Abstract
INTRODUCTION: Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease. Detection of antinuclear antibodies (ANAs) aids in the diagnosis of SLE. The indirect immunofluorescence (IIF) assay is often used a routine screening test for the detection of ANA. The pathogenic role and significance of various patterns produced in IIF is yet to be explored. AIM: This study aimed to detect ANA patterns generated by IIF and correlate these patterns with specific antibodies detected by line immunoassay. We also investigated the significance of each ANA pattern and its association with specific serological SLE markers, such as complement molecules, anti-dsDNA, antiphospholipid antibody, and C-reactive protein (CRP), along with associations with direct Coombs test (DCT). MATERIALS AND METHODS: We conducted a retrospective study that included 204 patients newly diagnosed with SLE according to the European Alliance of Associations for Rheumatology/American College of Rheumatology (EULAR/ACR) criteria. The detection and pattern determination of ANA was performed by IIF using HEp-20-10. Furthermore, line immunoassay was performed, and the antibody profile of each sample was obtained. Other immunodiagnostic markers were analyzed, including C3, C4, anti-dsDNA, antiphospholipid antibodies (anti-cardiolipin antibodies, anti-beta-2-glycoprotein I, and lupus anticoagulant), CRP, and DCT. RESULTS: Of the 204 samples, the most frequent ANA pattern observed was nucleus speckled (52.9%), followed by nucleus homogenous (27.5%), mixed (13.7%), and cytoplasm speckled (5.9%). The nucleus homogenous pattern showed the most pathogenic immune profile due to its close association with markers of disease activity, namely, high anti-dsDNA titer, low C3 level, and DCT positivity. Conclusion: This study showed that the most common pattern associated with SLE is nucleus speckled, followed by the nucleus homogenous pattern. Based on associations with specific serological markers, the nucleus homogenous pattern may be linked to a high disease activity in SLE.