AB1269\u2005RISK FACTORS ASSOCIATED WITH PERIPHERAL NEUROPATHY (PN) IN ANCA-ASSOCIATED VASCULITIS (AAV):

Abstract

Background: Few studies have reported on the risk factors associated with PN in AAV. Vasculitic PN in AAV has been associated with male sex, arthritis, cutaneous, mucous membranes, and ENT manifestations of vasculitis1,2,3. PN can lead to life quality impairment, as only 35% of the patients with PN have complete symptoms resolution within 6 months1. Objectives: Along with describing the prevalence of incidence of PN in our cohort, we undertook this study to identify the risk factors associated with PN in AAV. Methods: From 153 AAV patients (defined according to the EMA algorithm), 97 were eligible (complete data and no exclusion criteria -diabetes mellitus, axial disc disease, malignancies, herpetic neuralgia, other comorbidities). Clinical, electromyographic (EMG) and histopathological data were recorded. According to the presence (cases) or absence (controls) of clinical data for PN descriptive analysis is reported as means ± SD or medians (interquartile range-IQR). Categorical variables are reported as percentages. Student t-test and Mann-Whitney U-test were used for continuous variables, two-tailed Fisher exact test to compare proportions differences. To estimate PN predictors, bivariate and multivariate models to establish hazard ratios [HR] were built and analysed with Cox regression. Results: Thirty-two (33%) patients (19-GPA, 9-MPA, 4-EGPA; 17 prevalent, 15 incident) had PN. Mean age±SD was 47.2±13.0 at vasculitis diagnosis. The median follow-up was 55 months (IQR 37-79) until PN diagnosis. Main symptoms: paresthesias 97%, hypoesthesia 72%, hyporeflexia 53%, burning pain and weakness 47%, mononeuritis multiplex 44%. Diagnostic EMG support in 60%. The estimated incidence rate of PN was of 4/100 persons-year. Differences between cases (n-32) and controls (n-65) were smoking history (p=0.03), drug abuse (p=0.04), and a higher mean BVAS (p<0.001) at AAV diagnosis. The table shows the factors associated with a higher risk for the development of PN. After adjustment for covariates and in a multivariate analysis, a higher BVAS at baseline conferred risk for the presence of PN (HR=1.1, 95% CI 1.03-1.25, p=0.01). Table. Risk factors for development of PN in AAV expressed as hazard ratios after Cox regression analysis. Variable HR (95% CI) p value Drug abuse history 4.34 (1.2-15.6) 0.025 Arthritis 2.98 (1.01-8.7) 0.04 BVAS at AAV diagnosis 1.13 (1.03-1.23) 0.005 Conclusion: The risk for development of PN is related to overall higher disease activity when AAV is diagnosed. However, it may not be present after many years of its appearance. We had almost the same amount of incident cases than prevalent ones at diagnosis. Therefore, patients with a highly active disease need to be followed up specifically in order to detect PN during the disease course, probably with specialised neurological evaluation. References [1] - Suppiah R, Hadden RDM, Batra R, et al. Peripheral neuropathy in ANCA-associated vasculitis: outcomes from the European Vasculitis Study Group trials. Rheumatology. 2011;50:2214-22. [2] - de Groot K, Schimdt DK, Arlt AC, et al. Standarized Neurologic Evaluations of 128 Patients With Wegener Granulomatosis. Arch Neurol. 2001;58:1215-21. [3] - Nishino H, Rubino FA, DeRemee RA, et al. Neurological involvement in Wegener’s granulomatosis: an analysis of 324 consecutive patients at the Mayo Clinic. Ann Neurol 1993;33:4-9. Disclosure of Interests: None declared