Article Text

AB0693 Gender as A Determinant of Functional Status and Disease Activity Measures in Patients with Longstanding Ankylosing Spondylitis
  1. J. Nossent1,2,
  2. G. Bakland2
  1. 1School of Medicine, University of Western Australia, Crawley, Australia
  2. 2Rheumatology, Arctic University Norway, Tromso, Norway


Background Increasing evidence points to gender differences in disease presentation and course in Ankylosing Spondylitis (AS). This could reflect female specific AS characteristics or inequalities in health care provision.

Objectives To investigate the impact of gender and remoteness on functional outcome, quality of life (QOL) and disease activity measures in an AS cohort with longstanding disease.

Methods Cross sectional cohort study in TNFi naïve AS patients (n=227) in the Arctic region of Norway. Spinal function and functional indices (BASFI, Dougados Index), QOL measures (MHAQ, SF36) were obtained simultaneously with a range of biomarkers (ESR, CRP, IL-6, TNFa, IL-17, IL-23) during a research visit. Remoteness definition was living in a community with <10000 inhabitants. Associations between clinometric, QOL and serological findings were analysed by non-parametric methods.

Results Despite similar age at and disease duration since symptom onset (280 vs 265 months, p=0.5) female patients (n=66) had better spinal flexion (median 40 vs. 36°, p=0.035) and finger floor distance (7 vs. 16 cm, p=0.015) compared to male patients (n=161). While global disease scores (BASFI, Dougados Index, MHAQ and ASDAS-CRP) and comorbidity prevalence were comparable, female patients were more often work disabled (61 vs 49%, p=0.01). IL-6 levels correlate with ASDAS (Rs 0.4, p=0.005), occiput wall distance (Rs 0.32,p=0.012) and inversely with Schober (Rs -0.36 p=0.004), spinal flexion (Rs -0.27, p=0.03) and lateral movement (Rs= -0.31, p=0.013) in female patients only.

Conclusions While remoteness has little impact on the disease severity of AS in Northern Norway, the gender based variation in disease course in AS may be underpinned by differential activation of inflammatory cytokines.

Acknowledgement The authors want to acknowledge the technical assistance of Kirsten Nilsen, bioengineer at Uito

Disclosure of Interest None declared

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