Development of SLE among “potential SLE” patients seen in consultation: long‐term follow‐up
Identifieur interne : 001071 ( Main/Exploration ); précédent : 001070; suivant : 001072Development of SLE among “potential SLE” patients seen in consultation: long‐term follow‐up
Auteurs : M. Al Daabil [États-Unis] ; E. M. Massarotti [États-Unis] ; A. Fine [États-Unis] ; H. Tsao [États-Unis] ; P. Ho [États-Unis] ; P. H. Schur [États-Unis] ; B. L. Bermas [États-Unis] ; K. H. Costenbader [États-Unis]Source :
- International Journal of Clinical Practice [ 1368-5031 ] ; 2014-12.
Abstract
Objective: To identify factors associated with development of systemic lupus erythematosus (SLE) among patients evaluated at a tertiary care Lupus Center for potential SLE. Methods: We identified patients first seen at the Brigham and Women's Hospital Lupus Center between 1 January 1992 and 31 December 2012 and thought to have potential SLE by a board‐certified rheumatologist. All had 1–3 SLE ACR criteria at initial visit and > 2 follow‐up visits ≥ 3 months apart. We reviewed medical records through 15 May 2013 for: SLE signs and symptoms, autoimmune serologies, prescriptions and diagnoses by board‐certified rheumatologists. Bivariable analyses and multivariable logistic regression models were used to identify independent predictors of developing SLE. Results: Two hundred and sixty four patients met inclusion criteria. At initial visit, mean age was 39.2 (SD 12.4) years, 94% were female and 67% white. Mean number of SLE ACR criteria was 2.7 (SD 1.0) and 88% were antinuclear antibody (ANA) positive at initial consultation. Mean follow‐up time was 6.3 (SD 4.3) years and 67% were prescribed hydroxychloroquine in follow‐up. At most recent visit, 56 (21%) had been diagnosed with SLE; 47 (18%) were thought not to have SLE and 161 (61%) were still considered to have potential SLE. In multivariable regression models, oral ulcers (OR 2.40, 95% CI 1.03–5.58), anti‐dsDNA (OR 2.59, 95% CI 1.25–5.35) and baseline proteinuria or cellular casts (OR 16.20, 95% CI 1.63–161.02) were independent predictors of developing SLE. The most common other final diagnoses included fibromyalgia, Sjögren's syndrome, mixed connective tissue disease and cutaneous lupus. Conclusion: Among patients with potential SLE at initial consultation, 21% were diagnosed with definite SLE within 6.3 years. Oral ulcers, anti‐dsDNA and proteinuria or cellular casts were independent predictors of developing definite SLE. A better means of accurately identifying those who will develop SLE among those presenting with potential disease is necessary.
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DOI: 10.1111/ijcp.12466
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Al Daabil</name><affiliation wicri:level="3"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, MA, Boston</wicri:regionArea><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Massarotti, E M" sort="Massarotti, E M" uniqKey="Massarotti E" first="E. M." last="Massarotti">E. M. Massarotti</name><affiliation wicri:level="3"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, MA, Boston</wicri:regionArea><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Fine, A" sort="Fine, A" uniqKey="Fine A" first="A." last="Fine">A. Fine</name><affiliation wicri:level="3"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, MA, Boston</wicri:regionArea><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Tsao, H" sort="Tsao, H" uniqKey="Tsao H" first="H." last="Tsao">H. Tsao</name><affiliation wicri:level="3"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, MA, Boston</wicri:regionArea><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Ho, P" sort="Ho, P" uniqKey="Ho P" first="P." last="Ho">P. Ho</name><affiliation wicri:level="3"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, MA, Boston</wicri:regionArea><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Schur, P H" sort="Schur, P H" uniqKey="Schur P" first="P. H." last="Schur">P. H. Schur</name><affiliation wicri:level="3"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, MA, Boston</wicri:regionArea><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Bermas, B L" sort="Bermas, B L" uniqKey="Bermas B" first="B. L." last="Bermas">B. L. Bermas</name><affiliation wicri:level="3"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, MA, Boston</wicri:regionArea><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Costenbader, K H" sort="Costenbader, K H" uniqKey="Costenbader K" first="K. H." last="Costenbader">K. H. Costenbader</name><affiliation wicri:level="3"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, MA, Boston</wicri:regionArea><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName></affiliation><affiliation></affiliation><affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">International Journal of Clinical Practice</title><title level="j" type="alt">INTERNATIONAL JOURNAL OF CLINICAL PRACTICE</title><idno type="ISSN">1368-5031</idno><idno type="eISSN">1742-1241</idno><imprint><biblScope unit="vol">68</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="1508">1508</biblScope><biblScope unit="page" to="1513">1513</biblScope><biblScope unit="page-count">6</biblScope><date type="published" when="2014-12">2014-12</date></imprint><idno type="ISSN">1368-5031</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1368-5031</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Objective: To identify factors associated with development of systemic lupus erythematosus (SLE) among patients evaluated at a tertiary care Lupus Center for potential SLE. Methods: We identified patients first seen at the Brigham and Women's Hospital Lupus Center between 1 January 1992 and 31 December 2012 and thought to have potential SLE by a board‐certified rheumatologist. All had 1–3 SLE ACR criteria at initial visit and > 2 follow‐up visits ≥ 3 months apart. We reviewed medical records through 15 May 2013 for: SLE signs and symptoms, autoimmune serologies, prescriptions and diagnoses by board‐certified rheumatologists. Bivariable analyses and multivariable logistic regression models were used to identify independent predictors of developing SLE. Results: Two hundred and sixty four patients met inclusion criteria. At initial visit, mean age was 39.2 (SD 12.4) years, 94% were female and 67% white. Mean number of SLE ACR criteria was 2.7 (SD 1.0) and 88% were antinuclear antibody (ANA) positive at initial consultation. Mean follow‐up time was 6.3 (SD 4.3) years and 67% were prescribed hydroxychloroquine in follow‐up. At most recent visit, 56 (21%) had been diagnosed with SLE; 47 (18%) were thought not to have SLE and 161 (61%) were still considered to have potential SLE. In multivariable regression models, oral ulcers (OR 2.40, 95% CI 1.03–5.58), anti‐dsDNA (OR 2.59, 95% CI 1.25–5.35) and baseline proteinuria or cellular casts (OR 16.20, 95% CI 1.63–161.02) were independent predictors of developing SLE. The most common other final diagnoses included fibromyalgia, Sjögren's syndrome, mixed connective tissue disease and cutaneous lupus. Conclusion: Among patients with potential SLE at initial consultation, 21% were diagnosed with definite SLE within 6.3 years. Oral ulcers, anti‐dsDNA and proteinuria or cellular casts were independent predictors of developing definite SLE. A better means of accurately identifying those who will develop SLE among those presenting with potential disease is necessary.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Massachusetts</li></region><settlement><li>Boston</li></settlement></list><tree><country name="États-Unis"><region name="Massachusetts"><name sortKey="Al Daabil, M" sort="Al Daabil, M" uniqKey="Al Daabil M" first="M." last="Al Daabil">M. Al Daabil</name></region><name sortKey="Bermas, B L" sort="Bermas, B L" uniqKey="Bermas B" first="B. L." last="Bermas">B. L. Bermas</name><name sortKey="Costenbader, K H" sort="Costenbader, K H" uniqKey="Costenbader K" first="K. H." last="Costenbader">K. H. Costenbader</name><name sortKey="Fine, A" sort="Fine, A" uniqKey="Fine A" first="A." last="Fine">A. Fine</name><name sortKey="Ho, P" sort="Ho, P" uniqKey="Ho P" first="P." last="Ho">P. Ho</name><name sortKey="Massarotti, E M" sort="Massarotti, E M" uniqKey="Massarotti E" first="E. M." last="Massarotti">E. M. Massarotti</name><name sortKey="Schur, P H" sort="Schur, P H" uniqKey="Schur P" first="P. H." last="Schur">P. H. Schur</name><name sortKey="Tsao, H" sort="Tsao, H" uniqKey="Tsao H" first="H." last="Tsao">H. Tsao</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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