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Originally published as JCO Early Release 10.1200/JCO.2009.21.9881 on April 13 2009 © 2009 American Society of Clinical Oncology.
Reply to Y.X. Koo et al
Department of Clinical Oncology, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong Special Administrative Region, People's Republic of China We agree with Koo et al1 that patients who are to receive rituximab therapy should be screened for antibody to hepatitis B core antigen (anti-HBc) status if they are hepatitis B surface antigen (HBsAg) negative. We would like to emphasize that except for brief information provided in abstract and short case-report formats, there are limited data on this topic in the current literature; hence, additional detailed reports on similar populations are certainly warranted. We reviewed the abstract by Koo et al2 and would like to present additional information that is not provided in the authors' letter.1 The abstract describes 67 patients with lymphoma found to be HBsAg negative and anti-HBc positive who received systemic treatment. Seven patients (10.4%) received prophylactic lamivudine—a management approach Koo et al do not endorse in their letter. Of the 67 patients, 46 received systemic treatment including rituximab. We have been unable to ascertain whether the seven patients were among this group, because Koo et al fail to provide this information in their letter. In addition, we are still unable to comment on their reported low rate of hepatitis B virus (HBV) reactivation, because neither the abstract nor the letter provide information on type of lymphoma, sex, anti-HBs status, treatment regimen and duration of therapy, or frequency and duration of clinical, virologic, and biochemical follow-up, especially post-rituximab therapy, or other clinical information. This information would be particularly important because it was suggested in their abstract that clinical practice differed among physicians at their institute. Similarly, we are unable to comment on the study by Targhetta et al,3 because information on type of lymphoma, sex, anti-HBs status, and treatment regimen and duration of therapy, as well as other clinical information, is not available in the report. Data in our report,4 which described an HBV reactivation rate of 25% in the studied patient population, corresponded with those presented by Metzler et al5 at the 59th Annual Meeting of the American Association for the Study of Liver Diseases in November 2008 (San Francisco, CA). Metzler et al reported that no serologic or virologic data were available after the last dose of rituximab for seven of the 20 anti-HBc– and anti-HBs–positive patients treated with rituximab. Of the remaining 13 patients, three were found to have developed HBV reactivation after treatment with rituximab, which supports a similar incidence of HBV reactivation in our reported study. Nonetheless, we agree with Koo et al1 that in addition to the less informative anecdotal experience and isolated case reports, more information on experience of oncologists is needed. HBV reactivation is a phenomenon that includes two well-known major categories (ie, HBsAg positive v HBsAg negative/anti-HBc positive). These have both been well described and examined in reviews by experts.6,7 These reviews acknowledge that the definition of HBV reactivation has been arbitrary. Therefore, we disagree with the application by Koo et al1 of another term to describe the same condition; this may merely create more confusion for readers. We would like to confirm that our reported series4 involved consecutive patients treated at one institute in an endemic area where uniform protocol was available. Finally, we would like to clarify again that to prevent HBV reactivation and its associated morbidity and mortality, we suggested two possible approaches. The first was to closely monitor HBV DNA and serum biochemistry during and for at least 6 months after completion of rituximab therapy in anti-HBc–positive patients, particularly those who are also anti-HBs negative, and administer antiviral prophylaxis promptly on detection of reactivation. However, it has been commonly observed that this approach has not been universally successful, possibly because of delays in antiviral administration; it may not be cost effective, and it can be difficult to conduct in clinics that lack adequate laboratory support. We thus suggested the alternative of prophylactic antiviral therapy. Koo et al1 may consider the number of patients studied to have been too few. However, we maintain our study shows that physicians should take into account the cost of intense monitoring and assess whether to consider an alternative approach to a potentially ineffective therapy. AUTHORS' DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST The author(s) indicated no potential conflicts of interest. REFERENCES
1. Koo YX, Tan DSW, Tan BH, et al: Risk of hepatitis B virus reactivation in patients who are hepatitis B surface antigen negative/antibody to hepatitis B core antigen positive and the role of routine antiviral prophylaxis. J Clin Oncol 27:2570–2571, 2009. 2. Koo YX, Tan SW, Tan BH, et al: Risk of hepatitis B virus (HBV) reactivation and role of anti-viral prophylaxis in lymphoma patients with past HBV infection (HBV antigen negative but anti-hepatitis B core antibody positive) receiving chemo-immunotherapy. Blood 112: 2008 abstr 3768. 3. Targhetta C, Cabras MG, Mamusa AM, et al: Hepatitis B virus-related liver disease in isolated anti-hepatitis B-core positive lymphoma patients receiving chemo- or chemo-immunetherapy. Haematologica 93:951–952, 2008. 4. Yeo W, Chan TC, Leung NW, et al: Hepatitis B virus reactivation in lymphoma patients with prior resolved hepatitis B undergoing anticancer therapy with or without rituximab. J Clin Oncol 27:605–611, 2009. 5. Metzler F, Mederacke I, Manns MP, et al: Rituximab leads to reactivation of hepatitis B in individuals with resolved infection. Hepatology 48:685A; 2008 (suppl 4) abstr 848.[CrossRef] 6. Lok AS, McMahon BJ: Chronic hepatitis B. Hepatology 45:507–539, 2007.[CrossRef][Medline] 7. Yeo W, Johnson PJ: Diagnosis, prevention and management of hepatitis B virus reactivation during anticancer therapy. Hepatology 43:209–220, 2006.[CrossRef][Medline]
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Copyright © 2009 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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