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<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep372v1?rss=1">
<title><![CDATA[Genotype at the sIL-6R A358C polymorphism does not influence response to anti-TNF therapy in patients with rheumatoid arthritis]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep372v1?rss=1</link>
<description><![CDATA[
<p><b>Objectives.</b> To investigate the association between genotype at the soluble interleukin 6 receptor (sIL-6R) A358C single nucleotide polymorphism (SNP, rs8192284), previously reported to correlate with soluble receptor levels, and response to anti-TNF therapy in subjects with RA.</p>
<p><b>Methods.</b> In a large cohort of Caucasian RA patients treated with anti-TNF medications (total, <I>n</I> = 1050; etanercept, <I>n</I> = 455; infliximab, <I>n</I> = 450; and adalimumab, <I>n</I> = 142), the sIL-6R A358C polymorphism was genotyped using a Taqman 5'-allelic discrimination assay. Linear regression analysis adjusted for baseline 28 joint disease activity score (DAS28), baseline HAQ score, gender and use of concurrent DMARDs was used to assess the association of genotype at this polymorphism with response to anti-TNF therapy, defined by change in DAS28 after 6 months of treatment. Analyses were performed in the entire cohort, and also stratified by an anti-TNF agent. Additional analysis according to the EULAR response criteria was also performed, with the chi-squared test used to compare genotype groups.</p>
<p><b>Results.</b> No association between genotype at sIL-6R A358C and response to anti-TNF treatment was detected either in the cohort as a whole or after stratification by anti-TNF agent, in either the linear regression analysis or with response segregated according to EULAR criteria.</p>
<p><b>Conclusions.</b> This study shows that genotype at the functional sIL-6R A358C SNP is not associated with response to anti-TNF treatment in patients with RA.</p>
]]></description>
<dc:creator><![CDATA[Hassan, B., Maxwell, J. R., Hyrich, K. L., Biologics in Rheumatoid Arthritis Genetics and Genomics Study Syndicate, Barton, A., Worthington, J., Isaacs, J. D., Morgan, A. W., Wilson, A. G.]]></dc:creator>
<dc:date>Thu, 19 Nov 2009 05:10:44 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep372</dc:identifier>
<dc:title><![CDATA[Genotype at the sIL-6R A358C polymorphism does not influence response to anti-TNF therapy in patients with rheumatoid arthritis]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-19</prism:publicationDate>
<prism:section>Concise Report</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep356v1?rss=1">
<title><![CDATA[Rituximab as early therapy for pulmonary haemorrhage in systemic lupus erythematosus]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep356v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Narshi, C. B., Haider, S., Ford, C. M., Isenberg, D. A., Giles, I. P.]]></dc:creator>
<dc:date>Thu, 19 Nov 2009 05:10:40 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep356</dc:identifier>
<dc:title><![CDATA[Rituximab as early therapy for pulmonary haemorrhage in systemic lupus erythematosus]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-19</prism:publicationDate>
<prism:section>Letter to the Editor (Case Report)</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep352v1?rss=1">
<title><![CDATA[Disease activity and disability in children with juvenile idiopathic arthritis one year following presentation to paediatric rheumatology. Results from the Childhood Arthritis Prospective Study]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep352v1?rss=1</link>
<description><![CDATA[
<p><b>Objective.</b> Inflammatory arthritis in childhood is variable in terms of both presentation and outcome. This analysis describes disease activity in children with juvenile idiopathic arthritis (JIA) during the first year following presentation to a paediatric rheumatologist and identifies predictors of moderate to severe disability [defined using a Childhood HAQ (CHAQ) score &gt;=0.75] at 1 year.</p>
<p><b>Methods.</b> The Childhood Arthritis Prospective Study recruits children &lt;16 years with new inflammatory arthritis persisting for &gt;=2 weeks from five UK tertiary referral centres. Demographics, disease features, joint count, CHAQ, physician's global assessment, parent's general evaluation of well-being (PGE), ESR and treatment, are collected at first presentation, 6 months and then yearly. Independent predictors of CHAQ &gt;=0.75 at 1 year in children diagnosed with JIA were identified using multivariable logistic regression models.</p>
<p><b>Results.</b> Seven hundred and forty children with JIA were included; median age at presentation 7.6 years, 64% girls. During the first year, 85% received NSAIDs, 70% IA corticosteroids, 47% MTX and 27% systemic steroids (oral or i.v.). Median presenting CHAQ score was 0.63 and decreased to 0.25 at 1 year; 32% had CHAQ &gt;=0.75 at 1 year. The strongest predictor of CHAQ &gt;=0.75 at 1 year was CHAQ &gt;=0.75 at presentation (odds ratio 3.92; 95% CI 2.17, 7.09). Additional predictors included female gender and higher PGE</p>
<p><b>Conclusion.</b> Although CHAQ score improved in most children, the strongest predictor of persistent disability at 1 year was moderate to severe disability at first presentation. Follow-up beyond 1 year will assess whether CHAQ at presentation will continue to be a predictor of future poor outcome.</p>
]]></description>
<dc:creator><![CDATA[Hyrich, K. L., Lal, S. D., Foster, H. E., Thornton, J., Adib, N., Baildam, E., Gardner-Medwin, J., Wedderburn, L. R., Chieng, A., Davidson, J., Thomson, W.]]></dc:creator>
<dc:date>Thu, 19 Nov 2009 05:10:37 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep352</dc:identifier>
<dc:title><![CDATA[Disease activity and disability in children with juvenile idiopathic arthritis one year following presentation to paediatric rheumatology. Results from the Childhood Arthritis Prospective Study]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-19</prism:publicationDate>
<prism:section>Original Article</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep344v1?rss=1">
<title><![CDATA[Comment on: Clinical utility of ANA measured by ELISA compared with ANA measured by immunofluorescence: reply]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep344v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Maguire, G. A., Ginawi, A., Lee, J., Lim, A. Y. N., Wood, G., Houghton, S., Kumararatne, D. S., Hill Gaston, J. S.]]></dc:creator>
<dc:date>Thu, 19 Nov 2009 05:10:34 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep344</dc:identifier>
<dc:title><![CDATA[Comment on: Clinical utility of ANA measured by ELISA compared with ANA measured by immunofluorescence: reply]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-19</prism:publicationDate>
<prism:section>Letter to the Editor (Matters Arising)</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep368v1?rss=1">
<title><![CDATA[Genetic background of systemic sclerosis: autoimmune genes take centre stage]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep368v1?rss=1</link>
<description><![CDATA[
<p>SSc is a complex multiorgan disease. The key steps in its pathogenesis include early endothelial damage, dysregulation of the immune system with abnormal autoantibody production and fibroblast activation resulting in hyperproduction of extracellular matrix. The disease is caused by an interaction between susceptibility genes and environmental triggers since epidemiological data, including family and twin studies, reveal a genetic component in the pathogenesis of SSc. The candidate gene approach has mainly been employed to identify SSc susceptibility genes. We will focus on data obtained through large samples of well-phenotyped patients and replicated in independent cohorts. These case&ndash;control association studies have enabled the identification of several genes that are shared with other connective tissue disorders, and for some of these, putative autoimmune susceptibility genes have been identified. Indeed, we will mainly focus on <I>IRF</I>5 (rs2004640), <I>STAT</I>4 (rs7574865), <I>PTPN</I>22 (rs2476601) and <I>BANK</I>1 (rs3733197 and rs10516487) data. Some of these genes/loci are common to several autoimmune diseases, indicating a shared genetic background also contributing to SSc. Among connective tissue disorders, similarities for genetic markers with SLE are noteworthy. Most likely, these immune-modifying genes could interact and influence both disease phenotype and severity. Less evidence is available yet with regard to genetic markers relating to the vascular and fibrotic aspects of the disease.</p>
]]></description>
<dc:creator><![CDATA[Allanore, Y., Dieude, P., Boileau, C.]]></dc:creator>
<dc:date>Wed, 18 Nov 2009 07:21:05 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep368</dc:identifier>
<dc:title><![CDATA[Genetic background of systemic sclerosis: autoimmune genes take centre stage]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-18</prism:publicationDate>
<prism:section>Review</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep354v1?rss=1">
<title><![CDATA[Patient preferences in the choice of anti-TNF therapies in rheumatoid arthritis. Results from a questionnaire survey (RIVIERA study)]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep354v1?rss=1</link>
<description><![CDATA[
<p><b>Objective.</b> To identify the determinants of anti-TNF-naive patients&rsquo; preferences for the route of administration of anti-TNF agents.</p>
<p><b>Methods.</b> The study was carried out in 50 Italian rheumatology centres (802 patients). All patients completed a 31-item questionnaire addressing their perceptions of current treatment and the preferences for treatment with anti-TNF agents. Statistical methods included analysis of variance (ANOVA), <I>t</I>-test and chi-square test.</p>
<p><b>Results.</b> The response rate to the questionnaire was 97.6%. At the time of the survey, 310 (39.9%) patients were dissatisfied with current treatments, owing to inefficacy, side effects and inconvenience of administration. The i.v. and s.c. routes of administration were preferred by 50.2 and 49.8%, respectively. No significant difference was found in patients by gender, age, RA duration or number of drugs used. Reasons for the choice of i.v. administration were the safety of treatment at the hospital and the reassuring effect of physician presence. The s.c. administration was chosen for the convenience of treatment and in particular for home treatment. Patients dissatisfied with current therapy due to side effects preferred s.c. administration (<I>P</I> = 0.029), whereas patients choosing the i.v. route had slightly higher scores on &lsquo;today pain&rsquo; (<I>P</I> = 0.047) and &lsquo;articular pain&rsquo; (<I>P</I> = 0.023) of the Rheumatoid Arthritis Disease Activity Index (RADAI).</p>
<p><b>Conclusions.</b> Both i.v. and s.c. treatments were well accepted by patients. However, treatment choice has to be discussed with patients, as individual preference seems to be determined by personal attitudes towards safety and convenience, by past experience and by the perception of current disease status.</p>
]]></description>
<dc:creator><![CDATA[Scarpato, S., Antivalle, M., Favalli, E. G., Nacci, F., Frigelli, S., Bartoli, F., Bazzichi, L., Minisola, G., Matucci Cerinic, M., RIVIERA co-authors]]></dc:creator>
<dc:date>Tue, 17 Nov 2009 07:58:13 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep354</dc:identifier>
<dc:title><![CDATA[Patient preferences in the choice of anti-TNF therapies in rheumatoid arthritis. Results from a questionnaire survey (RIVIERA study)]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-17</prism:publicationDate>
<prism:section>Concise Report</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep348v1?rss=1">
<title><![CDATA[Evaluation of the CASPAR criteria for psoriatic arthritis in the Chinese population]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep348v1?rss=1</link>
<description><![CDATA[
<p><b>Objective.</b> To evaluate and validate the Classification of Psoriatic Arthritis (CASPAR) criteria for PsA in a Chinese population.</p>
<p><b>Methods.</b> Data were collected prospectively from consecutive Han Chinese clinic attendees with PsA and other chronic inflammatory arthritis. Subjects were classified according to Moll and Wright, European Spondyloarthropathy Study Group (ESSG) criteria for PsA, Vasey and Espinoza or CASPAR criteria. Sensitivity and specificity of each set of criteria were compared with the expert clinical diagnosis. Latent class analysis was used to calculate accuracy of criteria and confirm validity.</p>
<p><b>Results.</b> A total of 108 (53 males and 55 females) subjects with PsA were recruited. Mean (<scp>s.d</scp>.) age and duration of illness were 48.4 (12.0) and 9.55 (7.66) years, respectively. Data were compared with 195 controls with RA (<I>n</I> = 154) and AS (<I>n</I> = 41). The ESSG criteria have the lowest sensitivity, followed by the Moll and Wright criteria. The sensitivity and specificity for the CASPAR criteria were 98.2 and 99.5%, respectively, which is similar to reported values in European populations. The latent class model agreed closely with the clinical criteria.</p>
<p><b>Conclusions.</b> The CASPAR criteria performed well in a Chinese population, which is very different from the populations for which they were developed. The CASPAR criteria have higher sensitivity in classifying PsA.</p>
]]></description>
<dc:creator><![CDATA[Leung, Y. Y., Tam, L. S., Kwok, W. H., Lau, W. M., Li, T. K.-Y., Zhu, T. Y., Kun, E. W.-L., Li, E. K.-M.]]></dc:creator>
<dc:date>Tue, 17 Nov 2009 07:58:12 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep348</dc:identifier>
<dc:title><![CDATA[Evaluation of the CASPAR criteria for psoriatic arthritis in the Chinese population]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-17</prism:publicationDate>
<prism:section>Concise Report</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep347v1?rss=1">
<title><![CDATA[Juvenile idiopathic arthritis: improved outcome requires improved access to care]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep347v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Foster, H., Rapley, T., May, C.]]></dc:creator>
<dc:date>Tue, 17 Nov 2009 07:58:09 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep347</dc:identifier>
<dc:title><![CDATA[Juvenile idiopathic arthritis: improved outcome requires improved access to care]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-17</prism:publicationDate>
<prism:section>Editorial</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep338v1?rss=1">
<title><![CDATA[New classification of the shared epitope in rheumatoid arthritis: impact on the production of various anti-citrullinated protein antibodies]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep338v1?rss=1</link>
<description><![CDATA[
<p><b>Objective.</b> HLA-DR [shared epitope (SE)] alleles have recently been re-classified into <I>S1, S2, S3P</I> and <I>S3D</I> groups. <I>S2</I> and <I>S3P</I> have been associated with increased risk for RA. We assessed the impact of <I>S1, S2, S3P</I> and <I>S3D</I> alleles on anti-citrullinated protein antibody (ACPA) production. Instead of comparing allele-carriers to non-carriers, we studied each allele group individually, using the <I>X/X</I> (non-SE) genotype as reference.</p>
<p><b>Methods.</b> Serum and genomic DNA samples of 91 RA patients and 78 healthy controls were obtained. Various ACPAs and IgM RF were determined by ELISA. HLA-DRB1 genotyping and subtyping was performed by PCR. HLA-DRB1 alleles were re-classified as described above. Correlations between SE and ACPAs were determined.</p>
<p><b>Results.</b> Not only <I>S2</I> and <I>S3P</I>, but, to a lesser extent, <I>S1</I> and <I>S3D</I> alleles also predisposed to anti-cyclic citrullinated peptide (CCP) production (<I>P</I> &lt; 0.0001, <I>P</I> = 0.004, <I>P</I> = 0.01 and <I>P</I> = 0.027, respectively), with the following hierarchy of association: <I>S2</I>+<I>S3P</I> &gt; <I>S1</I>+<I>S3D</I> &gt; <I>X/X</I>. Similar associations were observed for anti-citrullinated vimentin. Anti-citrullinated fibrinogen (CF) exerted a different association pattern with the strongest correlation with <I>S1</I> alleles [odds ratio (OR) 16.00; <I>P</I> = 0.05]. In addition, HLA-DRB1*15 alleles may represent a special predisposing effect for anti-CF antibody production. Finally, in this study, RF production was associated only with the HLA-DRB1*0401 SE allele (<I>P</I> = 0.04).</p>
<p><b>Conclusions.</b> Our approach of comparing individual S allele carriers with <I>X/X</I> genotype patients allowed us to perform unequivocal analyses and demonstrate new associations. Thus, novel subgroups of RA could be identified with potential relevance for prognosis and therapy.</p>
]]></description>
<dc:creator><![CDATA[Gyetvai, A., Szekanecz, Z., Soos, L., Szabo, Z., Fekete, A., Kapitany, A., Teodorescu, M., Sipka, S., Szegedi, G., Lakos, G.]]></dc:creator>
<dc:date>Tue, 17 Nov 2009 07:58:03 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep338</dc:identifier>
<dc:title><![CDATA[New classification of the shared epitope in rheumatoid arthritis: impact on the production of various anti-citrullinated protein antibodies]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-17</prism:publicationDate>
<prism:section>Original Article</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep333v1?rss=1">
<title><![CDATA[An open-source, self-explanatory touch screen in routine care. Validity of filling in the Bath measures on Ankylosing Spondylitis Disease Activity Index, Function Index, the Health Assessment Questionnaire and Visual Analogue Scales in comparison with paper versions]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep333v1?rss=1</link>
<description><![CDATA[
<p><b>Objective.</b> The Danish DANBIO registry has developed open-source software for touch screens in the waiting room. The objective was to assess the validity of outcomes from self-explanatory patient questionnaires on touch screen in comparison with the traditional paper form in routine clinical care.</p>
<p><b>Methods.</b> Fifty-two AS patients and 59 RA patients completed Visual Analogue Scales (VASs) for pain, fatigue and global health, and Bath measures on Ankylosing Spondylitis Disease Activity Index (BASDAI) and Function Index (BASFI) (AS patients) or HAQs (RA patients) on touch screen and paper form in random order with a 1-h interval. Intra-class correlation coefficients (ICCs), 95% CIs and smallest detectable differences (SDDs) were calculated.</p>
<p><b>Results.</b> ICC ranged from 0.922 to 0.988 (<I>P</I> &lt; 0.001). The mean differences (95% CI) were: BASDAI [&ndash;0.5 (&ndash;14.5, 13.5) mm]; BASFI [&ndash;1.1 (&ndash;10.6, 8.4) mm]; Item 5 [&ndash;1.7 (&ndash;23.6, 20.2) mm] and Item 6 [&ndash;0.7 (&ndash;14.7, 13.3) mm] from BASDAI; HAQ score [0.023 (&ndash;0.183, 0.229)]. For VAS &ndash;0.4 to &ndash;2.8 mm (no significance for all except VAS global and VAS fatigue in RA). SDD for BASDAI was 14.0 mm; BASFI 9.5 mm; Item 5 21.8 mm; Item 6 14.0 mm; HAQ 0.206; VAS 11.1&ndash;18.8 mm.</p>
<p><b>Conclusions.</b> Self-explanatory touch screens based on the DANBIO open-source system generates valid results in AS and RA patients on completion of BASDAI, BASFI, HAQ and VAS scores for pain, fatigue and global health when compared with the traditional paper form. Implementation of touch screens in clinical practice is feasible and patients need no instruction.</p>
]]></description>
<dc:creator><![CDATA[Schefte, D. B., Hetland, M. L.]]></dc:creator>
<dc:date>Tue, 17 Nov 2009 07:58:00 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep333</dc:identifier>
<dc:title><![CDATA[An open-source, self-explanatory touch screen in routine care. Validity of filling in the Bath measures on Ankylosing Spondylitis Disease Activity Index, Function Index, the Health Assessment Questionnaire and Visual Analogue Scales in comparison with paper versions]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-17</prism:publicationDate>
<prism:section>Original Article</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep332v1?rss=1">
<title><![CDATA[Prescription and comorbidity screening following consultation for acute gout in primary care]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep332v1?rss=1</link>
<description><![CDATA[
<p><b>Objective.</b> To describe prescribing patterns and cardiovascular risk factor screening in patients, following consultation for acute gout in primary care.</p>
<p><b>Methods.</b> This study was undertaken in two inter-linked regional primary care databases: Consultations in Primary Care Archive (CiPCA) and Prescriptions in Primary Care Archive (PiPCA). During 2001&ndash;04, consultations in CiPCA were identified at 10 participating practices from gout-related Read morbidity codes. Lipid, blood pressure, glucose and renal function monitoring were identified from Read codes and consultation free text over the next month. Prescriptions for traditional NSAIDs, gastroprotective agents, colchicine, coxibs, corticosteroids, analgesic agents and urate-lowering therapies (ULTs) issued to these patients over the subsequent 12 months were identified from PiPCA.</p>
<p><b>Results.</b> Six hundred and seventy-three new gout consultations were identified. Monitoring of lipids (5%), blood pressure (26%), glucose (6%) and renal function (21%) within 1 month of index consultation were infrequently recorded. There were 583 consultations for acute gout. Traditional NSAIDs (68%) were most commonly prescribed, followed by colchicine (15%), coxibs (5%) and analgesia only (5%). Seven per cent did not receive a prescription. The most frequently prescribed traditional NSAIDs were diclofenac (41%) and indomethacin (32%). Gastroprotection was co-prescribed with NSAIDs for 17% of patients. Sixty six per cent of patients treated with colchicine were prescribed high-dose regimens (500 &micro;g at least four times daily). ULTs were prescribed within 12 months in 23% of patients. Nineteen per cent of ULTs were prescribed during acute attack.</p>
<p><b>Conclusions.</b> Primary care acute gout management is suboptimal. Education of general practitioners about acute gout management and cardiovascular risk is a priority.</p>
]]></description>
<dc:creator><![CDATA[Roddy, E., Mallen, C. D., Hider, S. L., Jordan, K. P.]]></dc:creator>
<dc:date>Tue, 17 Nov 2009 07:57:57 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep332</dc:identifier>
<dc:title><![CDATA[Prescription and comorbidity screening following consultation for acute gout in primary care]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-17</prism:publicationDate>
<prism:section>Original Article</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep328v1?rss=1">
<title><![CDATA[Identification of anti-prothrombin antibodies in the anti-phospholipid syndrome that display the prothrombinase activity]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep328v1?rss=1</link>
<description><![CDATA[
<p><b>Objective.</b> Prothrombin (PT) is one of the most important antigenic targets for aPL antibodies; however, the prothrombotic mechanism of anti-PT (aPT) antibodies in APS is not fully clarified. Considering that some autoantibodies possess the enzymatic activity, the aim of this study was to test the hypothesis that some aPT antibodies in APS may display prothrombinase activity.</p>
<p><b>Methods.</b> Six APS patient-derived PT-reactive monoclonal antibodies (mAbs) were analysed for prothrombinase activity on PT. One mAb with prothrombinase activity was examined for its proteolytic activity on PT. In addition, IgG was purified from plasma samples positive with IgG aPT antibodies, and their prothrombinase activity analysed.</p>
<p><b>Results.</b> Initial analysis of six mAbs revealed that, upon incubation with PT, IS6 mAb displayed prothrombinase activity and catalysed the proteolysis of PT to fragments. Analysis of plasma samples revealed that 9/21 (42.8%) APS patients had IgG antibodies against PT, based on a cut-off value equal to mean + 3 <scp>s.d</scp>. of the level in 21 normal controls. Importantly, of those samples positive for IgG aPT antibodies, two polyclonal IgG (P1 and P2) also displayed prothrombinase activity.</p>
<p><b>Conclusions.</b> In this study, we showed that some aPT antibodies displayed prothrombinase activity. Such catalytic aPT antibodies may contribute to thrombosis in APS.</p>
]]></description>
<dc:creator><![CDATA[Yang, Y.-H., Chang, C.-J., Chuang, Y.-H., Hsu, H.-Y., Chen, P. P., Chiang, B.-L.]]></dc:creator>
<dc:date>Tue, 17 Nov 2009 07:57:54 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep328</dc:identifier>
<dc:title><![CDATA[Identification of anti-prothrombin antibodies in the anti-phospholipid syndrome that display the prothrombinase activity]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-17</prism:publicationDate>
<prism:section>Original Article</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep337v1?rss=1">
<title><![CDATA[Rheumatologists: inflammation doctors of the future!]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep337v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Nikiphorou, E., Kerrigan, N., Mills, K., Merry, P.]]></dc:creator>
<dc:date>Mon, 16 Nov 2009 06:31:53 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep337</dc:identifier>
<dc:title><![CDATA[Rheumatologists: inflammation doctors of the future!]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-16</prism:publicationDate>
<prism:section>Letter to the Editor (Other)</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep331v1?rss=1">
<title><![CDATA[A systematic comparison of combination DMARD therapy and tumour necrosis inhibitor therapy with methotrexate in patients with early rheumatoid arthritis]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep331v1?rss=1</link>
<description><![CDATA[
<p><b>Objective.</b> We examined how combination DMARD therapies and TNF inhibitors therapies plus MTX (TNF/MTX) affect clinical and radiological outcomes compared with MTX monotherapy in early RA.</p>
<p><b>Methods.</b> We systematically searched EMBASE, PubMed and Ovid Medline for randomized controlled trials (RCTs) of combination therapy in early RA. We evaluated ACR responses, withdrawals for inefficacy and toxicity, HAQ and radiographic progression. Meta-analysis using Review Manager evaluated random effects odds ratios (ORs) and random effects weighted mean differences (WMDs) between treatments.</p>
<p><b>Results.</b> A preliminary search identified 2029 citations; 15 were relevant RCTs (4200 randomized patients). Patients with active disease were enrolled. Compared with MTX monotherapy, both combination DMARDs and TNF/MTX increased ACR20&ndash;70 responses (OR 1.64&ndash;2.02 and 2.03&ndash;2.30, respectively), reduced withdrawals for inefficacy (OR 0.52 and 0.29), reduced HAQ (WMD &ndash;0.17 and &ndash;0.16) and reduced annual X-ray progression (WMD &ndash;1.20 and &ndash;0.84%). DMARD combinations increased withdrawals for toxicity (OR 2.69; there was no difference with TNF/MTX). The only head-to-head RCT showed comparable efficacy for combination DMARDs and TNF/MTX combinations.</p>
<p><b>Conclusions.</b> In early active RA, both combination DMARDs and TNF/MTX are more effective than MTX monotherapy. DMARD and TNF/MTX combinations had equal efficacy on ACR response, withdrawals for inefficacy, disability and erosive progression. There is an apparent advantage for TNF/MTX combinations in the effect on toxicity with fewer consequent patients. We conclude that there is strong evidence in favour of combination treatment for RA but there is still uncertainty about which regimen is preferable.</p>
]]></description>
<dc:creator><![CDATA[Ma, M. H. Y., Kingsley, G. H., Scott, D. L.]]></dc:creator>
<dc:date>Mon, 16 Nov 2009 06:31:52 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep331</dc:identifier>
<dc:title><![CDATA[A systematic comparison of combination DMARD therapy and tumour necrosis inhibitor therapy with methotrexate in patients with early rheumatoid arthritis]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-16</prism:publicationDate>
<prism:section>Original Article</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep303av1?rss=1">
<title><![CDATA[BSR and BHPR guidelines for the management of polymyalgia rheumatica]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep303av1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Dasgupta, B., Borg, F. A., Hassan, N., Barraclough, K., Bourke, B., Fulcher, J., Hollywood, J., Hutchings, A., Kyle, V., Nott, J., Power, M., Samanta, A., on behalf of the BSR and BHPR Standards, Guidelines and Audit Working Group]]></dc:creator>
<dc:date>Thu, 12 Nov 2009 06:31:48 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep303a</dc:identifier>
<dc:title><![CDATA[BSR and BHPR guidelines for the management of polymyalgia rheumatica]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-12</prism:publicationDate>
<prism:section>Guidelines</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep349v1?rss=1">
<title><![CDATA[Comment on: New insights into the epidemiology of gout]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep349v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[White, J. S.]]></dc:creator>
<dc:date>Wed, 11 Nov 2009 07:22:25 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep349</dc:identifier>
<dc:title><![CDATA[Comment on: New insights into the epidemiology of gout]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-11</prism:publicationDate>
<prism:section>Letter to the Editor (Matters Arising)</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep342v1?rss=1">
<title><![CDATA[Comment on: Web resources for rare auto-inflammatory diseases: towards a common patient registry: reply]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep342v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Touitou, I.]]></dc:creator>
<dc:date>Wed, 11 Nov 2009 07:22:23 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep342</dc:identifier>
<dc:title><![CDATA[Comment on: Web resources for rare auto-inflammatory diseases: towards a common patient registry: reply]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-11</prism:publicationDate>
<prism:section>Letter to the Editor (Matters Arising)</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep325v1?rss=1">
<title><![CDATA[Initiation of rheumatoid arthritis treatments and the risk of serious infections]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep325v1?rss=1</link>
<description><![CDATA[
<p><b>Objective.</b> In clinical trials of RA patients on traditional DMARDs, the addition of TNF- antagonists increased infections compared with addition of placebo. Our objective was to compare serious infections following initiation of different RA regimens. Prior comparative studies of DMARD initiation have yielded conflicting results.</p>
<p><b>Methods.</b> We estimated hospitalization rates for infections following initiation of TNF- antagonists, other DMARDs and oral glucocorticoids in Tennessee Medicaid-enrolled RA patients (1995&ndash;2005). Exposure time was measured using pharmacy information and infections were identified using validated definitions. Initiation of RA regimens was compared using Cox regression models with MTX as the reference. Sensitivity analyses excluded glucocorticoid users, applied a first exposure carried forward approach, restricted observations to 2002&ndash;05 and first episodes of use and explored effects of unmeasured confounders.</p>
<p><b>Results.</b> We identified 28 906 new episodes of medication use, including TNF- antagonists (8%), MTX alone (15%) and glucocorticoids alone (57%). Compared with MTX initiation, TNF- antagonist initiation did not significantly increase the risk of hospitalizations for pneumonia [adjusted hazard ratio (aHR) 1.61; 95% CI 0.85, 3.03] or any infection (aHR 1.31; 95% CI 0.78, 2.19). Initiation of LEF, SSZ or HCQ did not increase serious infections, compared with MTX. Both initiation and concurrent glucocorticoid use were associated with a dose-dependent increase in serious infections. Sensitivity analyses showed consistent results.</p>
<p><b>Conclusions.</b> Compared with initiation of MTX alone, initiation of TNF- antagonists was not associated with a large increase in the risk of serious infections. Glucocorticoid use was associated with a dose-dependent increase in the risk of these infections.</p>
]]></description>
<dc:creator><![CDATA[Grijalva, C. G., Kaltenbach, L., Arbogast, P. G., Mitchel, E. F., Griffin, M. R.]]></dc:creator>
<dc:date>Wed, 11 Nov 2009 07:22:22 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep325</dc:identifier>
<dc:title><![CDATA[Initiation of rheumatoid arthritis treatments and the risk of serious infections]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-11</prism:publicationDate>
<prism:section>Original Article</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep341v1?rss=1">
<title><![CDATA[Comment on: Web resources for rare auto-inflammatory diseases: towards a common patient registry]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep341v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Yazici, Y., Yazici, H.]]></dc:creator>
<dc:date>Tue, 10 Nov 2009 05:01:34 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep341</dc:identifier>
<dc:title><![CDATA[Comment on: Web resources for rare auto-inflammatory diseases: towards a common patient registry]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-10</prism:publicationDate>
<prism:section>Letter to the Editor (Matters Arising)</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep353v1?rss=1">
<title><![CDATA[Ability of FRAX/NOGG guidelines to identify patients sustaining low trauma fractures]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep353v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bridges, M. J., Ruddick, S.]]></dc:creator>
<dc:date>Mon, 09 Nov 2009 03:39:18 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep353</dc:identifier>
<dc:title><![CDATA[Ability of FRAX/NOGG guidelines to identify patients sustaining low trauma fractures]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-09</prism:publicationDate>
<prism:section>Letter to the Editor (Other)</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep336v1?rss=1">
<title><![CDATA[A CLINICIAN'S GUIDE TO RHEUMATIC DISEASES IN CHILDREN. Edited by Thomas Lehman.]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep336v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[McErlane, F.]]></dc:creator>
<dc:date>Fri, 06 Nov 2009 07:11:35 PST</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep336</dc:identifier>
<dc:title><![CDATA[A CLINICIAN'S GUIDE TO RHEUMATIC DISEASES IN CHILDREN. Edited by Thomas Lehman.]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-11-06</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep330v1?rss=1">
<title><![CDATA[Comment on: Hepatotoxicity rates do not differ in patients with rheumatoid arthritis and psoriasis treated with methotrexate]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep330v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Lynch, M., Kirby, B.]]></dc:creator>
<dc:date>Sun, 25 Oct 2009 23:22:48 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep330</dc:identifier>
<dc:title><![CDATA[Comment on: Hepatotoxicity rates do not differ in patients with rheumatoid arthritis and psoriasis treated with methotrexate]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-10-25</prism:publicationDate>
<prism:section>Letter to the Editor (Matters Arising)</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep265v1?rss=1">
<title><![CDATA[Fibrocyte activation in rheumatoid arthritis]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep265v1?rss=1</link>
<description><![CDATA[
<p><b>Objectives.</b> RA is a common, relapsing autoimmune disease primarily affecting the joints. Fibroblast-like synovial (FLS) cells are thought to be responsible for pannus formation and secretion of factors that recruit leucocytes to affected joints, thereby promoting bone and cartilage destruction. Fibrocytes are multipotent circulating stem cells that may have a role in RA pathogenesis, perhaps as the precursors of the FLS cells, or by regulating FLS cell function.</p>
<p><b>Methods.</b> We utilized multidimensional phospho-specific flow cytometry to characterize the activation status of peripheral blood (PB) fibrocytes derived from human RA patients at different stages of disease and from mice with CIA.</p>
<p><b>Results.</b> Human PB fibrocytes from RA patients exhibited phosporylation activation of the p44/42 and p38 MAP kinases (MAPKs), and STAT3 (signal transducer and activator of transcription) and STAT-5 early in disease, within the first year of diagnosis. Similarly, in murine CIA, an increase in the total number of PB phosphoSTAT5-positive fibrocytes was observed at early time points in disease. Notably, in the affected paws of mice with CIA, we identified an increased number of fibrocytes, in contrast to the paws of control mice.</p>
<p><b>Conclusions.</b> These data suggest that activated fibrocytes may influence the disease process in RA and may serve as surrogate markers for disease in the PB of affected patients.</p>
]]></description>
<dc:creator><![CDATA[Galligan, C. L., Siminovitch, K. A., Keystone, E. C., Bykerk, V., Perez, O. D., Fish, E. N.]]></dc:creator>
<dc:date>Sun, 25 Oct 2009 23:22:41 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep265</dc:identifier>
<dc:title><![CDATA[Fibrocyte activation in rheumatoid arthritis]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-10-25</prism:publicationDate>
<prism:section>Original Article</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep329v1?rss=1">
<title><![CDATA[Therapeutic targets in rheumatoid arthritis: the interleukin-6 receptor]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep329v1?rss=1</link>
<description><![CDATA[
<p>RA is a chronic, debilitating disease in which articular inflammation and joint destruction are accompanied by systemic manifestations including anaemia, fatigue and osteoporosis. IL-6 is expressed abundantly in the SF of RA patients and is thought to mediate many of the local and systemic effects of this disease. Unlike a number of other cytokines, IL-6 can activate cells through both membrane-bound (IL-6R) and soluble receptors (sIL-6R), thus widening the number of cell types responsive to this cytokine. Indeed, trans-signalling, where IL-6 binds to the sIL-6R, homodimerizes with glycoprotein 130 subunits and induces signal transduction, has been found to play a key role in acute and chronic inflammation. Elevated levels of IL-6 and sIL-6R in the SF of RA patients can increase the risk of joint destruction and, at the joint level, IL-6/sIL-6R can stimulate pannus development through increased VEGF expression and increase bone resorption as a result of osteoclastogenesis. Systemic effects of IL-6, albeit through conventional or trans-signalling, include regulation of acute-phase protein synthesis, as well as hepcidin production and stimulation of the hypothalamo-pituitary-adrenal axis, the latter two actions potentially leading to anaemia and fatigue, respectively. This review aims to provide an insight into the biological effects of IL-6 in RA, examining how IL-6 can induce the articular and systemic effects of this disease.</p>
]]></description>
<dc:creator><![CDATA[Dayer, J.-M., Choy, E.]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 06:58:58 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep329</dc:identifier>
<dc:title><![CDATA[Therapeutic targets in rheumatoid arthritis: the interleukin-6 receptor]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-10-23</prism:publicationDate>
<prism:section>Review</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep315v1?rss=1">
<title><![CDATA[A case of early-onset sarcoidosis with a six-base deletion in the NOD2 gene]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep315v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Sakai, H., Ito, S., Nishikomori, R., Takaoka, Y., Kawai, T., Saito, M., Okafuji, I., Yasumi, T., Heike, T., Nakahata, T.]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 06:58:56 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep315</dc:identifier>
<dc:title><![CDATA[A case of early-onset sarcoidosis with a six-base deletion in the NOD2 gene]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-10-23</prism:publicationDate>
<prism:section>Letter to the Editor (Case Report)</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep323v1?rss=1">
<title><![CDATA[Comment on: Hepatotoxicity rates do not differ in patients with rheumatoid arthritis and psoriasis treated with methotrexate: reply]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep323v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Amital, H., Arnson, Y., Chodick, G., Shalev, V.]]></dc:creator>
<dc:date>Wed, 14 Oct 2009 05:34:51 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep323</dc:identifier>
<dc:title><![CDATA[Comment on: Hepatotoxicity rates do not differ in patients with rheumatoid arthritis and psoriasis treated with methotrexate: reply]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-10-14</prism:publicationDate>
<prism:section>Letter to the Editor (Matters Arising)</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep319v1?rss=1">
<title><![CDATA[Access to training in musculoskeletal ultrasound: a survey of UK rheumatology trainees]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep319v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Garrood, T., Platt, P.]]></dc:creator>
<dc:date>Wed, 07 Oct 2009 07:10:21 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep319</dc:identifier>
<dc:title><![CDATA[Access to training in musculoskeletal ultrasound: a survey of UK rheumatology trainees]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-10-07</prism:publicationDate>
<prism:section>Letter to the Editor (Other)</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep306v1?rss=1">
<title><![CDATA[The modern management of gout]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep306v1?rss=1</link>
<description><![CDATA[
<p>Gout is an inflammatory arthritis characterized by self-limiting but excruciatingly painful acute attacks. These are a consequence of monosodium urate (MSU) crystals being deposited within articular or periarticular tissue. Chronic tophaceous gout can develop after years of acute intermittent gout. Recent discoveries, including the role of the inflammasome and intracellular events demonstrating that pro-inflammatory cytokines, IL-1&beta;, -8 and TNF-, promote neutrophil influx genetic advances with the identification of the URAT-1 transporter and genetic variation in SLC 2A9 as a key regulator of urate homoeostasis, have given us deeper understanding of the pathophysiology of gout, and also allow for more targeted treatments. Hopefully, new and emerging therapeutic options will reduce treatment-resistant gout in patients who are unresponsive or unable to take traditional urate lowering therapy. The development of new therapies may also increase patient numbers being treated in the specialist setting, which may have several secondary benefits.</p>
]]></description>
<dc:creator><![CDATA[Rider, T. G., Jordan, K. M.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 23:00:55 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep306</dc:identifier>
<dc:title><![CDATA[The modern management of gout]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-10-05</prism:publicationDate>
<prism:section>Review</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep311v1?rss=1">
<title><![CDATA[Rheumatoid Arthritis National Clinical Guideline]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep311v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Watts, R. A.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 04:51:50 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep311</dc:identifier>
<dc:title><![CDATA[Rheumatoid Arthritis National Clinical Guideline]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep309v1?rss=1">
<title><![CDATA[A retrospective clinical analysis of pharmacological modalities used for symptomatic relief of Raynaud's phenomenon in children treated in a UK paediatric rheumatology centre]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep309v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Gargh, K., Baildam, E. M., Cleary, G. A., Beresford, M. W., Mccann, L. J.]]></dc:creator>
<dc:date>Thu, 01 Oct 2009 04:51:48 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep309</dc:identifier>
<dc:title><![CDATA[A retrospective clinical analysis of pharmacological modalities used for symptomatic relief of Raynaud's phenomenon in children treated in a UK paediatric rheumatology centre]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:section>Letter to the Editor (Other)</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep312v1?rss=1">
<title><![CDATA[ADOLESCENT RHEUMATOLOGY. By Janet McDonagh, Patience White.]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep312v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Woo, P.]]></dc:creator>
<dc:date>Wed, 30 Sep 2009 23:02:15 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep312</dc:identifier>
<dc:title><![CDATA[ADOLESCENT RHEUMATOLOGY. By Janet McDonagh, Patience White.]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-09-30</prism:publicationDate>
<prism:section>Book Review</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep307v1?rss=1">
<title><![CDATA[The clinical importance of ultrasound detectable forefoot bursae in rheumatoid arthritis]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep307v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bowen, C. J., Culliford, D., Dewbury, K., Sampson, M., Burridge, J., Hooper, L., Edwards, C. J., Arden, N. K.]]></dc:creator>
<dc:date>Wed, 30 Sep 2009 23:02:13 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep307</dc:identifier>
<dc:title><![CDATA[The clinical importance of ultrasound detectable forefoot bursae in rheumatoid arthritis]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-09-30</prism:publicationDate>
<prism:section>Letter to the Editor (Other)</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep225v1?rss=1">
<title><![CDATA[Association of myocardial infarctions with COX-2 inhibition may be related to immunomodulation towards a Th1 response resulting in atheromatous plaque instability: an evidence-based interpretation]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep225v1?rss=1</link>
<description><![CDATA[
<p>Cyclooxygenase (COX) inhibitors remain a major class of drugs in rheumatology and their widespread use is expected to continue. The view that a prothrombotic effect explains the increase in myocardial infarction (MI) associated with both COX-2 selective and traditional NSAIDs (tNSAIDs) has been increasingly questioned. We review the evidence that prostanoids direct the immune response away from a Th1 response and that consequently inhibition of prostaglandin synthesis results in augmentation of the Th1 response by limiting prostanoid synthesis. Although the role of prostanoids as mediators of inflammation in the periphery is well understood, the systemic immunomodulatory role of prostanoids shifting the immune response away from a Th1 type is less appreciated. Atherosclerosis is an inflammatory arterial disease driven by a Th1 type immune response. Moreover, the vulnerable phenotype of atheroma is associated with the cellular Th1 immune response in contrast to the stable plaque phenotype associated with a Th2 type response. We propose a class effect of COX-2 selective and tNSAIDs, which results in augmentation of Th1-mediated atherogenesis, associated with detrimental plaque remodelling, instability, rupture and embolization resulting in MI. Understanding of the Th1 mediated immunity, which underlies the cardiovascular, and the non-Th1, which underlies gastrointestinal adverse effects associated with the use of COX inhibitors, should lead to better risk assessment and the development of anti-inflammatory treatments with improved safety. Our explanation also emphasizes the pharmacological effects and consequences of immunomodulation in the inflammation associated with atherosclerosis and other Th1- as well as non-Th1-driven diseases.</p>
]]></description>
<dc:creator><![CDATA[Padol, I. T., Hunt, R. H.]]></dc:creator>
<dc:date>Thu, 24 Sep 2009 07:53:01 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep225</dc:identifier>
<dc:title><![CDATA[Association of myocardial infarctions with COX-2 inhibition may be related to immunomodulation towards a Th1 response resulting in atheromatous plaque instability: an evidence-based interpretation]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-09-24</prism:publicationDate>
<prism:section>Review</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep299v1?rss=1">
<title><![CDATA[Comment on: Clinical utility of ANA measured by ELISA compared with ANA measured by immunofluorescence]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep299v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Skogh, T., Dahle, C.]]></dc:creator>
<dc:date>Wed, 23 Sep 2009 08:40:04 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep299</dc:identifier>
<dc:title><![CDATA[Comment on: Clinical utility of ANA measured by ELISA compared with ANA measured by immunofluorescence]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-09-23</prism:publicationDate>
<prism:section>Letter to the Editor (Matters Arising)</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep298v1?rss=1">
<title><![CDATA[Hip involvement in ankylosing spondylitis: what is the verdict?]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep298v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Baraliakos, X., Braun, J.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 08:16:53 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep298</dc:identifier>
<dc:title><![CDATA[Hip involvement in ankylosing spondylitis: what is the verdict?]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-09-15</prism:publicationDate>
<prism:section>Editorial</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep093v2?rss=1">
<title><![CDATA[Experience with rituximab in scleroderma: results from a 1-year, proof-of-principle study]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep093v2?rss=1</link>
<description><![CDATA[
<p><b>Objective.</b> To assess the efficacy of rituximab (RTX) in SSc.</p>
<p><b>Methods.</b> Fourteen patients with SSc were evaluated. Eight patients were randomized to receive two cycles of RTX at baseline and 24 weeks [each cycle consisted of four weekly RTX infusions (375 mg/m<sup>2</sup>)] in addition to standard treatment, whereas six patients (control group) received standard treatment alone. Lung involvement was assessed by pulmonary function tests (PFTs) and chest high-resolution CT (HRCT). Skin involvement was assessed both clinically and histologically.</p>
<p><b>Results.</b> There was a significant increase of forced vital capacity (FVC) in the RTX group compared with baseline (mean &plusmn; <scp>s.d</scp>.: 68.13 &plusmn; 19.69 <I>vs</I> 75.63 &plusmn; 19.73, at baseline <I>vs</I> 1-year, respectively, <I>P =</I> 0.0018). The median percentage of improvement of FVC in the RTX group was 10.25%, whereas that of deterioration in the controls was 5.04% (<I>P</I> = 0.002). Similarly, diffusing capacity of carbon monoxide (DL<SUB>CO</SUB>) increased significantly in the RTX group compared with baseline (mean &plusmn; <scp>s.d</scp>.: 52.25 &plusmn; 20.71 <I>vs</I> 62 &plusmn; 23.21, at baseline <I>vs</I> 1-year respectively, <I>P</I> = 0.017). The median percentage of improvement of DL<SUB>CO</SUB> in the RTX group was 19.46%, whereas that of deterioration in the control group was 7.5% (<I>P</I> = 0.023). Skin thickening, assessed with the Modified Rodnan Skin Score (MRSS), improved significantly in the RTX group compared with the baseline score (mean &plusmn; <scp>s.d</scp>.: 13.5 &plusmn; 6.84 <I>vs</I> 8.37 &plusmn; 6.45 at baseline <I>vs</I> 1-year, respectively, <I>P</I> &lt; 0.001).</p>
<p><b>Conclusion.</b> Our results indicate that RTX may improve lung function in patients with SSc. To confirm our encouraging results we propose that larger scale, multicentre studies with longer evaluation periods are needed.</p>
]]></description>
<dc:creator><![CDATA[Daoussis, D., Liossis, S.-N. C., Tsamandas, A. C., Kalogeropoulou, C., Kazantzi, A., Sirinian, C., Karampetsou, M., Yiannopoulos, G., Andonopoulos, A. P.]]></dc:creator>
<dc:date>Tue, 15 Sep 2009 08:16:47 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep093</dc:identifier>
<dc:title><![CDATA[Experience with rituximab in scleroderma: results from a 1-year, proof-of-principle study]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-09-15</prism:publicationDate>
<prism:section>Original Article</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep281v1?rss=1">
<title><![CDATA[Fast microvascular remodelling in a patient with cancer-associated dermatomyositis: capillaroscopic follow-up]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep281v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[De Angelis, R., Bertolazzi, C., Filippucci, E., Gutierrez, M., Grassi, W.]]></dc:creator>
<dc:date>Wed, 09 Sep 2009 06:30:00 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep281</dc:identifier>
<dc:title><![CDATA[Fast microvascular remodelling in a patient with cancer-associated dermatomyositis: capillaroscopic follow-up]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-09-09</prism:publicationDate>
<prism:section>Clinical Vignette</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep267v1?rss=1">
<title><![CDATA[Intramedullary tuberculoma during infliximab therapy]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep267v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Ottaviani, S., Meyer, O., Dieude, P.]]></dc:creator>
<dc:date>Fri, 04 Sep 2009 07:52:07 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep267</dc:identifier>
<dc:title><![CDATA[Intramedullary tuberculoma during infliximab therapy]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-09-04</prism:publicationDate>
<prism:section>Clinical Vignette</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kep174v1?rss=1">
<title><![CDATA[Hip involvement in ankylosing spondylitis: epidemiology and risk factors associated with hip replacement surgery]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kep174v1?rss=1</link>
<description><![CDATA[
<p><b>Objectives.</b> Although clinicians recognize hip involvement, which frequently leads to hip replacement surgery, as an important feature of AS, data on the epidemiology, nature of the disease and therapeutic strategies are scarce. We aimed to describe the epidemiology of clinical and radiological hip involvement and define the risk factors for the hip replacement surgery in AS patients.</p>
<p><b>Methods.</b> Data from 3 datasets were merged, including 847 Belgian (ASPECT database), 1405 Spanish (REGISPONSER database) and 466 Ibero-American (RESPONDIA database) AS patients. The ASPECT and REGISPONSER database (Dataset A) are used for exploratory analysis; the RESPONDIA database (Dataset B) is used for confirmative analysis. Factors associated with hip involvement and the hip replacement surgery were analysed.</p>
<p><b>Results.</b> Twenty four (REGISPONSER) to 36% (RESPONDIA) of AS patients under rheumatologist's care presented clinical hip involvement, including the 5% (Dataset A) of AS patients who needed hip replacement surgery. Patients with hip involvement had significantly worse overall Bath Ankylosing Spondylitis Functional Index (BASFI) scores compared with patients without hip involvement (mean difference = 1.6, <I>P</I> &lt; 0.001) (Dataset A, confirmed in B). Corrected for disease duration, patients with early disease onset, enthesial and axial disease needed most frequently hip replacement surgery (Dataset A, confirmed in B).</p>
<p><b>Conclusion.</b> Hip involvement is commonly recognized by rheumatologists in AS patients, and involves about one out of the three to four patients with AS and is associated with impaired functioning reflected by higher overall BASFI scores. Early onset of disease, axial and enthesial disease are associated with the hip replacement surgery in AS.</p>
]]></description>
<dc:creator><![CDATA[Vander Cruyssen, B., Munoz-Gomariz, E., Font, P., Mulero, J., de Vlam, K., Boonen, A., Vazquez-Mellado, J., Flores, D., Vastesaeger, N., Collantes, E., on behalf of the ASPECT-REGISPONSER-RESPONDIA working group]]></dc:creator>
<dc:date>Tue, 14 Jul 2009 22:11:08 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kep174</dc:identifier>
<dc:title><![CDATA[Hip involvement in ankylosing spondylitis: epidemiology and risk factors associated with hip replacement surgery]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2009-07-14</prism:publicationDate>
<prism:section>Original Article</prism:section>
</item>

<item rdf:about="http://rheumatology.oxfordjournals.org/cgi/content/short/kel215bv1?rss=1">
<title><![CDATA[British Society for Rheumatology and British Health Professionals in Rheumatology Guideline for the Management of Rheumatoid Arthritis (The first 2 years)]]></title>
<link>http://rheumatology.oxfordjournals.org/cgi/content/short/kel215bv1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Luqmani, R., Hennell, S., Estrach, C., Birrell, F., Bosworth, A., Davenport, G., Fokke, C., Goodson, N., Jeffreson, P., Lamb, E., Mohammed, R., Oliver, S., Stableford, Z., Walsh, D., Washbrook, C., Webb, F., on behalf of the British Society for Rheumatology and British Health Professionals in Rheumatology Standards, Guidelines and Audit Working Group]]></dc:creator>
<dc:date>Thu, 13 Jul 2006 22:38:36 PDT</dc:date>
<dc:identifier>info:doi/10.1093/rheumatology/kel215b</dc:identifier>
<dc:title><![CDATA[British Society for Rheumatology and British Health Professionals in Rheumatology Guideline for the Management of Rheumatoid Arthritis (The first 2 years)]]></dc:title>
<dc:publisher>British Society for Rheumatology</dc:publisher>
<prism:publicationDate>2006-07-13</prism:publicationDate>
<prism:section>Guidelines</prism:section>
</item>

</rdf:RDF>