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IntroductionThere are no drugs specifically approved to treat cutaneous lupus. Inflammatory cells in lupus skin lesions can produce leukotrienes (LT), which promote tissue damage. In addition to hypersensitivity reactions, LT are also associated with cardiovascular diseases and elevated serum LT levels have been linked to worse atherosclerotic disease in lupus. Targeting LT could thus be an alternative to treat lupus. We present 4 cases of cutaneous lupus successfully treated with montelukast (MLK), a Cys‐LT antagonist.MethodsFour consecutive female systemic lupus erythematosus (SLE) patients with refractory skin lesions were treated with MLK (10 mg/d) in the Hospital Universitário Walter Cantídio of the Universidade Federal do Ceará. Skin lesions were scored using Revised Cutaneous LE Disease Area and Severity Index (RCLASI). Relative expression of the 5‐lipoxigenase (ALOX5) and 15‐lipoxigenase (ALOX15) genes was determined in peripheral blood cells (PBC) from lupus patients and 4 age‐matched female controls.ResultsAll patients experienced improvement of skin lesions measured using RCLASI scores within 2–12 weeks following initiation of MLK. The response was sustained for at least 3 months follow‐up and no adverse events were recorded. ALOX5 but not ALOX15 gene expression was significantly (P = 0.0425) increased in PBC from SLE patients vs controls.ConclusionThis is the first report of a fast and sustained successful response of cutaneous lupus to MLK. Given its acceptable safety profile, our data encourage development of a randomized trial as an attempt to reposition MLK as a safe, affordable alternative to treat cutaneous lupus.

BackgroundInflammatory back pain (IBP) is a major criterion in identifying axial spondyloarthritis. Whether socioeconomic issues impact prevalence of IBP assessed using standardized questionnaires has not been assessed. We determined IBP prevalence and performance of IBP questionnaires in a low-income, low-literacy population.MethodsIndividuals were interviewed in Fortaleza, Brazil, for the prevalence of IBP using Calin's, Berlin, and ASAS IBP questionnaires; monthly family income (US dollars), literacy (>/≤8 school years [SYs]), and smoking habit (present/absent) were registered.ResultsTwo hundred nineteen individuals were included (mean age, 38.2 ± 12.9 years), 110 (50.2%) men, 58 (26.4%) White, and 38 (17.3%) smokers. Overall, 152 (69.4%) declared

In view of the crucial role of tumor necrosis factor (TNF) in joint destruction, TNF inhibitors, including neutralizing anti-TNF antibodies and soluble TNF receptor constructs, are commonly used therapeutics for the treatment of arthropathies like rheumatoid arthritis (RA). However, not all patients achieve remission; moreover, there is a risk of increased susceptibility to infection with these agents. Spatially distinct from its receptor binding sites, TNF harbors a lectin-like domain, which exerts unique functions that can be mimicked by the 17 residue solnatide peptide. This domain binds to specific oligosaccharides such as N′N′-diacetylchitobiose and directly target the α subunit of the epithelial sodium channel. Solnatide was shown to have anti-inflammatory actions in acute lung injury and glomerulonephritis models. In this study, we evaluated whether the lectin-like domain of TNF can mitigate the development of immune-mediated arthritis in mice. In an antigen-induced arthritis model, solnatide reduced cell influx and release of pro-inflammatory mediators into the joints, associated with reduction in edema and tissue damage, as compared to controls indicating that TNF has anti-inflammatory effects in an acute model of joint inflammation via its lectin-like domain.

Although a rare condition, AAE can occur in SLE, either with deficiency or normal levels of C1 inhibitor. The investigation of AAE is challenging, especially when secondary to a disease with such a variable presentation. Thus, in the diagnostic approach of patients with AAE, one should always consider and look for evidence of autoimmune diseases, especially SLE.