ArticleLupus2024
Different patterns of longitudinal changes in antinuclear antibodies titers in children with systemic lupus erythematosus and Sjögren's syndrome.
Article in Lupus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- The Evolving Landscape of CAR T-Cell Therapy in Autoimmune Diseases: A State-of-the-Art Review (2025).Clinical reviews in allergy & immunology · 2026Review
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11 authors.
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Abstract
objectiveto investigate the trend of autoantibody titers during a 2-year follow-up in pediatric systemic lupus erythematosus (pSLE) and pediatric Sjögren's syndrome (pSS).
methodsAutoantibodies testing was performed every 3-4 months during 2 years from disease onset in a cohort of children with pSLE and pSS.
resultsWe enrolled 21 children with pSLE and 22 children with pSS. All pSLE patients at 2 years showed ANA titers significantly lower compared to disease onset. Eleven patients (73%) were still ANA positive at 2 years, while 4 (26%) became ANA negative. At diagnosis, 12 (80%) patients showed a homogeneous pattern, while 3 (20%) patients showed a speckled pattern. The latter remained ANA positive with the same pattern; only 2 patients with a homogenous pattern converted to speckled, 4 patients with a homogeneous pattern became ANA negative. ANA negative pSLE patients showed lower levels of interferon score compared to ANA positive patients. Anti-dsDNA titers declined equally in the two groups. All patients with pSS, at disease onset, were ANA and anti-Ro positive and 14 (66%) were anti-La positive. After 2 years of follow-up, 100% remained ANA positive but showed significant lower titers. During follow-up anti-Ro and anti-La titers remained stable.
conclusiondifferent patterns in changes of ANA and ENA titers in pSLE and pSS were shown. At 2 years of follow-up, all pSLE patients had a lower ANA titer and 26% became negative; however, all pSS patients remained both ANA and ENA positive. This evidence may be due to different pathogenetic pathways in SLE and pSS.
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