Risk of Reactivation of Latent HBV Hepatitis in Patients Under Neurosurgical Treatment

¹Department of Neurosurgery, Kohnan Hospital, Japan

²Departments of Pathology and Neurosurgery, Tohoku University Graduate School of Medicine, Japan

*Corresponding Author:

Yoshikazu Ogawa
Departments of Pathology and Neurosurgery
Tohoku University Graduate School of Medicine
1-1 Seiryo-machi, Aoba-ku, Sendai
Miyagi 980-8574, Japan
Tel: +81222482131
Fax: +81223041641
E-mail: yogawa@kohnan-sendai.or.jp

Received date: Oct 04, 2016; Accepted date: Oct 18, 2016; Published date: Oct 20, 2016

Citation: Ogawa Y, Tominaga T (2016) Risk of Reactivation of Latent HBV Hepatitis in Patients Under Neurosurgical Treatment . J Neuroinfect Dis 7:230. doi:10.4172/2314-7326.1000230

Copyright: © 2016 Ogawa Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Visit for more related articles at Journal of Neuroinfectious Diseases

Abstract

Reactivation of hepatitis B virus (HBV) is a risk in the 350 million HBV carriers worldwide. HBV reactivation may cause hepatocellular carcinoma, cirrhosis, and fulminant hepatitis, and HBV reactivation accompanied with malignant tumor and/or chemotherapy is a critical problem for the patients with chronic HBV infection. In addition, multiple risk factors causing immunosuppressive state can also induce HBV reactivation, which includes a few cases of intrinsic cortisol over secretion as Cushing’s syndrome or very low-dose steroid treatment for hypopituitarism after pituitary surgeries.

Appropriate screening methods and the discussion for preventive supplementation of antiviral drugs for HBV reactivation are required. For patients with pituitary tumors precise operative procedures and careful treatment planning are essentially required to avoid HBV reactivation.

Short Communication

Today HBV reactivation and hepatitis flare induced by cytotoxic chemotherapy has a keen interest in cancer patients with chronic HBV infection, especially in patients with hematological malignancies. Immunosuppressive state caused by immunosuppressive agents and anticancer drugs could precipitate an increase in HBV replication followed by a flare of hepatitis B, which may become severe or even fatal [1-9]. Inhibition of epigenetic regulator for the carcinoma therapy might directly lead the reactivation of latent HBV hepatitis or even HIV-1 [10]. Most patients who develop HBV reactivation are urged to suspend or postpone treatment of the underlying diseases, so establishment of preventive strategy in high-risk patients is extremely important.

One patient with Cushing’s syndrome and adrenal adenoma died of hepatic failure due to reactivation of HBV [5]. The immunosuppressive state in this patient resulted from intrinsic cortisol over secretion, which was considered to be the cause of reactivation of HBV. Immediate treatment is needed for HBV reactivation with both antiviral therapy and simultaneous remission from the immunosuppressive state. So early surgery after normalization of hepatic function is the best treatment strategy. This principle should be available for possible occurrence of brain tumors especially pituitary diseases. However great care is needed, as hypopituitarism is one of the serious complications after trans sphenoidal surgery and/or gamma knife therapy [11,12], and very low-dose steroid treatment can induce HBV reactivation [13]. Because postoperative hypopituitarism can result in HBV re-reactivation, avoidance of treatment-induced hypopituitarism is essentially required. The extreme care is needed for prevention of damage of pituitary gland, as delicate manipulation in surgery and making sufficient distance from residual tumor for the possible gamma knife therapy thereafter. Compatibility of this treatment dilemma could bring minimization of steroid supplementation and avoidance of HBV re-activation.

The strategy to prevent HBV reactivation is not well established. Strict monitoring or universal prophylaxis for hepatitis B core antibody-positive hepatitis is more appropriate and cost-effective with non-Hodgkin lymphoma [14]. Indications of the patients, the choice of antiviral drugs, and the duration of antiviral drug supplementation have to be established, and further investigations are needed to determine the appropriate screening methods and preventive supplementation of antiviral drugs for HBV reactivation.

References

1. Bae JH, Sohn JH, Lee HS, Park HS, Hyun YS, et al. (2012) A fatal case of hepatitis B virus (HBV) reactivation during long-term, very-low-dose steroid treatment in an inactive HBV carrier. Clin Mol Hepatol 18: 225-228.
2. Chan HL, Tsang SW, Hui Y, Leung NW, Chan FK, et al. (2002) The role of lamivudine and predictors of mortality in severe flare-up of chronic hepatitis B with jaundice.J Viral Hepat 9:424-428.
3. Hoofnagle JH (2009) Reactivation of hepatitis B. Hepatology 29:100-107.
4. Hui CK, Cheung WW, Zhang HY, Au WY, Yueng YH, et al. (2006) Kinetics and risk of de novo hepatitis B infection in HBsAg-negative patients undergoing cytotoxic chemotherapy. Gastroenterology131:59-68.
5. Kasumoto S, Tanaka Y, Mizokami M, Ueda R (2009) Reactivation of hepatitis B virus following systemic chemotherapy for malignant lymphoma. Int J Hematol90:13-23.
6. Lopez-Serrano P, de la Fuente Briongos E, Alonso EC, Pérez-Calle JL, Rodríguez CF (2015)Hepatitis B and immunosuppressive therapies for chronic inflammatory diseases: When and how to apply prophylaxis, with a special focus on corticosteroid therapy. World J Hepatol7:539-547.
7. Mori N, Suzuki F, Kawamura Y, Sezaki H, Hosaka T, et al. (2012) Determinants of the clinical outcome of patients with severe acute exacerbation of chronic hepatitis B virus infection. J Gastroenterol47:1022-1029.
8. Pei SN, Chen CH, Lee CM, Wang MC, Ma MC, et al. (2010) Reactivation of hepatitis B virus following rituximab-based regimens: a serious complication in both HBsAg-positive and HBsAg-negative patients. Ann Hematol89:255-262.
9. Perrillo RP, Gish R, Falck-Ytter YT (2015) American Gastroenterological Association Institute technical review on prevention and treatment of hepatitis B virus reactivation during immunosuppressive drug therapy. Gastroenterology148:221-244.
10. Imai K, Togami H, Okamoto T (2010) Involvement of histone H3 lysine 9 (H3K9)methyltransferase G9a in the maintenance of HIV-1 latency and its reactivation by BIX01294. J Biol Chem 285: 16538-16545.
11. Fatemi N, Dusick J, Mattozo C, McArthur DL, Cohan P, et al. (2008) Pituitary hormonal loss and recovery after transsphenoidal adenoma removal. Neurosurgery63: 709-719.
12. Xu Z, Lee Vance M, Schlesinger D, Sheehan JP (2013) Hypopituitarism after stereotactic radiotherapy for pituitary adenomas. Neurosurgery72: 630-637.
13. Tsou PL, Lee HS, Jeng YM, Huang TS (2002) Submassive liver necrosis in a hepatitis B carrier with Cushing��?s syndrome. J Formos Med Assoc101:156-158.
14. Masarone M, De Renzo A, La Mura V, Sasso FC, Romano M, et al. (2014) Management of the HBV reactivation in isolated HBcAb positive patients with Non Hodgkin Lymphoma. BMC Gastroenterol 14:31.