Background Psoriasis is a chronic inflammatory disease affecting 2–3% of the population [1,2]. Up to 30% of psoriasis patients develop psoriatic arthritis (PsA), and usually musculoskeletal symptoms start after the onset of skin disease. Psoriatic skin disease has a higher prevalence than arthritis what raises the question whether psoriasis patients without PsA are indeed spared from joint inflammation .
Detecting subclinical joint inflammation could help identify which patients with skin disease would benefit of treatment covering both skin and musculoskeletal inflammation.
Objectives To search for subclinical inflammatory joint disease in psoriasis patients without arthritis, and to determine whether such changes are associated with the later development of PsA.
Methods Eighty-five subjects without arthritis (55 with psoriasis and 30 healthy controls) received high field magnetic resonance imaging (MRI) of the hand. MRI scans were scored according to the PSAMRIS method . Psoriasis patients received complete clinical investigation, high-resolution peripheral quantitative computed tomography (HR-pQCT) to detect erosions and enthesiophytes and were followed up for at least one year for the development of PsA.
Results 47% of psoriasis patients showed at least one inflammatory lesion on MRI. Synovitis was the most prevalent inflammatory lesion (38%), while osteitis (11%), tenosynovitis (4%) and periarticular inflammation (4%) were less frequent. The mean (±SD) PSAMRIS synovitis score was 3.0±2.5 units. Enthesiophytes and bone erosions were not different between psoriasis patients with or without inflammatory MRI changes. The risk for developing PsA was as high as 55% if patients had subclinical synovitis and symptoms related to arthralgia, but only 15% of patients had normal MRIs and did not report of arthralgia.
Conclusions Prevalence of subclinical inflammatory lesions is high in patients with cutaneous psoriasis. Arthralgia associated with MRI synovitis constitutes a high-risk constellation for the development of PsA.
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Acknowledgement This study was supported by the Deutsche Forschungsgemeinschaft (SPP1468, CRC1181), the Marie Curie project OSTEOIMMUNE, the Metarthros project of the German Ministry of Science and Education, the IMI-funded project BTCure and the Pfizer Competitive Grant Award Germany.
Disclosure of Interest None declared