Rheumatology Advance Access originally published online on June 13, 2007
Rheumatology 2007 46(8):1381-1382; doi:10.1093/rheumatology/kem139
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Reply: Safety of anti-TNF-
therapy in rheumatoid arthritis (RA) and spondylarthropathies (SA) with concurrent B or C chronic hepatitis
Rheumatology Department and 1Hepatogastroenterology and nutrition federation, University Hospital, Nice, France
Correspondence to: C. ROUX. E-mail: roux101fr{at}yahoo.fr
SIR, We have read the comments of Raftery et al. [1] and appreciate their interest in our report. The two patients they described previously, and again now, with a longer follow-up, are both HBsAg-negative (absence of ongoing infection) meanwhile our three patients are HBs Ag-positive and must be considered carriers of B hepatitis and chronic HBV infection. We fully agree with their comment ‘Prophylactive antiviral therapy is indicated routinely in HBs Ag positive patients’. That situation is the most frequent in clinical practice.
Negative HBsAg test does not exclude, on a few occasions, an active HBV infection. Patients with occult HBV infection who are persistently HbsAg-negative, but with evidence of HBV DNA in the serum, have been reported [2,3]. Some of these patients have chronic HBV infection. Chronically infected patients either possess HBsAg escape mutants that are not recognized by the commercially available HBsAg assays or have very low levels of viraemia with undetectable HBsAg. Some of these patients with chronic HBV infection have anti-HBc as the sole marker of HBV infection (anti-HBc only) or can be completely negative for any serological marker of HBV infection (except HBV DNA).
This situation is infrequent, but up to 5% of the healthy blood donors have an isolated anti-HBc result [4].
So, the interpretation of those tests must be careful, and the decision to treat or not, needs probably to also consider other biological and/or clinical parameters. Moreover, HBV reactivation may occur after immunosuppressive therapy, in patients with resolved infection who are HBsAg-negative, anti-HBs-positive and anti-HBc-positive (as in patient 2 of Raftery et al.) [5].
Prophylactic treatment in such cases with prolonged immunosuppressive conditions also seems to be discussed, to prevent HBV reactivation, even if the risk is probably limited and if, unfortunately, lamivudine may potentially be associated with resistant HBV strains.
Reactivation is a potentially serious event, and as a weak risk of reactivation exist in case of HbsAg-negative, anti-HBs and/or anti-HBc-positive patients, the decision can be made individually based on the likelihood of reactivation and clinical and biological (ALAT, HBV DNA) follow-up should be recommended [6].
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- Raftery G, Griffiths B, Kay L, Kane D. Hepatitis B virus and tumour necrosis factor alpha blocking agents. Ann Rheum Dis (2004) 64(Suppl. 2). ii2–12eLetter 15 February 2006.
- Allain JP. Occult hepatitis B virus infection: implications in transfusion. Vox Sang (2004) 86:83–91.[CrossRef][Web of Science][Medline]
- Torbenson M, Thomas DL. Occult hepatitis B. Lancet Infect Dis (2002) 2:479–86.[CrossRef][Web of Science][Medline]
- Hatzakis A, Magiorkinis E, Haida C. HBV virological assessment. J Hepatol (2006) 44(Suppl. 1):S71–6.[Web of Science][Medline]
- Mindikoglu AL, Regev A, Schiff ER. Hepatitis B virus reactivation after cytotoxic chemotherapy: the disease and its prevention. Clin Gastroenterolog Hepatol (2006) 4:1076–81.[CrossRef]
- Calabrese LH, Zein NN, Vassilopoulos D. Hepatitis B virus (HBV) reactivation with immunosuppressive therapy in rheumatic diseases: assessment and preventive strategies. Ann Rheum Dis (2006) 65:983–9.
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