Peripheral Neuropathy Due to Systemic Lupus Erythematosus (SLE) Itself: Incidence, Disease Risk Factors and Outcome

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2012
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WILEY-BLACKWELL
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ARTHRITIS AND RHEUMATISM, v.64, n.10, suppl.S, p.S273-S273, 2012
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Background/Purpose: Peripheral neuropathy (PN) solely attributable to SLE itself is difficult to define since most of these patients are exposed to several other conditions that may cause this manifestation. The aim is to determine characteristics and outcome of PN attributed exclusively to SLE and its possible association with clinical/laboratorial features in a large cohort. Methods: SLE patients (ACR 1997) with PN were identified from our Lupus Outpatient Clinic computerized database of 1038 patients. Only patients with definitive PN proved by electroneuromyography were included. Exclusion criteria were conditions related to PN: diabetes mellitus, alcohol consumption, use of any drug related to neuropathy (thalidomide, statins, etc.), thyroid disease, infection, cancer, vitamin B12 deficiency, renal or hepatic failure, and other autoimmune disease (antiphospholipid syndrome, Sjogren’s syndrome, etc.). Medical records were extensively reviewed and included clinical/laboratorial data, treatment, and evolution. Each SLE patient with PN [n 22] was compared with 2 SLE patients without PN (controls) [n 44] that were age- and sex-matched and had similar disease duration. Results: PN exclusively attributed to SLE was identified in 22 patients (2.1%). The mean age (34.4 11.6 vs. 33.9 9.6 years, p 0.85) and disease duration (9.2 7.7 vs. 9.9 6.8 years, p 0.73) of PN were similar to controls. The interval between SLE onset and PN diagnosis was 4.9 5.7 years and the mean SLEDAI scores was higher in PN patients (5.4 7.6 vs. 1.8 2.9,p 0.001). The most common pattern on electroneuromyography was sensorimotor polyneuropathy of lower limbs (50%), followed by monon-europathy (26.9%), and polyradiculoneuropathy (15.3%). PN was associated to hematological involvement (72.7% vs. 43.2%,p 0.036), leukopenia (50% vs. 20.5%,p 0.022), lymphopenia (68.2% vs. 29.5%,p 0.004), cutaneous vasculitis (54.5% vs. 22.7%,p 0.014), and anti-Sm (50% vs. 15.9%,p 0.007). Multivariate analysis revealed that PN was related to anti-Sm (OR 5.36; 95%CI 1.37–20.99) and cutaneous vasculitis (OR 4.97; 95%CI 1.23–20.08). All SLE patients received corticosteroids, most of them associated with immunosuppressive drug (59% cyclophosphamide; 31.8% azathioprine). After immunosuppressive therapy, 63.6% improved of neurological symptoms and 31.8% remained stable. Conclusion: Our study suggested that PN attributed to SLE itself is rare in the absence of other conditions and seems to be strongly associated to anti-Sm antibodies and cutaneous vasculitis. A favorable outcome with immunosuppressive therapy is observed in most of SLE patients with this neurological manifestation.
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