Abstract
The purposes of this study were to determine the prevalence of metabolic syndrome (MetS) in patients with ankylosing spondylitis (AS) receiving anti-TNFα therapy and evaluate the association of the two conditions with clinical and laboratory findings and predictors of cardiovascular risk. In this cross-sectional study, 63 patients diagnosed with AS according to the modified New York criteria and treated with TNFα blockers and 33 healthy controls were submitted to clinical examination and anthropometric measurements. Glucose levels, lipid profile, and inflammatory markers were registered. The Framingham score (FS), atherogenic index of plasma (AIP), and waist-to-height ratio (WHtR) were calculated. MetS was diagnosed according to the revised National Cholesterol Education Program - Adult Treatment Panel III guidelines. The prevalence of MetS was higher among AS patients than controls (27 vs. 9.1%, p = 0.04). AS patients also had greater body mass index (27.6 kg/m2 ± 4.5 vs. 24.5 kg/m2 ± 2.7; p = 0.001) and WHtR (0.59 ± 0.08 vs. 0.49 ± 0.05; p < 0.01). Patients with MetS had higher FS (9.66 (4.08–20.5) vs. 2.54 (1.56–6.75); p < 0.001), WHtR (0.6444 ± 0.0706 vs. 0.5729 ± 0.0759; p = 0.001), and AIP (0.68 ± 0.46 vs. 0.34 ± 0.24; p = 0.02) than patients without MetS. When stratifying patients with and without MetS according to disease activity, the former had stronger predictors of cardiovascular risk than the latter, regardless of disease activity. MetS was more prevalent in AS patients than in controls. Predictors of cardiovascular risk were stronger in MetS patients than in non-MetS patients.
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The study was approved by the Hospital Geral de Fortaleza’s research ethics committee and filed under entry #880.336. All participants gave their informed written consent and the study was performed in accordance with the 1964 Declaration of Helsinki.
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Maia, D.G., Augusto, K.L., Bezerra, M.C. et al. Metabolic syndrome in patients with ankylosing spondylitis receiving anti-TNFα therapy: association with predictors of cardiovascular risk. Clin Rheumatol 36, 2371–2376 (2017). https://doi.org/10.1007/s10067-017-3623-8
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DOI: https://doi.org/10.1007/s10067-017-3623-8