11 research outputs found

    Convergent validity of the PsAQoL.

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    <p>PsAQoL, psoriatic arthritis quality of life; HAQ, health assessment questionnaire; Skin-17, Skindex-17.</p>*<p>P<0.01.</p

    Characteristics of the psoriatic arthritis (PsA) study population.

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    <p>Data obtained from self-reports.</p>A<p> = responders 1<sup>st</sup> series of questionnaires;</p>B<p> = 1<sup>st</sup> series PsAQoL complete; used for internal con- sistency assessment;</p>C<p> = 1<sup>st</sup> and 2<sup>nd</sup> series PsAQoL complete; used for calculating test-retest reliability;</p>D<p> = 1<sup>st</sup> series PsAQoL, HAQ and Skindex complete; used for convergent validity analyses.</p><p>PsA, psoriatic arthritis; n, number; y, years; SD, standard deviation; DMARD, disease-modifying antirheumatic drugs; anti-TNFα, anti-tumor necrosis factor α; NSAID, non-steroidal anti- inflammatory drug; PsAQoL, psoriatic arthrtitis quality of life; HAQ, health assessement questionnaire.</p

    Scores on the PsAQoL, HAQ and Skindex-17 at first and second assessment.

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    <p>PsAQoL, psoriatic arthritis quality of life; HAQ, health assessment questionnaire; Skin-17, Skindex-17; N, number of patients.</p

    Bland-Altman plot PsAQoL.

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    <p>Difference between the 1<sup>st</sup> and 2<sup>nd</sup> PsAQoL plotted against the mean of both assessments. PsAQoL, Psoriatic Arthritis Quality of Life; LOA, limits of agreement; CI, confidence interval.</p

    Disease activity over time in AS patients.

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    <p>ASDAS over time in patients starting TNF-α inhibitors (A) and receiving conventional treatment (B); BASDAI over time in patients starting TNF-α inhibitors (C) and receiving conventional treatment (D); CRP over time in patients starting TNF-α inhibitors (E) and receiving conventional treatment (F). *p<0.05 compared to baseline. Box-and-whisker plots: boxes indicate medians with interquartile ranges; + indicate means; whiskers indicate 5–95 percentile; • indicate outliers.</p

    Ankylosing spondylitis disease activity score is related to NSAID use, especially in patients treated with TNF-α inhibitors

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    <div><p>Background</p><p>Non-steroidal anti-inflammatory drugs (NSAIDs) are regarded as the cornerstone of conventional treatment for AS. However little is known about concomitant NSAID use during treatment (with TNF-α inhibitors) in daily clinical practice.</p><p>Methods and findings</p><p>Consecutive patients from the GLAS cohort were included. NSAID use and ASAS-NSAID index were evaluated at group level and at individual patient level during 52 weeks of follow-up. Analyses were stratified for treatment regimen. Generalized estimating equations (GEE) was used to evaluate NSAID use in relation to assessments of disease activity over time. In patients starting TNF-α inhibitors (n = 254), 79% used NSAIDs at baseline and this proportion decreased significantly to 38% at 52 weeks. ASAS-NSAID index also decreased significantly from median 65 to 0. In patients on conventional treatment (n = 139), 74% used NSAIDs at baseline with median ASAS-NSAID index of 50 and this remained stable during follow-up. At each follow-up visit, approximately half of the patients changed their type or dose of NSAIDs. GEE analysis over time showed that NSAID use was associated with AS disease activity score (p<0.05). This relation was more pronounced in patients treated with TNF-α inhibitors compared to conventional treatment (B = 0.825 vs. B = 0.250).</p><p>Conclusions</p><p>In this observational cohort of established AS patients, there was no difference in baseline NSAID use between patients with and without indication for TNF-α inhibitors. NSAID use decreased significantly after starting TNF-α inhibitors. During conventional treatment, NSAID use remained stable at group level. However, NSAID use changed frequently at individual patient level and was significantly associated with disease activity.</p></div
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