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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.semarthritisrheumatism.com/?rss=yes"><title>Seminars in Arthritis and Rheumatism</title><description>Seminars in Arthritis and Rheumatism RSS feed: Current Issue.    
 Seminars in Arthritis and Rheumatism  provides a broad interpretation of the field, including aspects of general medicine 
and orthopedics. Each bimonthly issue presents comprehensive review articles focusing on topics in rheumatology. It is of interest to 
rheumatologists, internal medicine specialists, orthopedic surgeons, immunologists and specialists in bone and marrow metabolism. 
 

 Seminars in  Arthritis and Rheumatism  is ranked 4th out of 26 journals in the Rheumatology category on the 2010 Journal Citation 
Reports®, published by Thomson Reuters, and has an Impact Factor of 4.724.   </description><link>http://www.semarthritisrheumatism.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:issn>0049-0172</prism:issn><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:publicationDate>June 2012</prism:publicationDate><prism:copyright> © 2012 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS004901721200114X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211002794/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211002782/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211002770/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211003593/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211003052/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211002836/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211003490/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS004901721100357X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211003465/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211003398/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211003611/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211003386/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211003374/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211003477/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211003581/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211002800/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211003453/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211003489/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211003568/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017212000650/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017211003982/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017212000224/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017212001163/abstract?rss=yes"/><rdf:li rdf:resource="http://www.semarthritisrheumatism.com/article/PIIS0049017212001175/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS004901721200114X/abstract?rss=yes"><title>Editor</title><link>http://www.semarthritisrheumatism.com/article/PIIS004901721200114X/abstract?rss=yes</link><description></description><dc:title>Editor</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0049-0172(12)00114-X</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>IFC</prism:startingPage><prism:endingPage>IFC</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211002794/abstract?rss=yes"><title>Korean Observational Study Network for Arthritis (KORONA): Establishment of a Prospective Multicenter Cohort for Rheumatoid Arthritis in South Korea</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211002794/abstract?rss=yes</link><description>
Objectives: 
The object of this study was to introduce the KORean Observational study Network for Arthritis (KORONA) registry with an emphasis on the design of the Korean rheumatoid arthritis (RA) national database, as well as to provide an overview of the RA patients who are currently registered in KORONA.

Methods: 
The KORONA was established in July 2009 by the Clinical Research Center for Rheumatoid Arthritis (CRCRA) in South Korea. KORONA is based on a prospective protocol and standard, defined data collection instruments. Demographic and clinical features, laboratory and radiologic data, health-related outcomes, treatment side effects, resource utilization, and health behaviors of the RA cohort patients are recorded in a database.

Results: 
A total of 23 institutions, which are about 38% of the rheumatologic departments at tertiary academic hospitals across South Korea, are part of KORONA. The quality control of data collection and management has been performed through annual monitoring and auditing, staff training, and providing standard operation protocol by the executive committee of CRCRA. As of 31 December 2010, 4721 patients with established RA were included in KORONA, because an annual survey had started to be performed in July 2010.

Conclusions: 
KORONA is the first nationwide Korean RA-specific cohort and it will provide valuable “real-world” information for Korean RA patients.
</description><dc:title>Korean Observational Study Network for Arthritis (KORONA): Establishment of a Prospective Multicenter Cohort for Rheumatoid Arthritis in South Korea</dc:title><dc:creator>Yoon-Kyoung Sung, Soo-Kyung Cho, Chan-Bum Choi, So-Yeon Park, Jeeseon Shim, Joong Kyong Ahn, So-Young Bang, Hoon-Suk Cha, Jung-Yoon Choe, Won Tae Chung, Minyoung Her, Seung-Jae Hong, Yun Kyung Hong, Chung-Il Joung, Jae-Bum Jun, Young Ok Jung, Young Mo Kang, Dong-Yook Kim, Hae-Rim Kim, Hyoun Ah Kim, Jinseok Kim, Seong-Kyu Kim, Sung-Il Kim, Tae-Hwan Kim, Tae-Jong Kim, Eunmi Koh, Choong Ki Lee, Hye-Soon Lee, Jisoo Lee, Sang-Heon Lee, Sang-Hoon Lee, Shin-Seok Lee, Sung Won Lee, Yeon-Ah Lee, Seong-Su Nah, Sung-Hoon Park, Dong Hyuk Sheen, Seung-Cheol Shim, Gwan Gyu Song, Chang-Hee Suh, Wan-Sik Uhm, Dae-Hyun Yoo, Wan-Hee Yoo, Bo Young Yoon, Sang-Cheol Bae</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.09.007</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2011-12-12</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2011-12-12</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Rheumatoid Arthritis</prism:section><prism:startingPage>745</prism:startingPage><prism:endingPage>751</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211002782/abstract?rss=yes"><title>Hand Tendon Involvement in Rheumatoid Arthritis: An Ultrasound Study</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211002782/abstract?rss=yes</link><description>
Objective: 
To assess the prevalence and the distribution of tendon involvement in the hands and wrists of patients with rheumatoid arthritis (RA) describing in detail the ultrasound (US) morphostructural and vascular tendon abnormalities.

Methods: 
Ninety consecutive RA patients were included in the study. The following tendons were scanned bilaterally: flexor pollicis longus tendon, flexor digitorum superficialis, and profundus tendons of the II to the V fingers (at both finger and carpal tunnel levels), flexor carpi radialis tendon, and extensor tendons of the 6 compartments on the dorsal aspect of the wrist. The presence of US findings indicative of tenosynovitis and tendon damage was investigated.

Results: 
Tenosynovitis was found in at least 1 anatomic site of 44 (48.8%) of 90 patients. Tendon damage was found in at least 1 anatomic site of 39 (43.3%) of 90 patients. The focal tendon echotexture derangement was found in 294 of 5400 (5.4%) tendons, the partial and complete tears in 14 (0.3%), and in 3 (0.06%) tendons, respectively. The most frequently involved tendons were the flexor tendons of the II, III, and IV fingers and the extensor carpi ulnaris tendon.

Conclusions: 
The present study provides evidence in favor of the ability of US to reveal a relatively high frequency of tendon involvement at the hand and wrist level in RA patients. These data can both facilitate US examinations in daily clinical practice and direct further investigations in the US assessment of tendon involvement in RA.
</description><dc:title>Hand Tendon Involvement in Rheumatoid Arthritis: An Ultrasound Study</dc:title><dc:creator>Emilio Filippucci, Alessandra Gabba, Luca Di Geso, Rita Girolimetti, Fausto Salaffi, Walter Grassi</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.09.006</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2011-11-07</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2011-11-07</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Rheumatoid Arthritis</prism:section><prism:startingPage>752</prism:startingPage><prism:endingPage>760</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211002770/abstract?rss=yes"><title>Ultrasound-Defined Remission and Active Disease in Rheumatoid Arthritis: Association with Clinical and Serologic Parameters</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211002770/abstract?rss=yes</link><description>
Objective: 
To assess the association of clinical and/or serological parameters with ultrasound-defined disease activity in rheumatoid arthritis (RA).

Methods: 
Retrospective analysis of 149 consecutive RA patients routinely assessed by sonography of the wrists, metacarpo-phalangeal, and proximal interphalangeal joints. Semiquantitative scoring of synovial hypertrophy/effusion and power Doppler (PD) signals was performed. Sonographic remission was defined by the absence of PD signals. Number of tender and swollen joints, global assessment of disease activity by the physician (VAS-phys) and patient (VAS-pt), C-reactive protein (CRP), erythrocyte sedimentation rate, duration of morning stiffness (MS), simplified disease activity index, disease activity score for 28 joints, clinical disease activity index, and health assessment questionnaires were recorded.

Results: 
PD signals as a sign of active disease were observed in 117 (78.5%) RA patients. CRP, erythrocyte sedimentation rate, and MS were higher in patients with PD signals than in patients in remission. CRP &gt;5.0 mg/L (normal values 0-5.0 mg/L), MS &gt;15 minutes, or the combination of both revealed odds ratios of 5.0, 3.0, or 18.9, respectively, to indicate sonography-defined active disease. The other parameters showed no association with the presence or absence of PD-signals.

Conclusions: 
Sonography-defined disease activity is associated with CRP and MS, whereas current composite scores and its clinical components did not match this definition.
</description><dc:title>Ultrasound-Defined Remission and Active Disease in Rheumatoid Arthritis: Association with Clinical and Serologic Parameters</dc:title><dc:creator>Christian Dejaco, Christina Duftner, Edith Wipfler-Freißmuth, Helmut Weiss, Winfried B. Graninger, Michael Schirmer</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.09.005</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2011-11-07</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2011-11-07</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Rheumatoid Arthritis</prism:section><prism:startingPage>761</prism:startingPage><prism:endingPage>767</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211003593/abstract?rss=yes"><title>Gait Analysis of the Lower Limb in Patients with Rheumatoid Arthritis: A Systematic Review</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211003593/abstract?rss=yes</link><description>
Introduction: 
In rheumatoid arthritis (RA), signs and symptoms of feet and ankle are common. To evaluate the dynamic function of feet and ankles, namely walking, a variety of gait studies have been published. In this systematic review, we provide a systematic overview of the available gait studies in RA, give a clinimetrical assignment, and review the general conclusions regarding gait in RA.

Methods: 
A systematic literature search within the databases PubMed, CINAHL, sportdiscus, Embase, and Scopus was described and performed and delivered 78 original gait studies that were included for further data extraction.

Results: 
The clinimetrical quality of the 78 included RA gait studies measured according a tailored QUADAS item list and proposed clinimetrical criteria by Terwee and coworkers are moderate. General conclusions regarding the walking abnormalities of RA patients point to a slower walk, longer double support time, and avoidance of extreme positions. Frequently found static features in RA are hallux valgus, pes planovalgus, and hind foot abnormalities.

Conclusions: 
Gait studies in RA patients show moderate clinimetrical properties, but are a challenging way of expressing walking disability. Future gait research should focus on more uniformity in methodology. When this need is satisfied, more clinical applicable conclusions can be drawn.
</description><dc:title>Gait Analysis of the Lower Limb in Patients with Rheumatoid Arthritis: A Systematic Review</dc:title><dc:creator>Hetty Baan, Rosemary Dubbeldam, Anand V. Nene, Martin A.F.J. van de Laar</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.11.009</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2012-02-10</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2012-02-10</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Rheumatoid Arthritis</prism:section><prism:startingPage>768</prism:startingPage><prism:endingPage>788.e8</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211003052/abstract?rss=yes"><title>Registry of the Spanish Network for Systemic Sclerosis: Clinical Pattern According to Cutaneous Subsets and Immunological Status</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211003052/abstract?rss=yes</link><description>
Objective: 
To investigate the incidence of clinical and immunological characteristics of a large cohort of Spanish patients with scleroderma (SSc) and identifying factors associated with particular organ manifestations assessed by a nationwide cross-sectional analysis.

Methods: 
We classified SSc patients in 4 subsets using a modification of LeRoy and Medsger classification that included: “prescleroderma” (pre-SSc), limited cutaneous SSc (lcSSc), diffuse cutaneous SSc (dcSSc), and SSc sine scleroderma (ssSSc). Fourteen Spanish centers participated in patient recruitment. On January 2008, the database included 916 consecutive Spanish SSc patients, 801 women (87.4%) and 115 men (12.6%), all of whom fulfilled the classification criteria proposed by LeRoy and Medsger. Epidemiological, clinical, and laboratory data were collected according to a standard protocol. Mean age at diagnosis was 51.2 ± 15.1 years and mean age at disease onset was 44.9.0 ± 15.8 years. lcSSc was the most frequent subset (61.8%) followed by dcSSc (26.5%), ssSSc (7.5%), and preSSc (4%) subsets. Gender ratios were as follows: dcSSc subset, 200 women and 43 men (4.7:1); lcSSc subset, 503 women and 63 men (ratio 7.9:1), and ssSSc subset, 62 women and 7 men (ratio 8.9:1). Digital ulcers, interstitial lung disease (ILD), musculoeskeletal and esophageal involvement, and scleroderma renal crisis were more frequent in dcSSc than lcSSc and ssSSc subsets. The incidence of pulmonary arterial hypertension assessed by echocardiography was similar in all subsets but mean estimated systolic pulmonary arterial pressure was higher in ssSSc than in lcSSc subset (47.3 ± 23.9 mm Hg vs 39.6 ± 19.2 mm Hg; P &lt; 0.03). Cardiac involvement was identified more frequently in ssSSc than in dcSSc and lcSSc subsets (49.3% vs 32.5% and 31.1%, respectively; P = 0.015 and P = 0.004 for both comparisons). Acro-osteolysis (8.2% vs 2.4%, P = 0.049), calcinosis (19.8% vs 7.2%, P &lt; 0.05), and sicca syndrome (37.5% vs 14.5%, P &lt; 0.0001) were more frequent in lcSSc than in ssSSc subsets. The frequency of clinical manifestations related to the presence of anticentromere antibodies or antitopoisomerase I antibodies was very similar to that identified in patients categorized to lcSSc and dcSSc, respectively. However, in multivariate studies, the ranking of the variables according to their overall explanatory effect on the model showed that the contributory effect of the antibody status was not greater than that of the clinical categorization into lcSSc and dcSSc for the majority of disease manifestations, but, in important manifestations, as ILD, absence of anticentromere antibodies was an independent predictor factor.

Conclusions: 
The classification of SSc into dcSSc, lcSSc, and ssSSc subsets is the one that most closely reflects the natural history of the disease, as they presented clear clinical differences. The immunological profile helps to define important visceral alteration as ILD. Finally, to improve early diagnosis of SSc, patients with preSSc should be considered both to trace the true evolution of the disease and to define which patients could benefit from therapeutic measures able to prevent the appearance of visceral involvements.
</description><dc:title>Registry of the Spanish Network for Systemic Sclerosis: Clinical Pattern According to Cutaneous Subsets and Immunological Status</dc:title><dc:creator>Carmen Pilar Simeón-Aznar, Vicent Fonollosa-Plá, Carles Tolosa-Vilella, Gerard Espinosa-Garriga, Manel Ramos-Casals, Mercedes Campillo-Grau, Francisco José García-Hernández, María Jesús Castillo-Palma, Julio Sánchez-Román, José Luis Callejas-Rubio, Norberto Ortego-Centeno, Maria Victoria Egurbide-Arberas, Luis Trapiellla-Martínez, María Gallego-Villalobos, Luis Sáez-Comet, José Velilla-Marco, María Teresa Camps-García, Enrique de Ramón-Garrido, Eva María Esteban Marcos, Lucio Pallarés-Ferreres, Carmen Hidalgo-Tenorio, José Mario Sabio-Sánchez, Ricardo Gómez-de la Torre, Gonzalo Salvador-Cervello, Juan José Rios-Blanco, Antonio Gil-Aguado, Miquel Vilardell-Tarrés</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.10.004</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2011-12-14</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2011-12-14</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Systemic Sclerosis</prism:section><prism:startingPage>789</prism:startingPage><prism:endingPage>800</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211002836/abstract?rss=yes"><title>Arthritis in Systemic Sclerosis: Systematic Review of the Literature and Suggestions for the Performance of Future Clinical Trials in Systemic Sclerosis Arthritis</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211002836/abstract?rss=yes</link><description>
Objectives: 
Musculoskeletal (MSK) pain is a frequent (between 40-80%) complaint of patients with systemic sclerosis (SSc). Unfortunately, there are virtually no systematic studies of the causes or the management of MSK involvement in SSc and with few exceptions there have been no controlled trials to determine what are and should be the best strategies for managing MSK pain and synovitis in patients with SSc.

Methods: 
A literature search was conducted for published reports that have addressed the clinical assessment of “arthritis” and “musculoskeletal” involvement in SSc. The literature search was a prelude to developing recommendations/suggestions for performing clinical trials (preferably randomized) in the future in SSc-related arthritis.

Results: 
The search netted a number of articles that reported clinical assessments of arthritis in SSc, but very few reported results of controlled clinical trials. Nevertheless, a prevalence of clinical arthritis and tools used to assess the involvement (clinical examination, functional assessments and assessments of quality of life, and radiographic imaging) was found.

Conclusions: 
Most of the tools used to assess arthritis in SSc patients have not been validated and additional work is needed to develop a “core set” of variables for assessment of arthritis in SSc and its response to treatment. This report furnishes the background information that can help provide the building blocks for the development of a “core set” that can be used to chart the efficacy of new treatments for SSc-related arthritis in the future.
</description><dc:title>Arthritis in Systemic Sclerosis: Systematic Review of the Literature and Suggestions for the Performance of Future Clinical Trials in Systemic Sclerosis Arthritis</dc:title><dc:creator>Philip J. Clements, Yannick Allanore, Dinesh Khanna, Minjit Singh, Daniel E. Furst</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.10.003</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2011-12-19</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2011-12-19</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Systemic Sclerosis</prism:section><prism:startingPage>801</prism:startingPage><prism:endingPage>814</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211003490/abstract?rss=yes"><title>Intrarenal Hemodynamic Parameters Correlate with Glomerular Filtration Rate and Digital Microvascular Damage in Patients with Systemic Sclerosis</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211003490/abstract?rss=yes</link><description>
Objectives: 
To evaluate intrarenal arterial stiffness by Doppler ultrasound and examine the correlation between renal Doppler indices, glomerular filtration rate, and digital microvascular damage in systemic sclerosis patients.

Methods: 
Thirty systemic sclerosis patients and 30 healthy controls were enrolled in this study. Doppler indices of intrarenal arterial stiffness, peak systolic flow velocity, end diastolic flow velocity, resistive index, pulsative index, and systolic/diastolic (S/D) ratio were measured on the interlobar artery of both kidneys. Glomerular filtration rate was measured using Tc99m diethylenetriamine pentaacetic acid (DTPA). Equation 7 from the Modification of Diet in Renal Disease was used to estimate glomerular filtration rate. Nailfold videocapillaroscopy findings were classified as early, active, and late patterns.

Results: 
The intrarenal arterial stiffness, evaluated by Doppler indices, was higher in systemic sclerosis patients than healthy controls. In systemic sclerosis patients pulsative index (r = −0.69), resistive index (r = −0.75), and S/D ratio (r = −0.74) showed a negative correlation with measured glomerular filtration rate (P &lt; 0001). High correlation (P = 0008) was observed between measured and estimated glomerular filtration rate (r = 0.55). Pulsative index, resistive index, and S/D ratio significantly increased with progression of capillaroscopic damage. Conversely, measured glomerular filtration rate significantly decreased with capillaroscopic damage progression.

Conclusions: 
Doppler indices of intrarenal arterial stiffness are noninvasive diagnostic tests to evaluate renal damage in SSc patients. Intrarenal arterial stiffness and glomerular filtration rate correlate with capillaroscopic microvascular damage.
</description><dc:title>Intrarenal Hemodynamic Parameters Correlate with Glomerular Filtration Rate and Digital Microvascular Damage in Patients with Systemic Sclerosis</dc:title><dc:creator>Edoardo Rosato, Antonietta Gigante, Biagio Barbano, Rosario Cianci, Ilenia Molinaro, Carmelina Rossi, Rita Massa, Antonio Amoroso, Simonetta Pisarri, Felice Salsano</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.11.005</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2011-12-22</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2011-12-22</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Systemic Sclerosis</prism:section><prism:startingPage>815</prism:startingPage><prism:endingPage>821</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS004901721100357X/abstract?rss=yes"><title>Treatment of Systemic Sclerosis-Associated Calcinosis: A Case Report of Rituximab-Induced Regression of CREST-Related Calcinosis and Review of the Literature</title><link>http://www.semarthritisrheumatism.com/article/PIIS004901721100357X/abstract?rss=yes</link><description>
Objectives: 
Calcinosis is frequently encountered in patients with systemic sclerosis (SSc) and may be associated with significant morbidity. No treatment has shown so far an unequivocal beneficial effect.

Methods: 
We performed an extensive internet search (MEDLINE) using the keywords calcinosis, calcification, scleroderma, systemic sclerosis, and treatment.

Results: 
Our patient had extensive Calcinosis, Raynaud, Esophagitis, Sclerodactyly, telangiectasia (CREST)-related calcinosis, frequently ulcerating and painful. Following 2 rituximab courses (consisting of 4 weekly infusions, 375 mg/m2 each), calcinosis significantly improved and pain disappeared. Pharmacologic agents used in the treatment of SSc-associated calcinosis include diltiazem, minocycline, warfarin, biphosphonates, and intravenous immunoglobulin. Other therapeutic approaches include surgical excision, laser vaporization, and extracorporeal shock wave lithotripsy.

Conclusions: 
Evidence for all existing therapies is weak and therefore larger scale controlled studies are needed. Rituximab appears as a promising treatment especially in view of recent evidence that this therapy may be also effective in the underlying disease.
</description><dc:title>Treatment of Systemic Sclerosis-Associated Calcinosis: A Case Report of Rituximab-Induced Regression of CREST-Related Calcinosis and Review of the Literature</dc:title><dc:creator>Dimitrios Daoussis, Ioannis Antonopoulos, Stamatis-Nick C. Liossis, Georgios Yiannopoulos, Andrew P. Andonopoulos</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.11.007</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2012-01-06</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2012-01-06</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Systemic Sclerosis</prism:section><prism:startingPage>822</prism:startingPage><prism:endingPage>829</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211003465/abstract?rss=yes"><title>Global Trend of Survival and Damage of Systemic Lupus Erythematosus: Meta-Analysis and Meta-Regression of Observational Studies from the 1950s to 2000s</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211003465/abstract?rss=yes</link><description>
Objective: 
To assess systemically with meta-analysis the trend of survival and its determinants, which are hindering further improvement of survival of patients with systemic lupus erythematosus (SLE) over the past 5 decades.

Methods: 
Retrospective, cross-sectional, and prospective observational studies addressing survival and damage in SLE patients published between 1 January 1950 and 31 July 2010 were identified in electronic databases. Using the random-effects model, effect size was calculated based on the logit of the overall 5- and 10-year survival rates. The pooled logit and its robust 95% confidence interval were transformed back into the 5- and 10-year survival rates, after adjusting for potential dependence on the data. Potential factors predicting the pooled survival rates were explored by meta-regression.

Results: 
Seventy-seven studies involving 18,998 SLE patients were analyzed. Between the 1950s and the 2000s, their overall survival significantly increased, from 74.8% to 94.8% and 63.2% to 91.4% for the overall 5-year and 10-year survival, respectively (P &lt; 0.001). The survival improvement, however, appeared to slow down between 1980 and 1990. Meta-regression revealed that neuropsychiatric and renal damage negatively affected the overall 5-year survival, whereas neuropsychiatric damage remained so for the 10-year survival for the past 50 years. Furthermore, the prevalence of neuropsychiatric damage has been significantly increasing over the past 5 decades.

Conclusions: 
For the past 50 years, damage involving the renal and neuropsychiatric systems has been negatively affecting survival of SLE patients. Early detection and aggressive management of renal and neuropsychiatric involvement may potentially improve further the survival of lupus patients.
</description><dc:title>Global Trend of Survival and Damage of Systemic Lupus Erythematosus: Meta-Analysis and Meta-Regression of Observational Studies from the 1950s to 2000s</dc:title><dc:creator>Anselm Mak, Mike W.-L. Cheung, Hui Jin Chiew, Yang Liu, Roger Chun-man Ho</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.11.002</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2012-01-18</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2012-01-18</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Systemic Lupus Erythematosus</prism:section><prism:startingPage>830</prism:startingPage><prism:endingPage>839</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211003398/abstract?rss=yes"><title>Measurement of Autoantibodies in Pediatric-Onset Systemic Lupus Erythematosus and Their Relationship with Disease-Associated Manifestations</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211003398/abstract?rss=yes</link><description>
Objective: 
To evaluate an autoantibody profile in pediatric-onset systemic lupus erythematosus (SLE) patients to determine clinical and statistical associations with disease-associated manifestations.

Methods: 
Sera from 53 SLE patients and 22 healthy individuals were collected. Antibodies to C1q, histone, chromatin, ribosomal P, dsDNA, and high-avidity dsDNA were measured by enzyme-linked immunosorbent assays. Patient records were evaluated for clinical and laboratory associations.

Results: 
The most prevalent autoantibodies found in the SLE cohort were anti-C1q antibodies (n = 32, 60%), which correlated significantly with proteinuria and decreased complement levels (P &lt; 0.05). Anti-C1q and antihistone antibodies were significantly elevated in patients with class III/IV nephritis compared with class I/II/V nephritis (P = 0.041). SLE patients with active nephritis at the time of sample collection demonstrated significantly elevated levels of anti-C1q antibodies compared with those without active nephritis, also exhibiting 100% sensitivity for active nephritis, proteinuria, and urinary casts. Antibodies to C1q, dsDNA, histone, and chromatin were significantly elevated in patients with active disease (P &lt; 0.01). Chart-documented anti-dsDNA antibodies were positive in 28 SLE patients, INOVA anti-dsDNA antibodies in 25 patients, and high-avidity anti-dsDNA antibodies in 8 patients. Antihistone correlated significantly with leukopenia and hemolytic anemia (P &lt; 0.05).

Conclusions: 
This study indicates the importance of measuring anti-C1q antibodies in pediatric-onset SLE patients because elevated anti-C1q antibodies may be more indicative of renal disease activity, showing significant correlation with proteinuria, urinary casts, and active nephritis. Antibodies to C1q, histone, chromatin, and dsDNA exhibited the strongest association with clinical features, indicating the importance of measuring all of these antibodies in pediatric-onset SLE patients.
</description><dc:title>Measurement of Autoantibodies in Pediatric-Onset Systemic Lupus Erythematosus and Their Relationship with Disease-Associated Manifestations</dc:title><dc:creator>Brooke E. Gilliam, Amanda K. Ombrello, Rufus W. Burlingame, Peri H. Pepmueller, Terry L. Moore</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.09.009</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2011-12-19</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2011-12-19</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Systemic Lupus Erythematosus</prism:section><prism:startingPage>840</prism:startingPage><prism:endingPage>848</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211003611/abstract?rss=yes"><title>A Prospective Functional MRI Study for Executive Function in Patients with Systemic Lupus Erythematosus Without Neuropsychiatric Symptoms</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211003611/abstract?rss=yes</link><description>
Objective: 
To study the functional brain activation signals before and after sufficient disease control in patients with systemic lupus erythematosus (SLE) without clinical neuropsychiatric symptoms.

Methods: 
Blood-oxygen-level-dependent signals during event-related functional magnetic resonance imaging brain were recorded, while 14 new-onset SLE patients and 14 demographically and intelligence quotient matched healthy controls performed the computer-based Wisconsin card sorting test for assessing executive function, which probes strategic planning and goal-directed task performance during feedback evaluation (FE) and response selection (RS), respectively. Composite beta maps were constructed by a general linear model to identify regions of cortical activation. Blood-oxygen-level-dependent functional magnetic resonance imaging signals were compared between (1) new-onset SLE patients and healthy controls and (2) SLE patients before and after sufficient control of their disease activity.

Results: 
During RS, SLE patients demonstrated significantly higher activation than healthy controls in both caudate bodies and Brodmann area (BA) 9 to enhance event anticipation, attention, and working memory, respectively, to compensate for the reduced activation during FE in BA6, 13, 24, and 32, which serve complex motor planning and decision-making, sensory integration, error detection, and conflict processing, respectively. Despite significant reduction of SLE activity, BA32 was activated during RS to compensate for reduced activation during FE in BA6, 9, 37, and 23/32, which serve motor planning, response inhibition and attention, color processing and word recognition, error detection, and conflict evaluation, respectively.

Conclusions: 
Even without clinically overt neuropsychiatric symptoms, SLE patients recruited additional pathways to execute goal-directed tasks to compensate for their reduced strategic planning skill despite clinically sufficient disease control.
</description><dc:title>A Prospective Functional MRI Study for Executive Function in Patients with Systemic Lupus Erythematosus Without Neuropsychiatric Symptoms</dc:title><dc:creator>Anselm Mak, Tao Ren, Erin Hui-yun Fu, Alicia Ai-cia Cheak, Roger Chun-man Ho</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.11.010</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2012-01-06</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2012-01-06</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Systemic Lupus Erythematosus</prism:section><prism:startingPage>849</prism:startingPage><prism:endingPage>858</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211003386/abstract?rss=yes"><title>Patients with Retinal Vasculitis Rarely Suffer from Systemic Vasculitis</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211003386/abstract?rss=yes</link><description>
Objectives: 
Systemic vasculitis is often mistakenly assumed to be a common cause of retinal vasculitis. We sought to determine the relationship between retinal vasculitis and systemic vasculitis.

Methods: 
A selected review was performed on 1390 charts of patients attending the uveitis clinic at the Oregon Health and Science University between 1985 and 2010. Included in the review were all patients with diagnoses commonly associated with retinal vasculitis and all patients who were diagnosed with a systemic vasculitis. Retinal vasculitis was identified by perivascular exudates, intraretinal hemorrhage, or cotton wool spots as seen on clinical examination or by vascular occlusion or leakage as identified by fluorescein angiogram.

Results: 
Two hundred seven or 14.9% of patients with uveitis had retinal vasculitis as a component of the intraocular inflammation. Thirty-five patients had retinal vasculitis that was primary, ie, not associated with a systemic disease, and the dominant manifestation of the uveitis. Fourteen of the patients with retinal vasculitis had Behcet's disease. Only 11 of the 1390 patients with uveitis had a systemic vasculitis. Of these 11, four had retinal vasculitis including 1 secondary to a cytomegalovirus retinitis. Thus, systemic vasculitis was directly responsible for 1.4% or 3 of 207 cases of retinal vasculitis. Nonvasculitic systemic diseases such as sarcoidosis (n = 13), syndromes confined to the eye such as pars planitis (n = 36), and intraocular infections (n = 29) were far more common causes of retinal vasculitis.

Conclusions: 
Retinal vasculitis is a relatively common feature of uveitis. Patients with retinal vasculitis, however, rarely suffer from 1 of the classical systemic vasculitides.
</description><dc:title>Patients with Retinal Vasculitis Rarely Suffer from Systemic Vasculitis</dc:title><dc:creator>James T. Rosenbaum, Jennifer Ku, Amro Ali, Dongseok Choi, Eric B. Suhler</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.10.006</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2011-12-19</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2011-12-19</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Vasculitis</prism:section><prism:startingPage>859</prism:startingPage><prism:endingPage>865</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211003374/abstract?rss=yes"><title>Utility of Erythrocyte Sedimentation Rate and C-Reactive Protein for the Diagnosis of Giant Cell Arteritis</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211003374/abstract?rss=yes</link><description>
Objectives: 
To evaluate the utility of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) for the diagnosis of giant cell arteritis (GCA) and to determine the frequency of normal ESR and CRP at diagnosis of GCA.

Methods: 
All patients undergoing temporal artery biopsy (TAB) between 2000 and 2008 were identified. Only subjects with both ESR and CRP at the time of TAB were included. The medical records of all patients were reviewed.

Results: 
We included 764 patients (65% women), mean age 72.7 (±9.27) years, who underwent TAB. Biopsy was consistent with GCA in 177 patients (23%). Elevated CRP and elevated ESR provided a sensitivity of 86.9% and 84.1%, respectively, for a positive TAB. The odds ratio of a concordantly elevated ESR and CRP for positive TAB was 3.06 (95% CI 2.03, 4.62), whereas the odds ratio for concordantly normal ESR and CRP was 0.49 (95% CI 0.29, 0.83). Seven patients (4%) with a positive TAB for GCA had a normal ESR and CRP at diagnosis. Compared with GCA patients with elevated markers of inflammation, a greater proportion of these patients had polymyalgia rheumatica symptoms (P = 0.008), whereas constitutional symptoms, anemia and thrombocytosis, were observed less often (P &lt; 0.05).

Conclusions: 
CRP is a more sensitive marker than ESR for a positive TAB that is diagnostic of GCA. There may be clinical utility in obtaining both tests in the evaluation of patients with suspected GCA. A small proportion of patients with GCA may have normal inflammatory markers at diagnosis.
</description><dc:title>Utility of Erythrocyte Sedimentation Rate and C-Reactive Protein for the Diagnosis of Giant Cell Arteritis</dc:title><dc:creator>Tanaz A. Kermani, Jean Schmidt, Cynthia S. Crowson, Steven R. Ytterberg, Gene G. Hunder, Eric L. Matteson, Kenneth J. Warrington</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.10.005</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2011-11-28</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2011-11-28</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Vasculitis</prism:section><prism:startingPage>866</prism:startingPage><prism:endingPage>871</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211003477/abstract?rss=yes"><title>HFE C282Y Homozygosity Is Associated with an Increased Risk of Total Hip Replacement for Osteoarthritis</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211003477/abstract?rss=yes</link><description>
Objective: 
The evidence for an association between mutations in the HFE (hemochromatosis) gene and the risk of hip or knee osteoarthritis is inconsistent. Total joint replacement is considered a surrogate measure for symptomatic end-stage osteoarthritis. We examined the relationship between HFE gene mutations and risk of total hip and knee replacement using a prospective cohort study.

Methods: 
The Melbourne Collaborative Cohort Study recruited participants between 1990 and 1994. Participants born in Australia, New Zealand, the United Kingdom, or Ireland (n = 27,848) were genotyped for the HFE C282Y mutation. Total hip and knee replacements for osteoarthritis during 2001 to 2009 were ascertained from the Australian Orthopaedic Association National Joint Replacement Registry. Hazard ratios (HR)/odds ratios (OR) and confidence intervals (CI) were obtained from Cox regression or logistic regression.

Results: 
Compared with those with no C282Y mutation, C282Y homozygotes had an increased risk of single total hip replacement (HR 1.94, 95% CI 1.04-3.62) and bilateral total hip replacement (OR 5.86, 95% CI 2.36-14.57) for osteoarthritis, adjusting for age, sex, body mass index, and educational level. Only 3 C282Y homozygotes had single total knee replacement; the HR was 0.51 (95% CI 0.16-1.57). C282Y/H63D compound heterozygosity was not related to the risk of total hip or knee replacement.

Conclusions: 
HFE C282Y homozygosity was associated with an increased risk of both single and bilateral total hip replacement for osteoarthritis.
</description><dc:title>HFE C282Y Homozygosity Is Associated with an Increased Risk of Total Hip Replacement for Osteoarthritis</dc:title><dc:creator>Yuanyuan Wang, Lyle C. Gurrin, Anita E. Wluka, Nadine A. Bertalli, Nicholas J. Osborne, Martin B. Delatycki, Graham G. Giles, Dallas R. English, John L. Hopper, Julie A. Simpson, Stephen Graves, Katrina J. Allen, Flavia M. Cicuttini</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.11.003</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2011-12-30</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2011-12-30</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Osteoarthritis</prism:section><prism:startingPage>872</prism:startingPage><prism:endingPage>878</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211003581/abstract?rss=yes"><title>Use of Diuretics and the Risk of Gouty Arthritis: A Systematic Review</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211003581/abstract?rss=yes</link><description>
Objective: 
To systematically review the literature investigating the relationship between use of diuretics and the risk of gouty arthritis.

Methods: 
PubMed (1950-October 2009), Embase (1974-October 2009), and the Cochrane Library (up to October 2009) were searched using keywords and MeSH terms diuretics, adverse effects, and gout. For this review, the technique of “best evidence synthesis” was used. Studies reporting frequency, absolute or relative risks, odds ratio, or rate ratio of gouty arthritis in diuretic users compared with nonusers were selected and evaluated. Studies had to be published in English. Checklists from the Dutch Cochrane Centre were used to assess the quality of randomized controlled trials (RCTs), cohort, and case-control studies.

Results: 
Two RCTs, 6 cohort studies, and 5 case-control studies met the inclusion criteria. The overall quality of the studies was moderate. In a RCT the rate ratio of gout for use of bendrofluazide vs placebo was 11.8 (95% CI 5.2-27.0). The other RCT found a rate ratio of 6.3 (95% CI 0.8-51) for use of hydrochlorothiazide plus triamterene vs placebo. Three cohort studies and 4 case-control studies found higher risks of gouty arthritis in users compared with nonusers of diuretics.

Conclusions: 
There is a trend toward a higher risk for acute gouty arthritis attacks in patients on loop and thiazide diuretics, but the magnitude and independence is not consistent. Therefore, stopping these useful drugs in patients who develop gouty arthritis is not supported by the results of this review.
</description><dc:title>Use of Diuretics and the Risk of Gouty Arthritis: A Systematic Review</dc:title><dc:creator>Berdine A.A. Hueskes, Elisabeth A. Roovers, Aukje K. Mantel-Teeuwisse, Hein J.E.M. Janssens, Eloy H. van de Lisdonk, Matthijs Janssen</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.11.008</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2012-01-06</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2012-01-06</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Gout</prism:section><prism:startingPage>879</prism:startingPage><prism:endingPage>889</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211002800/abstract?rss=yes"><title>Short-Term and Long-Term Outcome of Anti-Jo1-Positive Patients with Anti-Ro52 Antibody</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211002800/abstract?rss=yes</link><description>
Objectives: 
The aims of the present study were to (1) assess clinical features and long-term outcome in anti-Jo1-positive patients with anti-Ro52 antibody; (2) compare characteristics of anti-Jo1-positive patients with and without anti-Ro52 antibody; and (3) compare features of anti-Ro52-positive patients with and without anti-Jo1 antibody.

Methods: 
The medical records of 89 consecutive anti-Jo1-positive patients with antisynthetase syndrome (ASS) were reviewed; 36 of these patients had coexistent anti-Ro52 antibody. Furthermore, the medical records of 13 consecutive anti-Ro52-positive patients without anti-Jo1 antibody were also reviewed.

Results: 
Nine anti-Jo1-positive patients (25%) with anti-Ro-52 antibody achieved remission of ASS, whereas 19 other patients (52.8%) improved and 8 patients (22.2%) worsened their clinical status. Anti-Jo1-positive patients with anti-Ro52 antibody experienced ASS-related complications: interstitial lung disease (n = 28), esophageal dysfunction (n = 9), and joint manifestations (n = 25), including periarticular hydroxyapatite calcifications and erosions of metacarpophalangeal and interphalangeal joints and wrists (n = 3); 7 anti-Ro52-positive patients (19.4%) had cancer. Anti-Jo1-positive patients with anti-Ro52 antibody, compared with those without, more commonly experienced deterioration of myositis and joint involvement, symptomatic form of ILD, and cancer; they also had decreased survival rate (P = 0.05). We further found that anti-Ro52-positive patients with anti-Jo1 antibody, compared with those without, were younger and more frequently exhibited ILD with poorer prognosis.

Conclusions: 
Our series underlines that the presence of anti-Ro52 antibody is associated with a particular phenotype of ASS, leading to more severe myositis and joint impairment. Moreover, the coexistence of anti-Ro52 antibody seems to be associated with an increased risk of cancer. We therefore suggest that anti-Jo1-positive patients should routinely undergo the search for anti-Ro52 antibody, as this autoantibody appears to impact patients' prognosis.
</description><dc:title>Short-Term and Long-Term Outcome of Anti-Jo1-Positive Patients with Anti-Ro52 Antibody</dc:title><dc:creator>Isabelle Marie, Pierre Yves Hatron, Stéphane Dominique, Patrick Cherin, Luc Mouthon, Jean-François Menard, Hervé Levesque, Fabienne Jouen</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.09.008</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2011-11-11</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2011-11-11</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Miscellaneous</prism:section><prism:startingPage>890</prism:startingPage><prism:endingPage>899</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211003453/abstract?rss=yes"><title>Autoimmune Manifestations of Kikuchi Disease</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211003453/abstract?rss=yes</link><description>
Objectives: 
Kikuchi's disease (KD) has been associated with the presence of autoantibodies, systemic lupus erythematosus (SLE), and other autoimmune diseases. The aim of this study was to assess the frequency of autoimmune manifestations in a KD cohort with a long follow-up.

Methods: 
Twenty patients with histologically confirmed KD since January 1990 until December 2010 were studied; 12 of them were periodically followed up as outpatients. Another 7 patients were contacted by telephone to offer them a specific consultation and a complete autoimmunity study.

Results: 
Thirteen of 20 patients were women (65%) with a mean age of 29 years (range, 15-79). The age at diagnosis was higher in men (44 vs 27 years, P &lt; 0.05). Lymphopenia was present in 75% of the patients (15/20) and was the more frequent hematological abnormality. The mean follow-up of the 17 patients included in the autoimmunity study was 119 months (range, 15-252). Autoimmune diseases were detected in 9 women (53%): SLE was diagnosed in 4 patients (2 SLE before, 1 simultaneous, and 1 after KD), 2 patients developed primary Sjögren's syndrome after KD, 1 thyroiditis before KD, 1 SLE-like, and 1 antiphospholipid antibodies after KD. Leukocytoclastic vasculitis was found in 2 patients; 1 of them eventually developed SLE. Female sex, painful adenopathies, and cytopenias were significantly associated with autoimmune diseases.

Conclusions: 
Among patients with KD, only women developed autoimmune manifestations. Therefore, long-term follow-up and active surveillance of autoimmune diseases in patients with KD, especially women, are recommended.
</description><dc:title>Autoimmune Manifestations of Kikuchi Disease</dc:title><dc:creator>Bernardo Sopeña, Alberto Rivera, Caritina Vázquez-Triñanes, Enrique Fluiters, Joaquín González-Carreró, Margarita del Pozo, Mayka Freire, César Martínez-Vázquez</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.11.001</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2011-12-22</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2011-12-22</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Miscellaneous</prism:section><prism:startingPage>900</prism:startingPage><prism:endingPage>906</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211003489/abstract?rss=yes"><title>Treatment of Erdheim-Chester Disease with Long-Term High-Dose Interferon-α</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211003489/abstract?rss=yes</link><description>
Objectives: 
Erdheim-Chester disease (ECD) is a rare non-Langerhans cell histiocytosis, characterized by a foamy CD68+, CD1a− histiocyte tissue infiltration. Efficacy of standard doses of interferon-α-2a (IFNα) has been suggested in a small series but with variation, depending on the organs involved. Our aim was to report our single-center experience about the use of high-dose IFNα in ECD.

Methods: 
Twenty-four ECD patients have received high-dose IFNα (IFNα ≥18 mIU/wk or pegylated-IFNα ≥180 μg/wk). IFNα efficacy was evaluated clinically and morphologically using a standardized protocol (median follow-up 19 months).

Results: 
Indication for treatment was central nervous system and/or heart involvement (n = 20), exophthalmos (n = 1), and standard-dose IFNα inefficacy (n = 3). High-dose IFNα was effective in 16 patients (67%) with improvement (n = 11, 46%) and stabilization (n = 5, 21%). Late and gradual improvement was observed during prolonged follow-up in most patients. The efficacy of high-dose IFNα was dependent on the organs involved: central nervous system and heart improvement or stabilization occurred in 7/11 (64%) and 11/14 (79%) patients, respectively. Six patients (25%) worsened. High doses of IFNα were well-tolerated: 13 (54.2%) patients had side effects but treatment interruption was infrequent (n = 3, 12.5%).

Conclusions: 
High-dose IFNα may be effective in severe ECD. Improvement may be slow, and high-dose IFNα treatment should be prolonged.
</description><dc:title>Treatment of Erdheim-Chester Disease with Long-Term High-Dose Interferon-α</dc:title><dc:creator>Baptiste Hervier, Laurent Arnaud, Frederic Charlotte, Bertrand Wechsler, Jean Charles Piette, Zahir Amoura, Julien Haroche</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.11.004</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2012-02-10</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2012-02-10</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Miscellaneous</prism:section><prism:startingPage>907</prism:startingPage><prism:endingPage>913</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211003568/abstract?rss=yes"><title>Meta-Analysis on the Performance of Sonography for the Diagnosis of Carpal Tunnel Syndrome</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211003568/abstract?rss=yes</link><description>
Objective: 
We aimed to review and pool recent large methodological studies evaluating the diagnosis performance of ultrasonography vs electrodiagnostic testing (EDX).

Methods: 
Using the keywords: “carpal tunnel syndrome”, “ultrasound”, and “validity”, recent articles evaluating ultrasonography compared with a reference including EDX were selected from 4 databases (PubMed, Embase, Web of science, and BDSP) and from previous review for older articles, after 2 rounds. Relevant data for different thresholds of cross-sectional area of the median nerve were extracted from the articles to calculate the pooled sensitivity, specificity, and likelihood ratios. Different analyses were also performed to study potential sources of heterogeneity, such as calculation of area under the curve, using summary receiver operating characteristic curve.

Results: 
Among the 189 articles found, 13 articles were included. A cross-sectional area of the median nerve between 9.5 and 10.5 mm2 (study included once only), found for 11 studies, gave the pooled sensitivity as 0.84 [0.81 to 0.87] and the likelihood ratio for a negative test as 0.21 [0.17 to 0.27]. Specificity (0.78 [0.69-0.88]) and the likelihood ratio for a positive test (3.74 [2.30-6.10]) were heterogeneous. For a threshold at 7.0 to 8.5 mm2, pooled sensitivity was 0.94 [0.87 to 1.00], and for 11.5 to 13.0 mm2 specificity was 0.97 [0.91 to 1.00]. The only significant variable on potential sources of heterogeneity was the cross-sectional area of the median nerve threshold and area under the curve was 0.87 (asymmetric).

Conclusions: 
Pooling recent articles seems to confirm that sonography using cross-sectional area of the median nerve could not be an alternative to EDX for diagnosis of carpal tunnel syndrome but could give complementary results.
</description><dc:title>Meta-Analysis on the Performance of Sonography for the Diagnosis of Carpal Tunnel Syndrome</dc:title><dc:creator>Alexis Descatha, Laure Huard, François Aubert, Bruno Barbato, Olivier Gorand, Jean-François Chastang</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.11.006</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2012-01-13</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2012-01-13</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Miscellaneous</prism:section><prism:startingPage>914</prism:startingPage><prism:endingPage>922</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017212000650/abstract?rss=yes"><title>Proceedings of the 2012 Rheumatology Winter Clinical Symposia</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017212000650/abstract?rss=yes</link><description>
Recent years have witnessed important developments in rheumatology. Novel diagnostic methods, stratification approaches, and treatment paradigms have been brought into the clinic for a number of rheumatologic and autoimmune diseases. In addition, there have been developments in related medical disciplines that are relevant to the care of patients with rheumatic diseases. Keeping pace with these many developments is a challenge, and clinical rheumatologists have used various methods to educate themselves about these advances. In January 2012, the 5th annual Rheumatology Winter Clinical Symposium was held. At this meeting, faculty and participants held discussions and exchanged knowledge about new scientific data and how it may impact the care of rheumatology patients. Excerpts from some of the lectures from the Rheumatology Winter Clinical Symposium 2012 are included in this review. These and other presentations can be viewed in their entirety at http://www.r-w-c-s.com.
</description><dc:title>Proceedings of the 2012 Rheumatology Winter Clinical Symposia</dc:title><dc:creator>Arthur Kavanaugh, George Martin, John J. Cush, Martin J. Bergman, Roy Fleischmann, Orrin M. Troum, Vibeke Strand, Eric M. Ruderman, Alvin F. Wells</dc:creator><dc:identifier>10.1016/j.semarthrit.2012.03.002</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Proceedings</prism:section><prism:startingPage>923</prism:startingPage><prism:endingPage>926</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017211003982/abstract?rss=yes"><title>Injection of Botulinum Toxin for Treatment of Chronic Lateral Epicondylitis</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017211003982/abstract?rss=yes</link><description>We are pleased to read the article, “Injection of Botulinum Toxin for Treatment of Chronic Lateral Epicondylitis: Systematic Review and Meta-Analysis,” by Kalichman and coworkers in Seminars in Arthritis and Rheumatism (2011;40:532-8). The conclusions in their abstract stated that present literature provides support for use of botulinum toxin A injections into the forearm extensor muscles (60 units) for the treatment of chronic treatment-resistant lateral epicondylitis (). As they did not specify the proprietary name of the 60 units botulinum toxin type A, the readers may be misled if they only read the abstract without referring to the entire article.</description><dc:title>Injection of Botulinum Toxin for Treatment of Chronic Lateral Epicondylitis</dc:title><dc:creator>Yu-Ching Lin, Shu-Min Chen, Ta-Shen Kuan, Pei-Chun Hsieh, Yo-Hong Guo, I-Ling Lin, I-Ming Jou</dc:creator><dc:identifier>10.1016/j.semarthrit.2011.12.004</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2012-02-16</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2012-02-16</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>e1</prism:startingPage><prism:endingPage>e2</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017212000224/abstract?rss=yes"><title>Role of Interleukin-12 and - 18 in Lupus-like Syndrome Patients with Statin Use: Comment on: Association Between Statin Use and Lupus-like Syndrome Using Spontaneous Reports⁎</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017212000224/abstract?rss=yes</link><description>We read with great interest the recent contribution by de Jong et al. (). They assessed whether there was an association between statin use and the occurrence of lupus-like syndrome (LLS) and found that statins were associated with the reporting of LLS (reporting odds ratios 2.01; 95% confidence intervals 1.61-2.51). However, they did not explicate more detailed causality. We would like to suggest a possible pathomechanism in the development of LLS by using statin.</description><dc:title>Role of Interleukin-12 and - 18 in Lupus-like Syndrome Patients with Statin Use: Comment on: Association Between Statin Use and Lupus-like Syndrome Using Spontaneous Reports⁎</dc:title><dc:creator>Se Jin Park, Jae Il Shin</dc:creator><dc:identifier>10.1016/j.semarthrit.2012.01.006</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2012-03-12</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2012-03-12</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>e2</prism:startingPage><prism:endingPage>e3</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017212001163/abstract?rss=yes"><title>Contents</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017212001163/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0049-0172(12)00116-3</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A1</prism:startingPage><prism:endingPage>A3</prism:endingPage></item><item rdf:about="http://www.semarthritisrheumatism.com/article/PIIS0049017212001175/abstract?rss=yes"><title>Current Abstracts</title><link>http://www.semarthritisrheumatism.com/article/PIIS0049017212001175/abstract?rss=yes</link><description></description><dc:title>Current Abstracts</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0049-0172(12)00117-5</dc:identifier><dc:source>Seminars in Arthritis and Rheumatism 41, 6 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Seminars in Arthritis and Rheumatism</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>41</prism:volume><prism:number>6</prism:number><prism:issueIdentifier>S0049-0172(11)X0009-4</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A6</prism:startingPage><prism:endingPage>A12</prism:endingPage></item></rdf:RDF>
