year-old male underwent living donor liver transplantation for nonalcoholic steatohepatitis-related cirrhosis complicated with ascites, upper gastrointestinal bleeding, and hepatic encephalopathy. He was a known case of long-standing diabetes mellitus, systemic hypertension, and ischemic cerebrovascular stroke. Following an uneventful stay, he was discharged after 15 days on tacrolimus 1 mg twice a day, mycophenolate mofetil (MMF) 500 mg/day, prednisolone 15 mg/day, fluconazole 200 mg/day, valganciclovir 450 mg twice daily, and other medications for his comorbid states. The blood investigations showed stable graft function: alanine aminotransferase (AST) 9 U/L, aspartate aminotransferase (ALT) 34 U/L, total bilirubin 0.66 mg/dL, low hemoglobin 8.6 g/dL with normal total leucocyte count (TLC) 8870 cells/mm3 and platelets 300,000 /mm3, and adequate tacrolimus trough levels (6.9 ng/mL). Two weeks later, he presented with fatigue and dyspnea on exertion. Investigations revealed hemoglobin 5.8 g/dL, TLC 3370 cells/mm3, and platelets 289,000/mm3. Iron indices and vitamin B12 levels were normal. Reticulocyte count was 0.1%. Peripheral smear examination revealed normocytic normochromic anemia. His graft function was good with AST 12 U/L, ALT 30 U/L, total bilirubin 0.63 mg/dL, and tacrolimus trough level was 5.9 ng/mL. Cytomegalovirus and Epstein–Barr virus serology and viral load test using enzyme immunoassay and real-time polymerase chain reaction (PCR) were negative. His hemoglobin remained low (5.8–6.6 g/dL) in spite of two transfusions. Bone marrow examination showed severe red cell hypoplasia, giant erythroblasts with prominent eosinophilic intranuclear viral inclusions. These findings are consistent with parvovirus B19 (B19V) infection ([Fig. 1]). B19V immunoglobulin (Ig) M (enzyme immunoassay) was positive and B19V deoxyribonucleic acid levels (real-time PCR) were 1.27 × 1010 copies/mL. In view of these findings, his immunosuppression was optimized; MMF was stopped. His tacrolimus trough level was 5.3 ng/mL. He received intravenous Ig (IVIG) 400 mg/kg/day for 5 consecutive days. His hemoglobin level still remained low and he required more blood transfusions. Two cycles of IVIG were repeated after 20 and 40 days from the first dose. After the third dose, there was a dramatic response with rise in hemoglobin and TLC ([Fig. 2]). Currently, he is 1-year posttransplant and doing well. Repeat bone marrow biopsy and viral serology were not done.
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Anemia in postliver transplant period may be related to persisting hypersplenism, gastrointestinal bleeding, concomitant renal failure, adverse drug reactions to immunosuppressant drugs, nutritional deficiencies, and bone marrow suppression secondary to viral infections.[1] [2] [3] B19V infections have been described commonly in hematopoietic stem cell transplant recipients and renal transplantation. Only a handful of cases have been reported in liver transplant recipients and may be related to lesser immunosuppression in this group. In postliver transplant patients, infection with B19V commonly presents as pure red cell aplasia, pancytopenia, fever, and arthralgia followed by rash and carditis.[4] [5] B19V infection of the liver has been associated with poor outcomes in patients with cryptogenic acute liver failure.[6] Some patients may present with fulminant hepatic failure and aplastic anemia requiring liver transplant and bone marrow transplantation.[7] B19V infection should be considered in sudden decline in hemoglobin or transient aplastic anemia. The diagnosis is confirmed by serology (IgM and IgG positivity), PCR testing, and in situ hybridization in histological specimens. While there is no specific therapy, a triple drug regimen (of Ig, dehydrohydrocortisone, and cyclosporine) has been reported to be effective.[8] IVIG therapy has been reported to be effective and usually, a dose of 400 mg/kg/day for 5 days is used. The relapse rate is nearly 28% and these relapses are managed with a further course of IVIG.[9] Another important aspect of treatment is the optimization of immunosuppression and attaining the delicate balance between good graft function and minimum dose.
To conclude, the present case highlights that B19V infection is a rare but important cause of severe anemia in liver transplant recipients. Prompt testing and treatment would reduce the risk of bone marrow failure, morbidity, and mortality.
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Conflict of Interest
None declared.
Ethical Statement
Informed consent to publish obtained.
Authors' contribution
S.P., D.J., S.R.: Patient care, initial draft. M.J.: editing, analysis and preparing the manuscript.
Data Availability statement
The relevant data are provided in the manuscript.
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References
- 1 Ndimbie OK, Frezza E, Jordan JA, Koch W, van Thiel DH. Parvovirus B19 in anemic liver transplant recipients. Clin Diagn Lab Immunol 1996; 3 (06) 756-760
- 2 Misra S, Moore TB, Ament ME, Vargas JH, Busutill RW, McDiarmid SV. Profile of anemia in children after liver transplantation. Transplantation 2000; 70 (10) 1459-1463
- 3 Vales-Albertos LJ, García-Cárdenas M, Chávez-Becerra S, Gómez-Navarro B, Monteón-Ramos F, Cueto-Manzano AM. Pure red cell aplasia associated with parvovirus B19 infection in renal transplantation: the first case report in Mexico. Transplantation 2005; 79 (06) 739
- 4 Eid AJ, Brown RA, Patel R, Razonable RR. Parvovirus B19 infection after transplantation: a review of 98 cases. Clin Infect Dis 2006; 43 (01) 40-48
- 5 Zhang J, Ren B, Hui R, Sun Y, Liu Z, Zhou S. Clinical heterogeneity of human parvovirus B19 infection following adult liver transplantation. Medicine (Baltimore) 2018; 97 (34) e12074
- 6 Alves AD, Melgaço JG, Cássia Nc Garcia R. et al. Persistence of Parvovirus B19 in liver from transplanted patients with acute liver failure. Future Microbiol 2020; 15: 307-317
- 7 Bathla L, Grant WJ, Mercer DF, Vargas LM, Gebhart CL, Langnas AN. Parvovirus associated fulminant hepatic failure and aplastic anemia treated successfully with liver and bone marrow transplantation. A report of two cases. Am J Transplant 2014; 14 (11) 2645-2650
- 8 Bihari C, Rastogi A, Saxena P. et al. Parvovirus b19 associated hepatitis. Hepat Res Treat 2013; 2013: 472027
- 9 Bertoni E, Rosati A, Zanazzi M. et al. Unusual incidence of aplastic anaemia due to B-19 parvovirus infection in renal transplant recipients. Transplant Proc 1997; 29 (1-2): 818-819
Address for correspondence
Publikationsverlauf
Eingereicht: 16. Mai 2022
Angenommen: 04. Juni 2022
Artikel online veröffentlicht:
22. September 2023
© 2023. Gastroinstestinal Infection Society of India. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)
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References
- 1 Ndimbie OK, Frezza E, Jordan JA, Koch W, van Thiel DH. Parvovirus B19 in anemic liver transplant recipients. Clin Diagn Lab Immunol 1996; 3 (06) 756-760
- 2 Misra S, Moore TB, Ament ME, Vargas JH, Busutill RW, McDiarmid SV. Profile of anemia in children after liver transplantation. Transplantation 2000; 70 (10) 1459-1463
- 3 Vales-Albertos LJ, García-Cárdenas M, Chávez-Becerra S, Gómez-Navarro B, Monteón-Ramos F, Cueto-Manzano AM. Pure red cell aplasia associated with parvovirus B19 infection in renal transplantation: the first case report in Mexico. Transplantation 2005; 79 (06) 739
- 4 Eid AJ, Brown RA, Patel R, Razonable RR. Parvovirus B19 infection after transplantation: a review of 98 cases. Clin Infect Dis 2006; 43 (01) 40-48
- 5 Zhang J, Ren B, Hui R, Sun Y, Liu Z, Zhou S. Clinical heterogeneity of human parvovirus B19 infection following adult liver transplantation. Medicine (Baltimore) 2018; 97 (34) e12074
- 6 Alves AD, Melgaço JG, Cássia Nc Garcia R. et al. Persistence of Parvovirus B19 in liver from transplanted patients with acute liver failure. Future Microbiol 2020; 15: 307-317
- 7 Bathla L, Grant WJ, Mercer DF, Vargas LM, Gebhart CL, Langnas AN. Parvovirus associated fulminant hepatic failure and aplastic anemia treated successfully with liver and bone marrow transplantation. A report of two cases. Am J Transplant 2014; 14 (11) 2645-2650
- 8 Bihari C, Rastogi A, Saxena P. et al. Parvovirus b19 associated hepatitis. Hepat Res Treat 2013; 2013: 472027
- 9 Bertoni E, Rosati A, Zanazzi M. et al. Unusual incidence of aplastic anaemia due to B-19 parvovirus infection in renal transplant recipients. Transplant Proc 1997; 29 (1-2): 818-819
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