The lipid paradox is also present in early axial spondyloarthritis: results from the Swedish part of the SPondyloArthritis Caught Early (SPACE) cohort.

OBJECTIVE: Inverse associations between systemic inflammation and cholesterol ('the lipid paradox') have been reported in rheumatoid arthritis (RA) and, in established axial spondyloarthritis (axSpA), but little is known about this relationship in early axSpA, which is the focus of the present study. METHOD: In the Swedish part of the SPondyloArthritis Caught Early (SPACE) cohort (patients with chronic back pain for ≥3 months, ≤2 years; age at onset <45 years), serum levels of total cholesterol (TC) and apolipoproteins ApoA1 and ApoB were measured at inclusion, together with parameters reflecting inflammatory disease activity [C-reactive protein (CRP), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and sacroiliitis by magnetic resonance imaging (MRI) following Assessment of SpondyloArthritis international Society (ASAS) criteria]. All patients included in the analysis either had axSpA based on a high physician's level of confidence or fulfilled the ASAS criteria for axSpA. Associations between lipids/lipoproteins and inflammation were assessed using multivariable linear regression models. RESULTS: In the 64 patients included, there were inverse associations for CRP with TC, ApoA1, and ApoB in age-sex-adjusted models. The negative associations with CRP remained significant for TC and ApoB in multivariable models adjusted for age, sex, BASDAI, and current smoking (p = 0.048). There were no significant associations for the lipid parameters with BASDAI or inflammation on MRI of the sacroiliac joints. CONCLUSION: Inverse associations between systemic inflammation and lipids, particularly TC and ApoB, are present in early axSpA, similar to those shown for other inflammatory joint diseases. These patterns must be considered when including lipids in the evaluation of cardiovascular disease risk.

Validity of clinical psoriatic arthritis diagnoses made by rheumatologists in the Swedish National Patient Register.

OBJECTIVES: : Knowledge of the correspondence between clinical ICD diagnoses and classification criteria fulfilment is crucial to interpret studies identifying cases via ICD codes. We assessed the degree to which patients registered with ICD-10 diagnoses of psoriatic arthritis (PsA) in the Swedish National Patient Register (NPR) fulfil established PsA classification criteria. METHOD: Four hundred patients with at least one outpatient visit to one of five rheumatology or internal medicine departments (three university/two county departments across Sweden) in 2013-2015, with a main ICD-10 diagnosis of PsA (L40.5, M07.0-M07.3), were randomly selected (80 cases/site). Through a structured medical record review, positive predictive values (PPVs) for fulfilment of the following classification criteria were assessed: CASPAR, Moll and Wright, Vasey and Espinoza, and modified ESSG criteria for PsA. A subset analysis regarding CASPAR fulfilment was also performed among cases with available rheumatoid factor and peripheral X-ray status (central CASPAR items; n = 227). RESULTS: Of the 400 patients with a main ICD-10 diagnosis of PsA, 343 (86%) fulfilled at least one of the four PsA classification criteria. PPVs for the different criteria were: CASPAR 69% (82% in the subset analysis), Moll and Wright 51%, Vasey and Espinoza 76%, and modified ESSG 64%. Overall, only 6.5% of the 400 PsA diagnoses were judged as clearly incorrect by the medical record reviewers. CONCLUSION: The validity of rheumatologist-made, clinical ICD-10 diagnoses for PsA in the Swedish NPR is good, with PPVs of 69-82% for CASPAR fulfilment and 86% for meeting any established PsA classification criteria.

Immune-mediated skin lesions in patients treated with anti-tumour necrosis factor alpha inhibitors.

OBJECTIVE: To describe immune-mediated skin lesion (IMSL) development in patients during anti-tumour necrosis factor (TNF) therapy. METHODS: Two hundred and fifty-two patients with rheumatoid arthritis (RA) and 183 with spondyloarthropathies (SpA) treated with anti-TNF inhibitors were analysed to identify IMSLs. RESULTS: Of the 252 patients with RA (146 treated with infliximab, 72 with adalimumab, and 34 with etanercept), 32 developed IMSLs. Eleven patients developed psoriatic skin lesions, 10 presented with granuloma annulare (GA), five had skin vasculitis, two alopecia areata, two discoid lupus erythematosus, one lichenoid eruption (lichen planus), and one vitiligo. Of the 183 patients with SpA (138 treated with infliximab, 37 with etanercept, and eight with adalimumab), 10 cases with IMSLs were identified. All were treated with infliximab. More specifically, six patients with ankylosing spondylitis (AS) developed psoriatic skin lesions, one developed GA, one lichen planus, and one alopecia areata. In addition, one patient with psoriatic arthritis (PsA) developed skin vasculitis. The occurrence of these IMSLs ranged from 3 to 36 months with a median of 20 months. Of all the patients with IMSL development, two with psoriatic skin lesions, two with GA, and one with vasculitis stopped anti-TNF therapy because of the extent and severity of the skin lesions. CONCLUSIONS: Our results on patients treated with TNF antagonists strongly support a link between TNF inhibition and IMSL development. Although these clinical complications are rare, clinicians should be aware of their occurrence and should recognize them.

Granuloma annulare induced by anti-tumour necrosis factor therapy.

OBJECTIVE: To describe granuloma annulare (GA) skin lesion development in patients during anti-tumour necrosis factor (TNF) therapy. METHODS: 199 patients with rheumatoid arthritis and 127 suffering from spondyloarthropathies treated with anti-TNF antagonists were analysed to identify skin lesions suggesting GA. RESULTS: Nine cases of GA during anti-TNF therapy (123 treated with infliximab, 57 with adalimumab and 17 with etanercept) for rheumatoid arthritis were identified. Two have been treated with infliximab, six with adalimumab and one with etanercept, and here the development of GA was 4.5%. No patient with spondyloarthropathies developed such skin lesions. All patients developed the generalised form of GA. None had or developed diseases, or conditions known to be associated with GA. In seven patients the skin eruptions developed during the first year of anti-TNF treatment, while they developed in two patients during the second year. Two patients had to stop anti-TNF therapy due to the extent of skin lesions. All patients responded well to the local corticosteroid therapy. CONCLUSIONS: Our series strongly supports a link between TNF inhibition and the development of GA in some patients. When dealing with patients on these agents physicians should be aware of possible adverse events and the potential development of such complications.