Reactivation of chronic hepatitis B

Česká verzia

Authors: J. Šperl
Authors place of work: Klinika hepatogastroenterologie IKEM Praha, přednosta prof. MU Dr. Julius Špičák, CSc.
Published in the journal: Vnitř Lék 2013; 59(7): 591-596
Category:

Summary

Hepatitis B (HBV) is a DNA virus, which cannot be eradicated completely from the organism by treatment, only its replication can be suppressed to low levels. The pathogenesis of liver damage due to HBV is immune‑ mediated, the infected hepatocytes represent the target structures of immune reaction. In individuals who spontaneously achieved the state of inactive carriage of the virus or even achieved HBsAg negativity, we deal only with immune control of viral replication. Chemotherapy or immunosuppressive treatment disrupt the immune control of HBV infection, the virus replication substantially increases and hepatitis B reactivates. HBV reactivation manifests as further flare‑up of chronic inflammation with rapid progression of liver cirrhosis or even as a fulminant hepatitis with liver failure. The risk of reactivation increases with degree of induced immunosuppression, the highest risk is associated with corticosteroid and rituximab therapy. HBV reactivation threatens patients during solid tumours treatment as well as haemato‑ oncological malignancies, patients treated with immunosuppressive and biological therapies for systemic inflammatory diseases and inflammatory bowel diseases, as well as patients on maintenance haemodialysis, after kidney transplantation and patients with HBV/ HIV co‑ infection. HBV reactivation increases both morbidity and mortality in listed groups of patients. The patients threatened by HBV reactivation can be identified easily based on HBV serological markers assessment. Preemptive therapy with nucleos(t)ide analogues significantly reduces the risk of HBV reactivation, the effect of long‑term antiviral therapy is described in detail in kidney transplant recipients in whom the 3rd generation antivirals (entecavir and tenofovir) completely obviate the negative impact of HBV on long‑term survival. In oncological patients who are treated for a determined time period, we can use lamivudine, which is not suitable for long‑term treatment due to high risk of resistance emergence.

Key words:
hepatitis B – reactivation – screening – preemptive therapy

Zdroje

1. Werle‑ Lapostolle B, Bowden S, Locarnini Set al. Persistence of cccDNA during the natural history of chronic hepatitis B and decline during adefovir dipivoxil therapy. Gastroenterology 2004; 126: 1750– 1758.

2. Hui CK, Bowden S, Jackson K et al. Clinical significance of intrahepatic hepatitis B virus covalently closed circular DNA in chronic hepatitis B patients who received cytotoxic chemotherapy. Blood 2005; 105: 2616– 2617.

3. Iloeje UH, Yang HI, Su J et al. Predicting cirrhosis risk based on the level of circulating hepatitis B viral load. Gastroenterology 2006; 130: 678– 686.

4. Kremsdorf D, Soussan P, Paterlini‑Brechot P et al. Hepatitis B virus‑related hepatocellular carcinoma: paradigms for viral‑related human carcinogenesis. Oncogene 2006; 25: 3823– 3833.

5. Lau JY, Bain VG, Davies SE et al. High‑level expression of hepatitis B viral antigens in fibrosing cholestatic hepatitis. Gastroenterology 1992; 102: 956– 962.

6. Marcucci F, Mele A, Spada E et al. High prevalence of hepatitis B virus infection in B‑ cell non‑Hodgkinʼs lymphoma. Haematologica 2006; 91: 554– 557.

7. Hoofnagle JH. Reactivation of hepatitis B. Hepatology 2009; 49 (Suppl 5): S156– S165.

8. Lok AS, Liang RH, Chiu EK et al. Reactivation of hepatitis B virus replication in patients receiving cytotoxic therapy. Report of a prospective study. Gastroenterology 1991; 100: 182– 188.

9. European Association For the Study of the Liver. EASL clinical practice guidelines: management of chronic hepatitis B virus infection. J Hepatol 2012; 57: 167– 185.

10. Lok AS, McMahon BJ. Chronic hepatitis B: update 2009. Hepatology 2009; 50: 661– 662.

11. Lau GK, Yiu HH, Fong DY et al. Early is superior to deferred preemptive lamivudine therapy for hepatitis B patients undergoing chemotherapy. Gastroenterology 2003; 125: 1742– 1749.

12. Martyak LA, Taqavi E, Saab S. Lamivudine prophylaxis is effective in reducing hepatitis B reactivation and reactivation‑related mortality in chemotherapy patients: a meta‑analysis. Liver Int 2008; 28: 28– 38.

13. Lau GK, Leung YH, Fong DY et al. High hepatitis B virus (HBV) DNA viral load as the most important risk factor for HBV reactivation in patients positive for HBV surface antigen undergoing autologous hematopoietic cell transplantation. Blood 2002; 99: 2324– 2330.

14. Terrier B, Pol S, Thibault V et al. Management of the risk of hepatitis B virus reactivation in patients receiving immunosuppressive and immunomodulatory agents in internal medicine: data from the REACTI‑ B survey and proposal for a management algorithm. Rev Med Interne 2012; 33: 4– 12.

15. Yeo W, Zee B, Zhong S et al. Comprehensive analysis of risk factors associating with Hepatitis B virus (HBV) reactivation in cancer patients undergoing cytotoxic chemotherapy. Br J Cancer 2004; 90: 1306– 1311.

16. Loomba R, Rowley A, Wesley R et al. Systematic review: the effect of preventive lamivudine on hepatitis B reactivation during chemotherapy. Ann Intern Med 2008; 148: 519– 528.

17. Esteve M, Saro C, Gonzalez‑ Huix F et al. Chronic hepatitis B reactivation following infliximab therapy in Crohnʼs disease patients: need for primary prophylaxis. Gut 2004; 53: 1363– 1365.

18. Berger A, Preiser W, Kachel HG et al. HBV reactivation after kidney transplantation. J Clin Virol 2005; 32: 162– 165.

19. Vallet‑ Pichard A, Fontaine H, Mallet V et al.Viral hepatitis in solid organ transplantation other than liver. J Hepatol 2011; 55: 474– 482.

20. Mathurin P, Mouquet C, Poynard T et al. Impact of hepatitis B and C virus on kidney transplantation outcome. Hepatology 1999; 29: 257– 263.

21. Ahn HJ, Kim MS, Kim YS et al. Clinical out-come of renal transplantation in patients with positive pre‑transplant hepatitis B surface antigen. J Med Virol 2007; 79: 1655– 1663.

22. Cosconea S, Fontaine H, Meritet JF et al. Benefits associated with antiviral treatment in kidney allograft recipients with chronic hepatitis B virus infection. J Hepatol 2012; 57: 55– 60.

23. Sperl J, Frankova S, Spicak J et al. Further evidence of the benefits associated with antiviral treatment in kidney allograft recipients with chronic hepatitis B virus infection. J Hepatol 2013; 58: 833– 835.

24. Piroth L, Mahy S, Pol S et al. Current management and recommendations on hepatitis B therapy in HIV‑ coinfected patients. Hepatol Int 2011. In press.

25. Konopnicki D, Mocroft A, de Wit S et al. Hepatitis B and HIV: prevalence, AIDS progression, response to highly active antiretroviral therapy and increased mortality in the EuroSIDA cohort. AIDS 2005; 19: 593– 601.

26. Soriano V, Puoti M, Bonacini M et al. Care of patients with chronic hepatitis B and HIV co‑ infection: recommendations from an HIV‑ HBV International Panel. AIDS 2005; 19: 221– 240.