ArticleClinical rheumatology2014
Detection of asymptomatic cranial neuropathies in patients with systemic lupus erythematosus and their relation to antiribosomal P antibody levels and disease activity.
Article in Clinical rheumatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- The Discrepancy of ANA and Compartment Bead Patterns Suggestive of a Neuropsychiatry Systemic Lupus Erythematosus (NPSLE).Case reports in psychiatry · 2023Article
- Mouse models, antibodies, and neuroimaging: Current knowledge and future perspectives in neuropsychiatric systemic lupus erythematosus (NPSLE).Frontiers in psychiatry · 2023Review
- Progress in the Pathogenesis and Treatment of Neuropsychiatric Systemic Lupus Erythematosus.Journal of clinical medicine · 2022Review
- Peripheral Nervous System Disease in Systemic Lupus Erythematosus: Results From an International Inception Cohort Study.Arthritis & rheumatology (Hoboken, N.J.) · 2020Article
- Review
- Neurological Disease in Lupus: Toward a Personalized Medicine Approach.Frontiers in immunology · 2018Review
- Brainstem Reflexes in Systemic Lupus Erythematosus Patients Without Clinical Neurological Manifestations.Noro psikiyatri arsivi · 2017Article
- Immunotherapies for Neurological Manifestations in the Context of Systemic Autoimmunity.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The objectives of this study are to assess the risk of asymptomatic cranial neuropathy among patients with systemic lupus erythematosus (SLE) and find any association with disease activity and antiribosomal P antibodies. This study is a case-control study including 60 female patients and 30 healthy female controls. Disease activity was measured with the SLE disease activity index (SLEDAI). All patients were evaluated using evoked potentials, blink reflex, and levels of antiribosomal P antibodies. Patients with abnormal electrophysiological parameters had significantly higher levels of antiribosomal P antibodies (P = 0.034) and secondary antiphospholipid syndrome (P = 0.044). Antiribosomal P antibodies (odds ratio 5.4, 95 % confidence interval 1.002-1.03, P = 0.002) and presence of anti-DNA antibodies (odds ratio 1.01, 95 % confidence interval 1.2-24.8, P = 0.032) were independent risk factors for the presence of the abnormal electrophysiological parameters. Disease duration was positively correlated with wave 1 of the auditory brain reflex (P < 0.001) and a latency of the evoked blink reflex (component R1, P = 0.013). SLEDAI scores were positively correlated with latencies of the visually evoked potential (P100, P = 0.02), wave 1 of the auditory brain reflex (P < 0.001), and a latency of the evoked blink reflex (R2c, P = 0.005). Steroid dosage was negatively correlated with P100 latencies (P = 0.042) and components of the evoked blink reflex (R1, P = 0.042; R2i, P = 0.041; R2c, P < 0.001). Because abnormalities in the visually evoked potential and blink reflex were associated with antiribosomal P antibodies, they can be useful for detecting asymptomatic cranial neuropathy. Further studies on large number of patients should be done to determine any association.
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