Background Hepatitis B Virus (HBV) infection is widespread. Immunosuppressive agents may precipitate an increase in HBV replication followed by a flare of hepatitis B that may be severe and even fatal. There is no consensus about the minimal steroids dose or duration of therapy leading to HBV reactivation. There are no guidelines regarding the need for antiviral prophylactic treatment in steroid or DMARD’s treated HBV carriers.
Objectives To assess whether short courses of steroids induce HBV reactivation in patients (pts) with immunosuppressive therapy.
Methods A database search was performed for HBsAg positive or anti HB core positive, anti HBs negative pts hospitalized in our Rheumatology department during the years 2001-2010 and treated with steroids. Liver function tests (LFT), HBV serologic tests and serum HBV DNA at baseline and 1-3 months after discharge were recorded. A supervised treatment course was defined as intravenous methylprednisolone treatment for 7 days.
Results Complete data were found for 23 pts with a total of 73 supervised treatment courses (all anti-HBcore positive, anti-HBs negative, 18 pts HBsAg positive). The study group comprised pts with rheumatoid arthritis (11), psoriatic arthritis (3), ankylosing spondylitis (1), Behcet disease (1), idiopathic inflammatory myositis (1), SLE (1), systemic sclerosis (2), gout (2) and interstitial lung disease (1). All pts received intravenous methylprednisolone (mean dose 33.9±24mg/d, range 12.5-500) for 7 days. The concomitant medications included DMARDs in 15 pts (methotrexate -3, imuran -7, cyclophospamide-5, cellcept-1, cyclosporine-2), biologicals (7 pts-antiTNFα, 3-rituximab). Ten pts were on chronic steroid therapy, besides DMARDs (10.3±4.7mg, range 5-20mg). HBV DNA was positive at baseline in 7 pts. LFT (ALT) were elevated at baseline in 4 pts, (HBV DNA was positive in one of them) and returned to normal in all pts. Steroid therapy by itself did not trigger exacerbation of HBV hepatitis. Seroconversion to positive HBV DNA occurred in 3 pts, in one of them, accompanied by elevation of transaminases (ALTx4-7). The etiology was exposure to anti TNFα (1 pt), rituximab and cyclophosphamide (1pt) and azathioprine (1pt). ALT elevation (>3ULN) occurred in 2 pts, after cyclophosphamide treatment. Lamivudine therapy reduced the viral load and the LFT in all pts and even below detection in 2 pts. Six pts treated with lamivudine received 14 supervised treatment courses, No HBV reactivation occurred in lamivudine treated pts following recurrent biological or cyclophosphamide exposure.
Conclusions Short courses of steroids seem to be safe in HBV carriers, even in the presence of DMARDs. Lamivudine prophylaxis should be considered not only in pts exposed to biologicals, but also to cyclophosphamide. Larger prospective trials are needed to establish guidelines.
Disclosure of Interest None Declared