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OP0287 Ultrasonography-detected peripheral enthesitis in patients with axial spondyloarthritis – anatomical distribution, morphology and response to anti-tnf therapy
  1. S Seven,
  2. SJ Pedersen,
  3. M Østergaard,
  4. IJ Sørensen,
  5. UM Døhn,
  6. S Krabbe,
  7. L Terslev
  1. Copenhagen Center for Arthritis Research, Center for Rheumatology and Spine diseases, Rigshospitalet, Glostrup, Denmark


Background Peripheral enthesitis (PE) is a characteristic feature of spondyloarthritis (SpA) that may be asymptomatic and only detectable by imaging. Ultrasonography (US) has greater sensitivity than clinical examination for the detection of PE.[1]

Objectives The aim of the study was to investigate the anatomical distribution, morphological abnormalities and response to anti-tumor necrosis factor (anti-TNF) therapy of US-detected PE in patients with axial SpA (axSpA) initiating adalimumab (ADA).

Methods In a randomized, placebo-controlled, double-blinded investigator-initiated trial (NCT01029847), patients with axSpA according to the Assessment of SpA International Society (ASAS) criteria were randomized to subcutaneous ADA 40 mg every other week (eow) or placebo from baseline to week 6. From week 6 to 24, all patients received ADA 40 mg eow. Of 49 patients enrolled, 21 participated in the US sub-study. US assessment applying the OMERACT US definitions for enthesitis[2] of 10 peripheral entheseal regions (Tables 1 & 2) and clinical examination were performed at baseline, weeks 6 and 24. US was performed by an experienced investigator. Hypo-echogenicity, increased thickness and Doppler activity of the enthesis were considered signs of active inflammation, whereas insertional bone erosions, intratendinous calcifications and enthesophytes were regarded as signs of chronic lesions.[2]

Results See tables.

Table 1.

Distribution of US findings at baseline (n=21)

Conclusions In this axSpA cohort, US assessment primarily identified PE in the lower extremities, and predominantly chronic lesions. No change in chronic PE lesions were found during treatment indicating a low sensitivity to change of these lesions. The number of entheses with inflammatory activity was too low to detect any changes on US during ADA therapy.


  1. D'Agostino MA, et al. Ann Rheum Dis 2011, 70(8):1433–1440.

  2. Terslev L, et al. Arthritis Care Res (Hoboken) 2014, 66(5):741–748.


Disclosure of Interest None declared

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