Background Chronic and latent infections like tuberculosis (TB) are known triggers for developing autoimmunity. It is not known the consequences of latent TB infection (LTBI) in individuals who are genetically predisposed to develop autoimmune disease. Although several studies reported autoantibodies in first-degree relatives (FDR) of SLE, association between LTBI and these antibodies is not clear. This study focused on the prevalence of autoantibody levels in FDRs of SLE and assess any association with LTBI.
Methods This is a single center cross sectional study. FDRs of SLE who were apparently healthy and without past h/o TB were recruited (n=167). Demography, comorbidity and various autoantibodies (antibodies to beta-2 glycoprotein, cardiolipin, thyroid peroxidase, cyclic citrullinated peptide, glutamic acid decarboxylase, antinuclear antibody) were measured. LTBI was assessed using TB-IGRA (IFN-γ release assay). Based on results of TB-IGRA and seropositivity to antibodies, FDR were divided into 4 groups- Autoantibody positive and negative groups with and without LTBI. Basal IFN-γ and mycobacterium tuberculosis antigen specific IFN-γ levels were assessed in the unstimulated and stimulated tubes respectively.
Results In FDRs, overall prevalence of LTBI 25.7% (n=43) which is lesser than prevalence in the general population (40%). Prevalence of LTBI was numerically higher among FDRs positive for any autoantibody compared to the negative group (32.6% vs 21.8%), but without statistical significance. Seropositivity of various autoantibodies was comparable between those with and without LTBI. Basal and stimulated IFN-γ levels was lower in IGRA and autoantibodies positive group(p=0.014) compared to IGRA positive antibody negative group.
Conclusions This study showed higher prevalence of LTBI in antibody positive FDRs of SLE. Basal and stimulated IFN-γ levels were lower in antibody positive group, in contrast to SLE patients who have higher basal IFN-γ. Further longitudinal studies would be required to see the effect of these autoantibodies on LTBI and risk of progression to TB.
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