Increased Cardiovascular Risk in Psoriatic Arthritis: Results From a Case-Control Monocentric Study.

Background: Psoriatic arthritis (PsA) is associated with increased cardiovascular morbidity and mortality. The aims of our real-life study were to compare the prevalence of cardiovascular risk factors (CVRFs) and cardiovascular events (CVEs) among patients with PsA with a control population, to evaluate the impact of correcting factors in equations that assess cardiovascular risk (CVR) in PsA, and to determine the percentage of patients who reach the LDLc target as indicated by the European guidelines. Methods: In this observational cross-sectional monocentric case-control study, we used a standardized procedure to systematically assess patients with PsA aged 25-85 years who met the Classification for Psoriatic Arthritis (CASPAR) criteria. Controls were extracted from the MOnitoring NAtionaL du rISque Artériel (MONALISA) study. We compared the prevalence of CVRFs, CVEs, the CVR, and the percentage of patients reaching recommended LDLc target in both populations. The CVR was first assessed using SCORE and QRISK2 equations. Then, the SCORE equation was corrected by applying a 1.5 multiplication factor, as recommended by EULAR for rheumatoid arthritis (SCORE-PsA), and the QRISK2 was corrected using the "rheumatoid arthritis" item (QRISK2-PsA). Results: A total of 207 PsA and 414 controls were included. CVRFs and CVEs were more frequent in the PsA group. After controlling for age and gender, atherothrombotic disease was increased in the PsA population (SCORE p = 0.002, QRISK2 p = 0.001). Using the SCORE-PsA increased the percentage of patients with a high or very high CVR from 39.3 to 45.3% in the PsA group. Similarly, using the QRISK2-PsA increased the percentage of patients with a CVR ≥ 10% from 44.9 to 53.2%. The percentages of patients with PsA with high LDLc in the high and very high CVR groups were not significantly different from controls, despite a trend in favor of patients with PsA. Of the 83 PsA with a QRISK2 ≥ 10%, only 22.9% were treated with statin vs. 35.8% of the 134 controls. The QRISK2-PsA score did not alter these results. Conclusion: In real-life, patients with PsA have a higher prevalence of CVRFs, as well as a higher prevalence of CVEs compared to the general population. The CVR is higher in the PsA population than in the controls either using the SCORE and QRISK2 equations or using the corrected SCORE- PsA and QRISK2-PsA equations.

Link between traditional cardiovascular risk factors and inflammation in patients with early arthritis: results from a French multicenter cohort.

OBJECTIVE: To compare the characteristics of traditional cardiovascular risk factors for untreated patients with early arthritis (EA) and healthy subjects, and to look for a link between cardiovascular risk factors and inflammation in EA patients. METHODS: This multicenter case-control study enrolled 607 patients with EA (ESPOIR cohort) and 1,821 age- and sex-matched controls (World Health Organization MONICA survey). Lipid levels, blood pressure, glucose levels, and exposure to smoking were characterized in patients and controls. Systemic inflammation was quantified in EA patients. Traditional cardiovascular risk factor characteristics were compared between patients with EA and controls. The link between cardiovascular risk factors and inflammation was assessed in EA patients. RESULTS: Mean ± SEM total cholesterol (2.14 ± 0.022 versus 2.34 ± 0.017 gm/liter; P < 0.001), high-density lipoprotein (HDL) cholesterol (0.60 ± 0.011 versus 0.63 ± 0.007 gm/liter; P = 0.020), and low-density lipoprotein (LDL) cholesterol (1.28 ± 0.025 versus 1.51 ± 0.016 gm/liter; P < 0.001) were lower in EA patients than in controls. Triglycerides, triglycerides/HDL ratio, and pulse pressure were higher in patients with EA. Diastolic blood pressure and glucose levels were lower in EA patients. Former or current smokers were more frequent in patients with EA. Total and HDL cholesterol levels were negatively associated with C-reactive protein or serum interleukin-6 levels. CONCLUSION: Total, HDL, and LDL cholesterol, triglycerides, diastolic blood pressure, pulse pressure, glucose, and triglycerides/HDL ratio differ between patients with EA and controls. Some of these risk factors appear to be linked to systemic inflammation. Such initial differences could modulate the risk of cardiovascular events later in the course of arthritis.

Maintenance of cytomegalovirus-specific CD4pos T-cell response in rheumatoid arthritis patients receiving anti-tumor necrosis factor treatments.

INTRODUCTION: Anti-tumor necrosis factor (TNF)-α biotherapies have considerably changed the treatment of rheumatoid arthritis (RA). However, serious infections are a major concern in patients with rheumatic diseases treated with anti-TNF-α. Little is known about viral, especially latent, infections in anti-TNF-α treatments. Infections by cytomegalovirus (CMV), a ß-herpes virus, are frequent and induce a strong CD4pos T-cell immunity, which participates in the control of infection. We thus have chosen to analyze the CD4pos T-cell response to CMV antigens as a model of antiviral response in RA patients treated with anti-TNF-α. CD28 expression was evaluated. METHODS: We have measured the CD4pos response to CMV antigens in RA patients, before and after initiation of treatment with an anti-TNF-α agent. The intracellular production of interferon (IFN)-γ in total and CD28neg CD4pos T cells in response to CMV antigens (Ags) was evaluated with flow cytometry. The proliferation of total CD4pos T cells in the presence of CMV antigens was measured with 3H-thymidine incorporation. RESULTS: Anti-TNF-α treatments impaired neither the anti-CD4pos anti-CMV IFN-γ response nor the proliferative response in patients. The percentage of CD28neg CD4pos cells remained constant. CONCLUSIONS: Our data suggest that the CD4pos T-cell response against CMV is not altered by anti-TNF-α treatments and that infection remains controlled in treated RA patients latently infected with CMV. Our observation brings new insight into the current knowledge of the risks of infection in patients treated with anti-TNF-α biotherapies.

Remitting seronegative symmetrical synovitis pitting oedema after BCG instillation.

Remitting seronegative symmetrical synovitis pitting oedema (RS3PE) is a distinct form of seronegative rheumatoid arthritis like polyarthritis. It is characterized by late onset symmetrical joint involvement and pitting oedema of hands and feet (JAMA 254(19):2763-2767, [1]). Polyarthritis secondary to intravesical Bacillus Calmette Guerin (BCG) therapy has been reported (Clin Rheumatol 21:536-537, [2]). To our knowledge, about 0.5% of patients receiving BCG instillation presented polyarthritis, but only one case of RS3PE has been reported (J Rheumatol 28:1699-1701, [3]). We described the second case of RS3PE following intravesical BCG instillation of bladder carcinoma.

Tumor necrosis factor receptor II gene polymorphism and severity of rheumatoid arthritis.

OBJECTIVE: The gene encoding tumor necrosis factor receptor type II (TNFRII) is a strong candidate in the pathogenesis of rheumatoid arthritis (RA). An association between a single-nucleotide polymorphism (196M/R) in exon 6 of the TNFRII gene and familial RA was recently reported. The present study was undertaken to test the hypothesis that there is an association between this polymorphism and the severity of RA. METHODS: One hundred two white patients with early RA were included in this prospective study. The French version of the Health Assessment Questionnaire (F-HAQ) and a radiographic damage score (modified Sharp/van der Heijde method) were used to quantify the functional and structural severity of RA at baseline and after 4 years of followup. TNFRII 196M/R polymorphism genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism analysis. RESULTS: Among the 102 patients with RA, 63 (61.8%) were homozygous for the 196M allele, 36 (35.3%) were heterozygous for alleles 196M and 196R, and 3 (2.9%) were homozygous for the 196R allele. At baseline, the median radiographic and F-HAQ scores did not differ between RA patients who carried the 196R allele and those who did not. After 4 years of followup, the F-HAQ score was higher in RA patients carrying the 196R allele (median 1 [interquartile range (IQR) 0.125, 1.375]) than in noncarriers (0.375 [IQR 0, 1]) (P = 0.02), while the median radiographic score did not differ between RA patients who carried the 196R allele and those who did not. CONCLUSION: The results of the present study support the hypothesis that there is an association between the TNFRII 196 M/R gene polymorphism and the functional severity of early RA.

The therapeutic approach to osteoarthritis.

Ideally, treatment is based on etiology, if possible on pathophysiology, and in practice on anatomical and clinical findings. A systematic search for the etiological factors of osteoarthritis (OA) shows that the various mechanisms are frequently associated. Etiological treatments are rare. We may mention acetabular tectoplasty in hip dysplasia with minimal joint space narrowing. Valgus osteotomy would also be indicated for early medial tibiofemoral OA in genu varum if we had definite proof that, if left untreated, this deformity inevitably leads to clinically severe OA. This is not the case. One of the limitations of this etiological treatment lies in the fact that we do not know which patients are at risk of developing painful OA. Instead, certain risk factors for OA are known, so that primary and secondary prevention of the disease is possible. While age, sex and genetic predisposition are not amenable to preventive action, the same does not apply to the following factors: obesity, sports, and occupational activity. Thanks to in vitro studies of cultured normal and osteoarthritic chondrocytes and to experimental models of OA in animals, the pathophysiological mechanisms of OA are beginning to be better known. The prospect thus arises of "therapeutic manipulations" of precise pharmacological targets, even if it is still too soon to speak of true pathophysiological treatment of this disease. For instance, various interventions along the IL-1 pathway can be envisaged and have all been tested in animals. In practice, treating OA means taking into consideration its various signs: pain which appears to be mechanical and more or less chronic, joint stiffness, instability, effusion, and--the consequence of these symptoms--the professional, social and personal handicap of the patient. The treatment of OA must be approached from a global perspective, associating whenever possible symptomatic treatment, disease-modifying treatment, education and rehabilitation. In other words, the treatment of OA requires an overall approach, associating pharmacological and non-pharmacological modalities.