Is a positive family history of spondyloarthritis relevant for diagnosing axial spondyloarthritis once HLA-B27 status is known?

OBJECTIVES: A positive family history (PFH) of spondyloarthritis, in particular a PFH of AS or acute anterior uveitis, is associated with HLA-B27 carriership in chronic back pain patients. As it is unknown, the study aimed to investigate if a PFH contributes to diagnosing axial spondyloarthritis (axSpA) once HLA-B27 status is known. METHODS: In axSpA-suspected patients from the Assessment of SpondyloArthritis international Society (ASAS), DEvenir des Spondyloarthropathies Indifférenciéés Récentes (DESIR) and SPondyloArthritis Caught Early (SPACE) cohorts, logistic regression analyses were performed with HLA-B27 status and PFH according to the ASAS definition (ASAS-PFH) as determinants and clinical axSpA diagnosis as outcome at baseline. Analyses were repeated with a PFH of AS or acute anterior uveitis. RESULTS: In total, 1818 patients suspected of axSpA were analysed (ASAS n = 594, DESIR n = 647, and SPACE n = 577). In patients from the ASAS, DESIR and SPACE cohorts, respectively 23%, 39% and 38% had an ASAS-PFH, 52%, 58% and 43% were HLA-B27 positive, and 62%, 47% and 54% were diagnosed with axSpA. HLA-B27 was independently associated with an axSpA diagnosis in each cohort but an ASAS-PFH was not [ASAS cohort: HLA-B27 odds ratio (OR): 6.9 (95% CI: 4.7, 10.2), ASAS-PFH OR: 0.9 (95% CI: 0.6, 1.4); DESIR: HLA-B27 OR: 2.1 (95% CI: 1.5, 2.9), ASAS-PFH OR: 1.0 (95% CI 0.7, 1.3); SPACE: HLA-B27 OR: 10.4 (95% CI: 6.9, 15.7), ASAS-PFH OR: 1.0 (95% CI: 0.7, 1.5)]. Similar negative results were found for PFH of AS and acute anterior uveitis. CONCLUSION: In three independent cohorts with different ethnical backgrounds, ASAS, DESIR and SPACE, a PFH was not associated independently of HLA-B27 with a diagnosis of axSpA. This indicates that in the vast majority of patients presenting with back pain, a PFH does not contribute to the likelihood of an axSpA diagnosis if HLA-B27 status is known.

Left Ventricular Systolic Myocardial Function in Ankylosing Spondylitis.

OBJECTIVE: Subclinical left ventricular (LV) myocardial dysfunction is associated with an increased risk of cardiovascular disease (CVD), but it is not known whether subclinical LV myocardial dysfunction is present in patients with ankylosing spondylitis (AS) independent of CVD risk factors. METHODS: Conventional and speckle tracking echocardiography were performed in 106 patients with AS (mean ± SD age 48 ± 12 years; 59% men) and 106 matched controls (mean ± SD age 51 ± 12 years; 59% men). LV systolic myocardial function was assessed by peak systolic global longitudinal strain (GLS). RESULTS: CVD risk factors were similarly distributed in patients with AS and controls, but more controls received statin therapy (P = 0.05). GLS was significantly lower in patients with AS compared to controls (mean ± SD -17.7 ± 2.5% versus -18.4 ± 2.3%; P = 0.03). In univariable linear regression analyses in the total study population, lower GLS was associated with having AS, male sex, higher body mass index, higher LV mass index, and lower LV ejection fraction (all P < 0.05). Having AS retained an independent association with lower GLS when adjusted for these factors in multivariable analyses (ß = 0.16, P = 0.02). In patients with AS, lower GLS was independently associated with larger aortic root diameter in multivariable analyses (ß = 0.24, P = 0.02), while no association with AS disease activity, disease duration, or use of antirheumatic medication was observed. CONCLUSION: Patients with AS had lower GLS compared with controls, independent of confounders. In AS patients, lower GLS was associated with larger aortic root diameter. Prospective studies should test whether lower GLS contributes to the observed higher CVD risk in patients with AS.

Serum inflammatory biomarkers fail to identify early axial spondyloarthritis: results from the SpondyloArthritis Caught Early (SPACE) cohort.

INTRODUCTION: Decreasing the diagnostic delay in axial spondyloarthritis (axSpA) remains a major challenge. Here, we assessed the value of serum inflammatory biomarkers to distinguish early axSpA from other pathologies in a large cohort of patients referred with early back pain. METHODS: Serum c reactive protein (CRP), erythrocyte sedimentation rate (ESR) and calprotectin were determined in the SPondyloArthritis Caught Early (SPACE) cohort (n=310), an early back pain inception cohort. Additionally, explorative serum biomarkers derived from the literature (interleukin-27 (IL-27), human ß-defensin-2 (hBD-2) and lipcolin-2 (LCN-2)) were determined by ELISA in full-blown patients with ankylosing spondylitis (AS) (n=21) and healthy controls (n=20). RESULTS: Serum CRP and ESR levels were not elevated in early axSpA versus 'control' back pain patients. Serum calprotectin was elevated in early axSpA versus controls (p=0.01) but failed to identify early axSpA at the individual level (positive predictive value of 38.7%). As to explorative biomarkers, serum levels of IL-27 were not detectable, and hBD-2 and LCN-2 serum levels were not elevated in full-blown AS versus healthy controls (p=0.572, p=0.562, respectively). Therefore, these markers were not further determined in the SPACE cohort. CONCLUSIONS: None of the candidate serum inflammatory markers were useful as diagnostic markers in the early phase of axSpA.