Background and objectives: Information on the performance of ixekizumab (IXE) in patients with psoriatic arthritis (PsA) in clinical practice is scarce. We aimed to analyze the retention rate and safety of IXE in patients with PsA in routine clinical practice. Methods: A retrospective longitudinal observational single-center study of all patients with PsA who had received at least one dose of IXE. Adverse events (AEs) and drug retention rate were the main study focus. Survival was analyzed using Kaplan–Meier curves and predictive factors using multivariate Cox regression analysis. The hazard ratio (HR) was used as a measure of the association. Results: Seventy-two patients were included (52 women and 20 men). Median disease duration was 5 years (IQR 3–9). More than 90% received ≥2 biologic and/or targeted synthetic disease-modifying anti-rheumatic drugs (DMARDs) prior to IXE. Ixekizumab showed a 1-year retention rate of 65% and a 2-year retention rate of 57%. Regarding discontinuation due to AEs, 0.18 AEs per person-year were identified. The number of previous biologics did not influence drug survival but prior use of methotrexate (HR 2.31 (95% CI 1.05–5.10), p < 0.05) and depression (HR 2.40 (95% CI 1.07–5.41), p < 0.05) increased the risk of IXE discontinuation. Conclusions: Ixekizumab showed a good retention rate in a PsA population mostly refractory to biologic and targeted synthetic DMARDs. Drug survival was consistently good regardless of age, gender, metabolic comorbidities, smoking status, or prior number of biologic therapies. This information may be of interest to better position this drug in the PsA treatment algorithms.

The human leukocyte antigen-C ∗ 06 (HLA-C ∗ 06, formerly HLA-Cw6) is the main genetic biomarker in psoriatic disease. It has been related to several phenotypic traits in psoriatic disease, but its role in relation to cardiometabolic comorbidities is unknown at present. Here, we analyze the potential connections between this biomarker and the cardiometabolic profile of these patients. We carried out a cross-sectional observational study including 400 patients recruited at a single university hospital. Clinical and classical cardiometabolic factors were compared between HLA-C ∗ 06-positive and HLA-C ∗ 06-negative individuals (OR with 95% CI). Multivariate regression analyses were carried out to check for disease traits associated with different cardiometabolic risk factors. The study population included 215 men (53.8%) and 185 women (46.2%), mean age of 46 ± 15   years , and an average disease evolution of 17 ± 12.6   years . Ninety-three (23.3%) patients met CASPAR criteria for psoriatic arthritis. HLA-C ∗ 06 carriers ( n : 160, 40%) showed an earlier age at disease onset, psoriasis family history, and more severe skin disease (type I disease). After correcting for age, sex, and disease duration, they also showed less hypertension (13.8% vs. 24.2%, OR 0.7 (95% CI: 0.42-0.78), p = 0.025 ), lower waist circumference ( 94.4 ± 13.7 vs. 98.3 ± 13.8   cm ), and lower BMI ( 27 ± 4.4 vs. 28.1 ± 4.8 , p < 0.05 ). We confirmed the well-known association between HLA-C ∗ 06 and type I psoriatic disease. As a novel finding, patients carrying HLA-C ∗ 06 showed a better cardiometabolic profile. In any case, these findings need further confirmation.

Psoriatic arthritis (PsA) is a chronic inflammatory arthritis that affects one-third of patients with psoriasis (PsO). PsA is a relatively common condition in rheumatology clinics. In fact, the prevalence of PsA increased to approximately 0.6% of the general population in a recent epidemiological study carried out in Spain.1

Background and aims: Breastfeeding is recognized as one of the most influential drivers of the gut microbiome. In turn, alterations in the gut microbiome may play a role in the development and severity of spondyloarthritis (SpA). We aimed to analyze different disease outcomes in patients with axial SpA (axSpA) based on the history of breastfeeding. Patients and methods: A random sample was selected from a large database of axSpA patients. Patients were divided based on history of breastfeeding and several disease outcomes were compared. Both groups were also compared based on disease severity. Adjusted linear and logistic regression statistical methods were used. Results: The study included 105 patients (46 women and 59 men), and the median age was 45 years (IQR: 16–72), and the mean age at diagnosis was 34.3 ± 10.9 years. Sixty-one patients (58.1%) were breastfed, with a median duration of 4 (IQR: 1–24) months. After the fully adjusted model, BASDAI [−1.13 (95%CI: −2.04, −0.23), p = 0.015] and ASDAS [−0.38 (95%CI: −0.72, −0.04), p = 0.030] scores were significantly lower in breastfed patients. Forty-two percent had severe disease. In the adjusted logistic model for age, sex, disease duration, family history, HLA-B27, biologic therapy, smoking, and obesity, breastfeeding had a protective effect against the development of severe disease (OR 0.22, 95%CI: 0.08–0.57, p = 0.003). The selected sample size was sufficient to detect this difference with a statistical power of 87% and a confidence level of 95%. Conclusion: Breastfeeding might exert a protective effect against severe disease in patients with axSpA. These data need further confirmation.

Background and aims: The effect of smoking on disease activity and quality of life (QoL) in spondyloarthritis (SpA) is far from clear. We aimed to evaluate the relationship between smoking and these outcomes in patients with axial SpA (axSpA) and psoriatic arthritis (PsA). Patients and methods: This cross-sectional observational multicenter study included 242 patients with axSpA and 90 with PsA. The association between conventional cardiovascular risk factors and disease activity as well as QoL, in both SpA phenotypes was evaluated. For this, univariate and multivariate regression analyses were performed, as well as confirmatory meta-analyses. Results: Regardless of age, sex, or disease duration, patients with axSpA showed significantly less association with obesity (OR 0.50 (0.26–0.96), p = 0.03) and hypertension (OR 0.33 (0.18–0.62), p = 0.0005). However, axSpA was significantly associated with smoking (OR 2.62 (1.36–5.04), p = 0.004). Patients with axSpA were more likely to be in a category of high disease activity compared with PsA (OR 2.86, p = 0.0006). Regardless of sex, age, disease duration, and education level, smoking was significantly associated with higher disease activity in axSpA (OR 1.88, p = 0.027). A fixed-effects model meta-analysis (OR 1.70, p = 0.038) confirmed the association between tobacco and disease activity. No relationship was found between smoking (or other cardiometabolic risk factors) and structural damage or worse QoL in either disease. Conclusions: Although the cardiometabolic risk profile is clearly different between both SpA phenotypes, the only clear link between these factors and increased disease activity was observed between smoking and axSpA. Our findings need further confirmation.