In some chronic conditions, patient-specific tools with individualized items have proved to be more sensitive outcome instruments than fixed-item tools; their use has not yet been investigated in chronic low back pain (cLBP).

Thrombosis is an important cause of morbidity and mortality in SLE. We have explored the factors associated with time to the occurrence of thrombotic events in SLE patients to expand our cohort's previous observations.

The purpose of this study was to examine prevalence trends of serious extra-articular manifestations (EAMs) in a data set representing both hospitalized and ambulatory patients with RA.

The discovery of regulatory T cells almost 15 years ago initiated a new and exciting research area. The growing evidence for a critical role of these cells in controlling autoimmune responses has raised expectations for therapeutic application of regulatory T cells in patients with autoimmune arthritis. Here, we review recent studies investigating the presence, phenotype and function of these cells in patients with RA and juvenile idiopathic arthritis (JIA) and consider their therapeutic potential. Both direct and indirect methods to target these cells will be discussed. Arguably, a therapeutic approach that combines multiple regulatory T-cell-enhancing strategies could be most successful for clinical application.

To evaluate the efficacy and safety of three dosing and repeat treatment regimens of rituximab (RTX) plus MTX in patients with active RA.

T cells contribute to the initiation and perpetuation of autoimmunity in systemic lupus erythematosus (SLE), and seem to be directly involved in the development of related organ pathology. Defects associated with CD8(+) and T-regulatory (T(REG)) cell function manifest in parallel with the expanded CD3(+)CD4(-)CD8(-) T cell lineage. The cytokine expression pattern is uniquely characterized by decreased expression of interleukin (IL)-2 and increased production of IL-17 and related cytokines. Therapeutic approaches that limit the cognate interaction between T cells and B cells, prevent inappropriate tissue homing and restore T(REG) cell function and the normal cytokine milieu have been entertained. Biochemical characterization of SLE T cells has revealed distinct early and late signaling aberrations, and has enabled the identification of novel molecular targets that can be corrected with small molecules, and biomarkers that may foretell disease activity and predict organ damage.

To describe working status in patients with RA, AS and PsA treated with anti-TNF therapy registered with the British Society for Rheumatology Biologics Register.

Although NSAIDs have a well-established place for certain indications in the management of OA and RA, they are associated with significant gastrointestinal (GI) toxicity. The risk of NSAID-related upper GI events, such as dyspepsia or peptic ulcer and complications such as perforation or bleeding, is well characterized. Non-selective NSAIDs increase the risk of peptic ulcer disease approximately 5-fold, and that of upper GI bleeding 4-fold, whereas selective cyclo-oxygenase-2 (COX) inhibitors are associated with a significantly lower GI toxicity than non-selective agents. There is evidence that, while the incidence of NSAID-related upper GI complications has decreased in recent years, that of lower GI complications is increasing. Observational studies and analyses from studies, primarily designed to investigate upper GI events, suggest that lower GI complications are relatively common in NSAID users and that COX-2 selective inhibitors are associated with a lower risk of these events. Such events have been poorly characterized, but are associated with significant mortality; indeed, they may have even more serious consequences than the better characterized upper GI events. There is thus a strong case for evaluating the impact of such complications in prospective outcome studies. To facilitate such studies a new endpoint, Clinically Significant Upper or Lower GI Events, has been introduced that captures both upper and lower GI events.

For the family physician, NSAIDs, both traditional and cyclo-oxygenase-2 inhibitors, are a valuable contribution to managing arthritis and other rheumatological conditions in primary care. Yet, many of the patients seen by the family doctor have complex comorbidities and polypharmacy issues. This review looks at the main considerations for primary-care physicians while choosing an anti-inflammatory treatment for a hypothetical patient case study. In addition to looking at the evidence for gastrointestinal and cardiovascular risk, the concomitant use of aspirin with an NSAID is also examined. New evidence for interaction between selective serotonin re-uptake inhibitors is reviewed and the interaction between angiotensin-converting enzyme inhibitors and NSAIDs is considered. Making careful judgements based on individual needs, medical history and comorbidities is recommended based on the evidence reviewed.

There is a range of pharmacological options available to the rheumatologist for treating arthritis. Non-selective NSAIDs or Cox-2 selective inhibitors are widely prescribed to reduce inflammation and alleviate pain; however, they must be used with caution in individuals with an increased cardiovascular, renal or gastrointestinal (GI) risk. The potential cardiovascular risks of Cox-2 selective inhibitors came to light over a decade ago. The conflicting nature of the study data reflects some context dependency, but the evidence shows a varying degree of cardiovascular risk with both Cox-2 selective inhibitors and non-selective NSAIDs. This risk appears to be dose dependent, which may have important ramifications for arthritis patients who require long-term treatment with high doses of anti-inflammatory drugs. The renal effects of non-selective NSAIDs have been well characterized. An increased risk of adverse renal events was found with rofecoxib but not celecoxib, suggesting that this is not a class effect of Cox-2 selective inhibitors. Upper GI effects of non-selective NSAID treatment, ranging from abdominal pain to ulceration and bleeding are extensively documented. Concomitant prescription of a proton pump inhibitor can help in the upper GI tract, but probably not in the lower. Evidence suggests that Cox-2 selective inhibitors are better tolerated in the entire GI tract. More evidence is required, and a composite end-point is being evaluated. Appropriate treatment strategies are needed depending on the level of upper and lower GI risk. Rheumatologists must be vigilant in assessing benefit-risk when prescribing a Cox-2 selective inhibitor or non-selective NSAID and should choose appropriate agents for each individual patient.

Foot and ankle problems are highly prevalent in the general population; however, little is known about the characteristics of those seeking medical assessment for these problems. The objective of this study was to explore the extent and types of musculoskeletal foot and ankle problems in primary care.

To describe quality of life (QoL) in an ANCA-associated vasculitis (AAV) cohort and make comparisons with a general population sample. In addition, we aimed to take preliminary steps to identify potential disease and psycho-social factors which may determine QoL impairment.

Recently, a non-synonymous (Gly307Ser) variant, rs763361, in the CD226 gene was shown to be associated with multiple autoimmune diseases (ADs) in European Caucasian populations. However, shared autoimmunity with CD226 has not been evaluated in non-European populations. The aim of the present study is to assess the association of this single nucleotide polymorphism (SNP) with ADs in non-European populations.

EF is a rare fibrosing disorder that may involve skin and internal organs. Current therapies include moderate- to high-dose glucocorticoids with or without use of immunosuppressives.

To evaluate, by musculoskeletal ultrasound (MSUS), articular involvement in primary SS (pSS) patients by analysing hand and wrist changes, and to correlate them with clinical evaluation and laboratory tests.

Recent whole-genome and candidate gene association studies in RA have identified a number of single nucleotide polymorphisms (SNPs) that predispose to disease with moderate risk. It remains poorly understood how recently identified genetic factors may contribute to RA severity. We therefore sought to investigate the role of recently identified RA susceptibility SNP markers in predicting erosive outcome in patients with recent-onset inflammatory polyarthritis (IP).

To obtain an objective, unbiased assessment of skin fibrosis in patients with SSc for use in clinical trials of SSc disease-modifying therapeutics.