To determine the associations between depression, cardiovascular risk factors and coronary artery calcification (CAC) in women with SLE and controls.

To study the membrane expression of endothelial protein C receptor (mEPCR) in the renal microvasculature in lupus nephritis (LN) as a potential marker of injury and/or prognostic indicator for response to therapy.

Vasculitis may be associated with infection, immunization or anti-microbial drugs. Infections are responsible for a number of different types of vasculitis. Conversely, patients with vasculitis may develop infections, which sometimes mimic relapse. The aim of this review is to summarize the various aspects of the inter-relationship between vasculitis and infection, and the physiopathological mechanisms involved, in light of our current knowledge from animal models. Currently, a causal relationship between infection and vasculitis has only been established in a few instances and many mechanisms remain hypothetical. This inter-relationship is further assessed from the point of view of clinical presentation and therapeutic options, based on case reports and prospective observational data.

Damage accrual in SLE has been previously shown to be an independent predictor of mortality. We sought to discern which SLICC Damage Index (SDI) domains are the most important predictors of survival in SLE.

To determine the first signs and symptoms, and the clinical, biological and radiological characteristics of patients with early SpA.

We examined the association between candidate single nucleotide polymorphisms (SNPs) and disease activity in RA patients on MTX.

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease, in which neuropsychiatric manifestations are a common cause of significant morbidity. The American College of Rheumatology has identified 19 distinct neuropsychiatric syndromes associated with SLE, although the 1982 American College of Rheumatology classification criteria for SLE recognize only two: seizures and psychosis. Neurocognitive impairment (NCI) is one of the most common and clinically challenging manifestations of SLE, but its pathophysiology remains poorly understood. This Review examines the epidemiology and pathophysiology of NCI in children and adolescents with SLE, as well as the diagnostic and therapeutic approaches that are available for these patients. As few published studies specifically address NCI in pediatric SLE, new directions for research are also discussed.

Psoriasis vulgaris and psoriatic arthritis (PsA) are inter-related heritable diseases. Psoriatic skin is characterized by hyperproliferative, poorly differentiated keratinocytes and severe inflammation. Psoriatic joints are characterized by highly inflamed synovia and entheses with focal erosions of cartilage and bone. Genetic analyses have uncovered risk factors shared by both psoriasis and PsA. Predisposition to psoriasis and PsA arising from common variation is most strongly conferred by the HLA class I region. Other genetic risk factors implicate the interleukin (IL)-23 pathway and the induction and regulation of type 17 T-helper cells in the pathogenesis of both diseases. Secretion of cytokines, such as IL-22 and IL-17, could result in the hyperproliferative phenotype of keratinocytes and potentially synoviocytes, leading to a vicious cycle of cellular proliferation and inflammation in both the skin and joints. In synovial tissue, disease-related cytokines could also promote osteoclast formation, resulting in bone erosion. The next step will be to identify genetic risk factors specifically associated with PsA. Although therapies that target tumor necrosis factor are often highly successful in the treatment of both diseases, genetic findings are likely to lead to the development of treatments tailored to an individual's genetic profile.

This longitudinal study investigated survival, risk factors and causes of death in the multicentre ItinérAIR-Sclérodermie cohort of patients with SSc without severe pulmonary fibrosis or severe left heart disease at baseline.

Complement activation products contribute to a large number of inflammatory diseases, including RA. We have investigated whether osteoprotegerin (OPG) may concur with the soluble terminal complement complex (SC5b-9) to the inflammatory cascade characterizing RA.

Human endogenous uveitis is one of the sight-threatening diseases associated with variety of systemic disorders, such as Behcet's disease and sarcoidosis. Recently, biosynthesized antibodies against inflammatory cytokines have been recognized to be useful to control the regional inflammation. In this study, we focused on the possibility of IL-6-based biological therapies for endogenous uveitis. We initially confirmed the significant increase of several inflammatory soluble factors including IL-6 in the vitreous fluids from refractory/chronic engogenous uveitis patients.

Using prospectively collected registry data to investigate sick leave (sickness benefit and sickness compensation) over a 7-yr period in patients with AS in comparison with population-based controls matched for age, sex and residential area.

To identify whether a shared genetic influence accounts for the occurrence of OA at different skeletal sites.

To study health care utilization in veterans with SpAs.

RA is a systemic inflammatory arthritis that leads to local and systemic bone loss. Osteoporosis or the systemic bone loss associated with RA increases the risk for fragility fractures, which can affect quality of life dramatically in RA patients. Although traditional and RA-related risk factors have been defined and studied for osteoporosis associated with RA, genetic factors such as polymorphic variants in the traditional candidate genes for osteoporosis, such as the vitamin D receptor (VDR), type 1 collagen A1 (COLIA1) and oestrogen receptor-alpha (ESR1), have not been well elucidated in RA patients. This review summarizes the currently available literature on the association of VDR polymorphisms with local and systemic bone loss in RA. It also discusses potential targets for genetic research in this area, such as polymorphisms in genes, such as IL-6 (IL6) and TNF receptor type 2 (TNFRSF1B), which control the inflammatory response in RA and may influence bone loss in RA. Defining such genetic factors, in addition to traditional and RA-related risk factors for osteoporosis in RA, may facilitate early identification of patients at high risk for fractures who can then be targeted for treatment.

To compare patient self-report of knee flexion, extension, range of motion (ROM) and American Knee Society (AKS) Pain, Knee and Functional scores with a clinician assessment.

To examine the frequency and correlates of fatigue and its impact on physical and social functioning in patients with scleroderma, and to investigate whether fatigue mediates an association between pain and physical function.

Loss of articular cartilage caused by extracellular matrix breakdown is the hallmark of arthritis. Degradative fragments of cartilage oligomeric matrix protein (COMP) have been observed in arthritic patients. ADAMTS-7 and ADAMTS-12, two members of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family, have been associated with COMP degradation in vitro, and are significantly overexpressed in the cartilage and synovium of patients with rheumatoid arthritis. Recent studies have demonstrated the importance of COMP degradation by ADAMTS-7 and ADAMTS-12. Specifically, the size of COMP fragments generated by ADAMTS-7 or ADAMTS-12 is similar to that of COMP-degradative fragments seen in arthritic patients. In addition, antibodies against ADAMTS-7 or ADAMTS-12 dramatically inhibit tumor necrosis factor-induced and interleukin-1beta-induced COMP degradation in cartilage explants. Furthermore, suppression of ADAMTS-7 or ADAMTS-12 expression using the small interfering RNA silencing approach in human chondrocytes markedly prevents COMP degradation. COMP degradation mediated by ADAMTS-7 and ADAMTS-12 is inhibited by alpha(2)-macroglobulin. More significantly, granulin-epithelin precursor, a newly characterized chondrogenic growth factor, disturbs the interaction between COMP and ADAMTS-7 and ADAMTS-12, preventing COMP degradation by these enzymes. This Review summarizes the evidence demonstrating that ADAMTS-7 and ADAMTS-12 are newly identified enzymes responsible for COMP degradation in arthritis, and that alpha(2)-macroglobulin and granulin-epithelin precursor represent their endogenous inhibitors.