Hepatitis B virus reactivation in rheumatoid arthritis and ankylosing spondylitis patients treated with anti-TNFα agents: A retrospective analysis of 49 cases

Han Hee Ryu, Eun Young Lee, Kichul Shin, In Ah Choi, Yun Jong Lee, Bin Yoo, Min Chan Park, Yong Beom Park, Sang Cheol Bae, Wan Hee Yoo, Sung Il Kim, Eun Bong Lee, Yeong Wook Song

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Abstract

Clinical guidelines regarding anti-viral prophylaxis for HBV surface antigen (HBsAg) carriers starting anti-TNFα agents are not yet fully established, even in endemic regions of HBV infection. We retrospectively collected the clinical data of 52 HBsAg carriers with rheumatoid arthritis (RA) or ankylosing spondylitis (AS) that had been administered anti-TNFα treatment at seven medical centers in South Korea. Periodic data of liver function tests and serum HBV DNA were both utilized to assess HBV reactivation. The YMDD motif mutation of HBV DNA polymerase was tested in lamivudine-treated patients with elevated HBV DNA. Three of the 52 patients were excluded from the analysis. Of the 49 analyzed patients, 20 patients received anti-viral prophylaxis (15 lamivudine, five entecavir) with anti-TNFα treatment. The remaining 29 patients were treated with anti-viral agents if needed at the discretion of the clinician and did not receive prophylaxis. Of the 29 patients who did not receive primary prophylaxis, two (6.9%) developed viral reactivation within a year of anti- TNFα treatment. In the prophylaxis group, one patient developed viral reactivation at week 64 of anti-TNFα therapy attributed to YMDD mutation caused by lamivudine. Patients with HBV reactivation all responded well to antiviral therapy. In summary, anti-viral prophylaxis helped preventing HBV reactivation in HBsAg carriers with RA or AS starting anti-TNFα, yet mutation in the YMDD motif of HBV DNA polymerase could be detrimental to some patients under long-term lamivudine prophylaxis.

Original languageEnglish
Pages (from-to)931-936
Number of pages6
JournalClinical Rheumatology
Volume31
Issue number6
DOIs
Publication statusPublished - 2012 Jun 1

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Ankylosing Spondylitis
Hepatitis B virus
Rheumatoid Arthritis
Lamivudine
Surface Antigens
DNA-Directed DNA Polymerase
Mutation
Therapeutics
Republic of Korea
Liver Function Tests
DNA
Antiviral Agents
Guidelines
Infection

All Science Journal Classification (ASJC) codes

  • Rheumatology

Cite this

Ryu, Han Hee ; Lee, Eun Young ; Shin, Kichul ; Choi, In Ah ; Lee, Yun Jong ; Yoo, Bin ; Park, Min Chan ; Park, Yong Beom ; Bae, Sang Cheol ; Yoo, Wan Hee ; Kim, Sung Il ; Lee, Eun Bong ; Song, Yeong Wook. / Hepatitis B virus reactivation in rheumatoid arthritis and ankylosing spondylitis patients treated with anti-TNFα agents : A retrospective analysis of 49 cases. In: Clinical Rheumatology. 2012 ; Vol. 31, No. 6. pp. 931-936.
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abstract = "Clinical guidelines regarding anti-viral prophylaxis for HBV surface antigen (HBsAg) carriers starting anti-TNFα agents are not yet fully established, even in endemic regions of HBV infection. We retrospectively collected the clinical data of 52 HBsAg carriers with rheumatoid arthritis (RA) or ankylosing spondylitis (AS) that had been administered anti-TNFα treatment at seven medical centers in South Korea. Periodic data of liver function tests and serum HBV DNA were both utilized to assess HBV reactivation. The YMDD motif mutation of HBV DNA polymerase was tested in lamivudine-treated patients with elevated HBV DNA. Three of the 52 patients were excluded from the analysis. Of the 49 analyzed patients, 20 patients received anti-viral prophylaxis (15 lamivudine, five entecavir) with anti-TNFα treatment. The remaining 29 patients were treated with anti-viral agents if needed at the discretion of the clinician and did not receive prophylaxis. Of the 29 patients who did not receive primary prophylaxis, two (6.9{\%}) developed viral reactivation within a year of anti- TNFα treatment. In the prophylaxis group, one patient developed viral reactivation at week 64 of anti-TNFα therapy attributed to YMDD mutation caused by lamivudine. Patients with HBV reactivation all responded well to antiviral therapy. In summary, anti-viral prophylaxis helped preventing HBV reactivation in HBsAg carriers with RA or AS starting anti-TNFα, yet mutation in the YMDD motif of HBV DNA polymerase could be detrimental to some patients under long-term lamivudine prophylaxis.",
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Hepatitis B virus reactivation in rheumatoid arthritis and ankylosing spondylitis patients treated with anti-TNFα agents : A retrospective analysis of 49 cases. / Ryu, Han Hee; Lee, Eun Young; Shin, Kichul; Choi, In Ah; Lee, Yun Jong; Yoo, Bin; Park, Min Chan; Park, Yong Beom; Bae, Sang Cheol; Yoo, Wan Hee; Kim, Sung Il; Lee, Eun Bong; Song, Yeong Wook.

In: Clinical Rheumatology, Vol. 31, No. 6, 01.06.2012, p. 931-936.

Research output: Contribution to journalArticle

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T1 - Hepatitis B virus reactivation in rheumatoid arthritis and ankylosing spondylitis patients treated with anti-TNFα agents

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AU - Ryu, Han Hee

AU - Lee, Eun Young

AU - Shin, Kichul

AU - Choi, In Ah

AU - Lee, Yun Jong

AU - Yoo, Bin

AU - Park, Min Chan

AU - Park, Yong Beom

AU - Bae, Sang Cheol

AU - Yoo, Wan Hee

AU - Kim, Sung Il

AU - Lee, Eun Bong

AU - Song, Yeong Wook

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AB - Clinical guidelines regarding anti-viral prophylaxis for HBV surface antigen (HBsAg) carriers starting anti-TNFα agents are not yet fully established, even in endemic regions of HBV infection. We retrospectively collected the clinical data of 52 HBsAg carriers with rheumatoid arthritis (RA) or ankylosing spondylitis (AS) that had been administered anti-TNFα treatment at seven medical centers in South Korea. Periodic data of liver function tests and serum HBV DNA were both utilized to assess HBV reactivation. The YMDD motif mutation of HBV DNA polymerase was tested in lamivudine-treated patients with elevated HBV DNA. Three of the 52 patients were excluded from the analysis. Of the 49 analyzed patients, 20 patients received anti-viral prophylaxis (15 lamivudine, five entecavir) with anti-TNFα treatment. The remaining 29 patients were treated with anti-viral agents if needed at the discretion of the clinician and did not receive prophylaxis. Of the 29 patients who did not receive primary prophylaxis, two (6.9%) developed viral reactivation within a year of anti- TNFα treatment. In the prophylaxis group, one patient developed viral reactivation at week 64 of anti-TNFα therapy attributed to YMDD mutation caused by lamivudine. Patients with HBV reactivation all responded well to antiviral therapy. In summary, anti-viral prophylaxis helped preventing HBV reactivation in HBsAg carriers with RA or AS starting anti-TNFα, yet mutation in the YMDD motif of HBV DNA polymerase could be detrimental to some patients under long-term lamivudine prophylaxis.

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