RESUMO

OBJECTIVE: The aims of this study were to determine the frequency of asymptomatic sensorineural hearing loss (SNHL) in systemic lupus erythematosus (SLE) and to determine the association between SNHL and demographic, clinical, and laboratory features and cardiovascular risk factors. METHODS: We conducted a cross-sectional study including consecutive female SLE patients. We performed audiometry and clinical and laboratory evaluation and determined cardiovascular risk factors in all patients. Statistical analysis included principal component analysis and logistic regression. RESULTS: Eighty-nine women were included with mean age of 38.98 (SD, 7.77) years and mean disease duration of 10.29 (SD, 9.19) years. Asymptomatic SNHL was observed in 14 patients (16%). In logistic regression model, only low-density lipoprotein levels (z = 2.64; P = 0.008) were associated with SNHL. CONCLUSIONS: We observed asymptomatic SNHL in 16% of SLE and an association with low-density lipoprotein levels suggesting atherosclerosis as a mechanism. Follow-up is needed to determine clinical implications.

Assuntos

Doenças Assintomáticas/epidemiologia , Doenças Cardiovasculares/epidemiologia , LDL-Colesterol/sangue , Perda Auditiva Neurossensorial , Lúpus Eritematoso Sistêmico , Adulto , Audiometria/métodos , Brasil/epidemiologia , Estudos Transversais , Feminino , Perda Auditiva Neurossensorial/sangue , Perda Auditiva Neurossensorial/diagnóstico , Perda Auditiva Neurossensorial/etiologia , Humanos , Lúpus Eritematoso Sistêmico/complicações , Lúpus Eritematoso Sistêmico/epidemiologia , Pessoa de Meia-Idade , Fatores de Risco , Estatística como Assunto , Avaliação de Sintomas/métodos

RESUMO

In the autoimmune disease systemic lupus erythematosus (SLE), our normal antiviral defenses are inappropriately activated, resulting in over-activity of the type I interferon (IFN) pathway. This increased activity of the type I IFN pathway is an important primary pathogenic factor in the disease. Emerging evidence has implicated the antiviral helicases in this process. The antiviral helicases normally function as nucleic acid receptors in viral immunity. Genetic variations in antiviral helicase genes have been associated with SLE, supporting the idea that helicase pathways are involved in the primary pathogenesis of SLE. Studies have documented functional consequences of these genetic variations within the type I IFN pathway in human cell lines and SLE patients. In this review, we summarize the function of helicases in the anti-viral immune response, and how this response is dysregulated in SLE patients. In particular, we will focus on known functional genetic polymorphisms in the IFIH1 (MDA5) and mitochondrial antiviral signaling protein genes which have been implicated in human SLE. These data provide fascinating evidence for dysregulation of helicase-mediated innate immunity in SLE, and may support novel therapeutic strategies in the disease.