No evidence of autoimmune disorders in antiretroviral-experienced HIV-1-infected individuals after long-term treatment with raltegravir

Background: The HIV integrase inhibitor raltegravir (RAL) can exacerbate autoimmune diseasesin genetically predisposed mice. To evaluate whether this may occur in clinical practice, weclinically monitored HIV positive patients treated with RAL and measured a panel ofautoantibodies (auto-Abs) during the first year of RAL treatment.Methods: This was a longitudinal study in 109 antiretroviral-experienced patients who started aRAL-based regimen and were followed up for more than two years. Forty-five of them were testedat baseline (before starting RAL) and after 12 months for the presence of the following auto-Abs:anti-nuclear antibodies (ANA), anti-double-stranded (ds)DNA, anti-smooth-muscle antibodies(ASMA), anti-thyreoglobulin (anti-TG) and anti-thyroid peroxidase (anti-TPO) antibodies, anticardiolipin(anti-CL) IgG and IgM, anti-nuclear extractable antigens (ENA) including anti-SMRNP antigen, anti–Ro (SSA) antigen and anti-La (SSB) antigen.Results: A low rate of clinically relevant autoimmune diseases was observed at study entry (3/109,2.8%, 95%CI = 0.004 – 0.059). No exacerbations were observed during follow-up. During thesecond year of RAL-based therapy a previously healthy patient developed psoriasis. At baseline17/45 (37.8%) patients tested for the presence of auto-Abs were positive. Most subjects (13) werepositive for anti-CL. After 12 months of RAL exposure 9/45 subjects were positive ( 20%, p =0063). A positive correlation was found between HIV-1 RNA and anti-CL antibody concentration(p = 0.010).Conclusions: According to these results, RAL does not promote antibody-mediated immunedisorders at least in the mid-term. A prolonged follow up and an extension of autoAbs’ panel arerecommended to support these results.