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ID PMID Title PublicationDate abstract
18799090 High-grade inflammation, circulating adiponectin concentrations and cardiovascular risk fa 2008 Jul OBJECTIVE: To assess whether obesity and systemic inflammation are potential determinants of circulating adiponectin concentrations and whether low adiponectin levels cluster with metabolic syndrome features that are previously documented cardiovascular risk factors in rheumatoid arthritis (RA). METHODS: We investigated 33 RA patients who were treated with the TNF-alpha antagonist infliximab, immediately prior to an infliximab infusion. Adiponectin levels were also determined immediately after administration of an infliximab dose. RESULTS: Adiponectin concentrations correlated with age (R=0.465, p=0.008) and were higher in women (mean [95% confidence interval]=21,595 [15,366 to 30,349] ng/ml) than in men (9,310 [5,653 to 15,335] ng/ml)(p=0.008). C-reactive protein (CRP) levels correlated with circulating adiponectin concentrations (partial (p) R=-0.370, p=0.04), independent of age and gender. By contrast, the body mass index (BMI) did not correlate with adiponectin levels (pR=-0.039, p=0.8). Adiponectin concentrations correlated with triglycerides/HDL cholesterol ratios (pR=-0.396, p=0.03), total cholesterol/HDL cholesterol ratios (pR=-0.444, p=0.01) and high fasting plasma glucose levels (pR=-0.366, p=0.04), independent of CRP levels and the BMI. Adiponectin levels did not change (p=0.3) upon infliximab administration. CONCLUSION: In this cohort, high-grade inflammation was independently and negatively correlated with circulating adiponectin concentrations whereas low adiponectin levels clustered with metabolic syndrome features that reportedly contribute to atherogenesis in RA. Circulating adiponectin may be involved in cardiovascular disease in RA. The impact of inflammation on circulating adiponectin concentrations is not likely to be TNF-alpha mediated in RA.
18391680 A rare case of enterobacter endocarditis superimposed on a mitral valve rheumatoid nodule. 2008 Apr We present the case of a 56-year-old man with longstanding seropositive active erosive and deforming rheumatoid arthritis with no peripheral rheumatoid nodules; he immigrated from the former Soviet Union (where he did not receive any disease-modifying antirheumatic drugs) to Israel in 1995. In February 2005, he had a buccogingival mucosal abscess on his lower lip, which was treated by surgical drainage, followed by prolonged antibiotic therapy. One and a half years later, he had 2 episodes of transient ischemic attacks characterized by speech difficulties and moderate weakness on his right side. Transesophageal echocardiogram revealed a mass on the anterior mitral valve leaflet. Repeated blood cultures were negative, and the patient was afebrile all the time. The patient underwent mitral valve replacement and the histologic findings of the mass were typical of both a rheumatoid nodule and bacterial endocarditis. The patient recovered fully after 6 weeks of antibiotic therapy. Emboli from a rheumatoid nodule should always be considered in patients with rheumatoid arthritis who present with transient ischemic attacks.
17870033 Mortality in established rheumatoid arthritis. 2007 Oct Rheumatoid arthritis (RA) is associated with reduced life expectancy. Whether the development of RA initiates this process of premature ageing or is part of it is not clear. The excess mortality is apparent within the first few years of disease and increases with RA disease duration. Most of the excess deaths are attributable to infection, cardiovascular disease (in particular coronary heart disease) and respiratory disease. Deaths due to lung cancer and non-Hodgkin's lymphoma, but not other cancers, are also increased. There is some evidence that effective disease-modifying therapy can improve survival but, overall, survival in RA patients has not improved to the same degree as in the general population over recent decades.
18021889 Comorbidities in psoriasis. 2007 Nov Epidemiological studies have shown that, in psoriasis patients, associated disorders may occur more frequently than expected. Such comorbidities include psoriatic arthritis, psoriatic pustular diseases, Crohn disease, and signs of metabolic syndrome, which leads to atherosclerosis with coronary heart disease. Although the disorders represent separate entities, they appear to follow overlapping pathogenic pathways. Comorbidities often become clinically manifest years after onset of psoriasis and are frequently seen in severe disease. Persistent low-grade inflammation with secretion of proinflammatory cytokines (eg, tumor necrosis factor alpha) favors the development of insulin resistance and metabolic syndrome. In addition, biochemical and immunologic observations point toward an inflammatory immune mechanism that uses tools of the innate defense armamentarium.
17984195 Detection of rheumatoid arthritis bone erosions by two different dedicated extremity MRI u 2008 Jul OBJECTIVES: To compare the ability of two different dedicated extremity MRI (E-MRI) units and conventional radiography (CR) for identifying bone erosions in rheumatoid arthritis (RA) metacarpophalangeal (MCP) and wrist joints. METHODS: CR and two MRI examinations (using 0.2 T Esaote Artoscan and 0.2 T portable MagneVu MV1000 units) of 418 bones in the dominant wrist and second to fifth MCP joints of 15 patients with RA and 4 healthy controls were performed and evaluated blindly for bones being visible and for erosions. RESULTS: In MCP joints, MagneVu visualised 18.5% of bones entirely and 71.1% were 67-99% visualised. In wrists, MagneVu visualised 1.5% of bones entirely, 39.8% were 67-99% visualised and 19% were not visualised at all. Artoscan and CR visualised all bones entirely. Artoscan, MagneVu and CR found 22, 19 and 15 bones with erosions in MCP joints and 66, 40 and 13 bones with erosions in wrist joints, respectively. With the previously validated Artoscan unit as standard reference, MagneVu and CR had sensitivities of 0.82 and 0.55, respectively, in MCP joint bones and 0.41 and 0.14 in wrist bones. Specificities of CR and MagneVu were comparable (0.82-0.99). The MagneVu unit was particularly more sensitive than CR for metacarpal heads and carpal bones. MagneVu MRI and CR detected 100% and 89%, respectively, of large erosions (Outcome Measures in Rheumatoid Arthritis Clinical Trials-Rheumatoid Arthritis MRI Scoring System (OMERACT-RAMRIS) score >1 on Artoscan) in MCP joints and 69% and 15.8% of large erosions in wrists. CONCLUSIONS: Both E-MRI units detected more erosions than CR, in particular due to a higher sensitivity in metacarpal heads and carpal bones. The MagneVu unit detected fewer erosions than the Artoscan unit due to a lower average image quality and a smaller proportion of bones being visualised.
17143328 Inducible bronchus-associated lymphoid tissue (iBALT) in patients with pulmonary complicat 2006 Dec Bronchus-associated lymphoid tissue (BALT) was originally described as a mucosal lymphoid organ in the lungs of some species. However, while the lungs of naive mice and humans typically lack BALT, pulmonary infection in mice leads to the development of inducible BALT (iBALT), which is located in peribronchial, perivascular, and interstitial areas throughout the lung. Here we investigated whether iBALT forms in patients with a variety of interstitial lung diseases. We show that while iBALT can be found in the lungs of patients suffering from multiple diseases, well-developed iBALT is most prevalent in patients with pulmonary complications of RA and Sjögren syndrome. In these patients, iBALT consisted of numerous B cell follicles containing germinal centers and follicular dendritic cells. A loosely defined T cell area surrounded the B cell follicles while lymphatics and high endothelial venules were found at the B cell/T cell interface. Increased expression of lymphoid-organizing chemokines, such as CXCL13 and CCL21, as well as molecules involved in the immunopathology of RA, such as B cell-activating factor of the TNF family (BAFF), ICOS ligand, and lymphotoxin, correlated with more well-developed iBALT. Finally, the presence of iBALT correlated with tissue damage in the lungs of RA patients, suggesting that iBALT participates in local RA pathogenesis.
18075712 TNF-alpha blockade induces a reversible but transient effect on endothelial dysfunction in 2008 Jul Considerable evidence indicates that patients with rheumatoid arthritis (RA) are at greater risk of developing atherosclerosis and cardiovascular disease. Recent studies support the predictive ability of endothelial function measures for subsequent atherosclerotic events. We have investigated the effects of infliximab, a chimeric monoclonal anti-tumor necrosis factor (TNF) antibody, on endothelial vasodilation, measured by brachial ultrasonography and on the levels of inflammatory biomarkers and adhesion molecules in ten consecutive patients with severe long-standing RA, despite methotrexate therapy, during the loading phase of infliximab therapy. Flow-mediated dilation (FMD) in RA patients at baseline was significantly impaired compared with healthy controls (7.71 +/- 2.78% vs 14.91 +/- 6.41%; p = 0.008) and improved significantly after infliximab infusion (12.63 +/- 1.63% vs 7.71 +/- 2.78%; p = 0.005). At baseline, a statistically significant correlation between C-reactive protein levels and FMD was found (r = -0.69, p = 0.026). However, this improvement was transitory, as FMD values returned to baseline values before each infliximab infusion at weeks 2, 6 and 14. There were no significant differences in baseline brachial artery diameter between visits, although at each time, the diameter was increased. According to European League Against Rheumatism response criteria, all ten patients were good responders. No significant differences were observed in intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1, vascular endothelial growth factor and E-selectin plasma levels before and after each infusions. This study demonstrates that endothelial dysfunction is a reversible phenomenon in RA. The addition of anti-TNFalpha treatment reduces inflammatory symptoms in patients with severe RA. The improvement of endothelial function during the loading phase of therapy is transitory, suggesting an enhanced and persistent TNF-alpha generation within the arterial wall.
18251219 [Rheumatoid arthritis and ankylosing spondylitis--rheumatologic highlights 2007]. 2008 Jan 9 The use of biological therapy is now firmly established in the management of inflammatory rheumatism. The anti-TNFalpha have rightly become agents of choice over the last 10 years, and the recent literature reminds us of their places and indications in ankylosing spondylitis. However, not all patients respond, and the availability of new treatments is certainly a welcome addition. Abatacept is a new treatment for rheumatoid arthritis with an innovative mode of action. It appears effective and safe, and some data as well as practical aspects on its use are presented. Nevertheless, we must still learn to integrate it into our therapeutic strategies, as we are presently doing with rituximab.
17133559 Individualized monitoring of drug bioavailability and immunogenicity in rheumatoid arthrit 2006 Dec OBJECTIVE: Infliximab, an anti-tumor necrosis factor alpha (anti-TNFalpha) antibody, is effective in the treatment of several immunoinflammatory diseases. However, many patients experience primary or secondary response failure, suggesting that individualization of treatment regimens may be beneficial. This study was undertaken to investigate whether serologic monitoring of infliximab bioavailability and immunogenicity in individual patients would be useful in optimizing treatment regimens to improve efficacy and tolerability. METHODS: To avoid the use of solid-phase assays, two radioimmunoassays were developed: one for measurement of levels of anti-infliximab antibody, and a functional one for measurement of TNFalpha binding due to infliximab. Sera from 106 randomly selected rheumatoid arthritis patients were tested within 6 months of therapy initiation, and associations between findings of serum assays and disease activity, infusion reactions, and treatment failure occurring within 18 months were assessed. RESULTS: Trough serum infliximab levels after the first 2 intravenous infusions of infliximab at 3 mg/kg varied considerably between patients (range 0-22 microg/ml). At this stage, only 13% of the patients were anti-infliximab antibody positive. With subsequent infusions, the frequency of antibody positivity rose to 30% and 44% (at 3 months and 6 months, respectively), accompanied by diminished trough levels of infliximab. Indeed, low infliximab levels at 1.5 months predicted antibody development and later treatment failure. There were highly significant correlations between high levels of antibodies and later dose increases, side effects, and cessation of therapy. High baseline disease activity, judged by C-reactive protein level and Disease Activity Score, was associated with low levels of infliximab at the early stage of treatment and later development of anti-infliximab antibodies. Cotreatment with methotrexate resulted in slightly reduced antibody levels after 6 months; other disease-modifying antirheumatic drugs and prednisolone had no effect. CONCLUSION: Development of anti-infliximab antibodies, heralded by low preinfusion serum infliximab levels, is associated with increased risk of infusion reaction and treatment failure. Early monitoring may help optimize dosing regimens for individual patients, diminish side effects, and prevent prolonged use of inadequate infliximab therapy.
18633630 [Fractalkine--a proinflammatory chemokine in rheumatoid arthritis]. 2008 Sep Fractalkine (CX3CL1), so far the only member of the CX3C class of chemokines, and its receptor, CX3CR1, are strongly expressed in the chronically inflamed synovial tissue of patients with rheumatoid arthritis (RA). Due to the specific binding of Fractalkine to its receptor, many proinflammatory reactions involved in the pathogenesis of RA are triggered. Functionally, fractalkine plays an important proinflammatory role in RA pathogenesis as characterized by induction of synovial angiogenesis, chemotaxis, activation of monocytes and T cells as well as the stimulation of proliferation and synthesis of matrix degrading enzymes (matrix metalloproteinases, MMP) in synovial fibroblasts. Fractalkine thus may represent a novel target molecule for therapeutic intervention in RA.
18953538 Assessment of adenosine deaminase levels in rheumatoid arthritis patients receiving anti-T 2009 Apr Anti-TNF-alpha agents are increasingly used in rheumatoid arthritis (RA) treatment and that is known to increase the risk of tuberculosis (TB) reactivation. Adenosine deaminase (ADA) levels are shown to increase to high levels in TB patients. Our aim is to investigate the serum ADA levels in RA patients being treated with anti-TNF-alpha and to compare the results with the patients on DMARD therapy. The study groups comprised of 56 RA patients (45 female, mean age 49) who were treated either with two or three DMARDs, 32 RA patients with anti-TNF-alpha treatment (26 female, mean age 46) and 20 healthy controls (10 female, mean age 48). All patients fulfilled the 1987 ACR criteria for RA. DAS28 score was calculated for all subjects. When compared to healthy controls, ADA levels were measured statistically higher both in patient groups (P = 0.046, 0.002). ADA levels in anti-TNF-alpha group were similar to conventional therapy (11.3 +/- 2.7, 10.9 +/- 4.01; P = 0.76). PPD was positive in 17 RA patients in the anti-TNF-alpha treatment group (%53). The ADA levels were found to be similar in the anti-TNF-alpha group when compared according to the PPD positivity (positive, 12.4 +/- 3.7; negative, 10.5 +/- 2.1; P = 0.02). No correlation was found between the ADA levels and age, disease duration, ESR, CRP, DAS 28 and HAQ score. In this study, we observed that RA patients at remission taking DMARD or anti-TNF-alpha therapy have similar levels of serum ADA. Although serum ADA levels during TB infection increase much higher, in our study, ADA levels of all RA patients were lower than 15 IU/L. Elevated ADA levels may be a clue for diagnosis of TB in patients who were on anti-TNF-alpha therapy.
16568505 Treatment of rheumatoid arthritis patients with abatacept and methotrexate significantly i 2006 Apr OBJECTIVE: This study examined the effect of abatacept, a costimulation modulator, on the health-related quality of life (HRQOL) of patients with rheumatoid arthritis (RA). METHODS: Three hundred thirty-nine patients with RA on a background of methotrexate (MTX), who participated in a multicenter, double-blind, placebo-controlled trial, were randomized to abatacept 2 mg/kg, abatacept 10 mg/kg, or placebo. HRQOL was assessed at pretreatment, and at 3, 6, and 12 months posttreatment using the SF-36 Health Survey (SF-36). Changes in SF-36 scores from baseline to 12 months were compared across treatment and placebo groups to examine HRQOL benefits of abatacept. A link between American College of Rheumatology improvement and changes in SF-36 scores was established to demonstrate the association between HRQOL outcomes and clinical response. RESULTS: After 12 months of treatment, patients randomized to abatacept 10 mg/kg showed significantly better HRQOL outcomes overall versus patients randomized to placebo (MANOVA F = 4.71, p < 0.001) or to abatacept 2 mg/kg (MANOVA F = 1.97, p = 0.05). Differences in SF-36 change scores between abatacept 10 mg/kg and placebo groups reached statistical significance on all 8 domain scales, the 2 summary measures, and the SF-36 utility index (SF-6D). Differences in SF-36 change scores between abatacept 10 mg/kg and abatacept 2 mg/kg reached statistical significance on 5 of the 8 domain scales, the physical summary measure, and the SF-6D. Improvement in HRQOL was highly related to clinical response. CONCLUSION Abatacept 10 mg/kg plus MTX demonstrated a stronger HRQOL response than placebo plus MTX. The abatacept 2 mg/kg arm showed a very weak and transient response.
18821680 Marked differences in fine specificity and isotype usage of the anti-citrullinated protein 2008 Oct OBJECTIVE: Anti-citrullinated protein antibodies (ACPAs) display high association with rheumatoid arthritis (RA) and are implicated in its pathogenesis. The presence of ACPAs is known to precede the onset of RA. In order to identify the features that could confer its pathogenicity, we extensively characterized this antibody response in a unique North American native population of patients with RA and their unaffected relatives. METHODS: The levels of IgA, IgM, and IgG ACPAs, as well as IgM and IgA rheumatoid factor (RF), were measured in serum samples obtained from 81 patients with RA and 195 of their unaffected relatives. The isotype distribution, the fine specificity of the ACPA response, and its association with RF were compared in health and disease. RESULTS: ACPA positivity was observed in 19% of the healthy relatives and approximately 91% of the patients with RA. ACPA isotype usage was strikingly lower in unaffected relatives than in patients with RA (1-2 versus 5-6 isotypes). Fine specificity studies showed that reactivity to citrullinated fibrinogen and vimentin was present in sera from patients with RA, while it was virtually absent in their unaffected relatives. Finally, the ACPA and RF responses were associated in patients with RA but were discordant in their healthy relatives. Extended analyses revealed that the presence of ACPAs was associated with RA irrespective of RF status, while the association of RF with disease relied on its interaction with ACPAs. CONCLUSION: The fine specificity and isotype usage of the ACPA response are qualitatively different in health and disease. Epitope spreading and expansion of the isotype repertoire might be necessary for development of RA, and this could be facilitated by the presence of RF antibodies.
17456523 Bone mineral density in patients with recently diagnosed, active rheumatoid arthritis. 2007 Nov OBJECTIVES: Osteoporosis is a well-known extra-articular phenomenon in patients with uncontrolled, long-standing rheumatoid arthritis (RA). In the present study, the extent of osteoporosis and reduced bone mineral density (BMD) and the disease-related and demographic factors that are associated with osteoporosis and reduced BMD were examined in patients with recently diagnosed, active RA. METHODS: BMD of the total hip and the lumbar spine was measured using dual-energy x ray absorptiometry in 381 patients with recently diagnosed active RA, who had never been treated with DMARDs or corticosteroids. Osteoporosis was defined as a T score
17644821 The anti-allergic drug, N-(3',4'-dimethoxycinnamonyl) anthranilic acid, exhibits potent an 2007 Sep OBJECTIVES: The degradation of tryptophan by indoleamine 2,3-dioxygenase yields a number of immunomodulatory metabolites, including 3-hydroxyanthranilic acid, 3-hydroxykynurenic acid and quinolinic acid. N-(3',4'-dimethoxycinnamonyl) anthranilic acid (3,4-DAA) is a synthetic anthranilic acid derivative that has been used therapeutically in Japan for many years as an anti-allergic drug and has recently been shown to be effective in a murine model of multiple sclerosis. METHODS: In the present study, we tested the efficacy of 3,4-DAA in collagen-induced arthritis, a mouse model of rheumatoid arthritis, and analysed its mechanism of action. RESULTS: Administration of 3,4-DAA after arthritis onset reduced clinical and histological severity of arthritis and reduced pain. It completely abrogated thermal and mechanical hyperalgesia. 3,4-DAA also suppressed Th1 cell activity in lymph node cell cultures and raised serum levels of IL-10. In vitro, 3,4-DAA suppressed IFNgamma production and proliferation of both T and B lymphocytes in a manner comparable with the endogenous tryptophan metabolite, 3-hydroxyanthranilic acid, suggesting similar mechanisms of action. CONCLUSION: It is concluded that 3,4-DAA has both anti-inflammatory and analgesic properties, and may therefore be useful in filling an unmet need, in the treatment of rheumatoid and other forms of arthritis, especially in the light of its analgesic properties.
16308252 Auditory pathway in rheumatoid arthritis. A comparative study and surgical perspectives. 2006 Jan CONCLUSION: Rheumatoid arthritis (RA) patients present with both conductive and sensorineural deafness. OBJECTIVE: To evaluate the prevalence and features of hearing impairment in patients with RA. MATERIAL AND METHODS: A total of 28 RA patients underwent a rheumatological evaluation, including determination of rheumatoid factor, protein 2-glycoprotein I level and the Lee index. An audiological assessment consisting of pure-tone audiometry (PTA) and determination of auditory brainstem responses (ABRs) and transient evoked otoacoustic emissions (TEOAEs) was performed. The results were compared with those of 28 age- and sex-matched healthy subjects. Four selected RA patients underwent stapedectomy; PTA and TEOAEs were evaluated 6 months postoperatively. RESULTS: Increased air conduction thresholds at 250, 500 and 1000 Hz were found in RA subjects in comparison to controls (p<0.001). RA patients showed higher air-bone gaps in PTA (p<0.05) and an increased Wave I latency in ABRs (p=0.03). Decreased reproducibility (p<0.001) and amplitude (p<0.001) of TEOAEs were found in RA subjects in comparison to controls. A significant correlation between disease duration and echo amplitude was noticed (r=0.389). After stapedectomy, a reduction in the air-bone conduction gap (11 vs 2 dB HL) was noticed; no significant difference in TEOAEs was found.
18084807 A clinical, electrophysiological, and pathological study of neuropathy in rheumatoid arthr 2008 Jul Neuropathy in rheumatoid arthritis (RA) may result secondary to entrapment, vasculitis, and drug toxicity. We aimed to study clinical and electrophysiological neuropathy and pathological changes in sural nerve in patients with RA. One hundred eight patients of RA, fulfilling American College of Rheumatology 1987 criteria (mean age, 45.83 years; M/F 1:3, 80.3% seropositive) were examined clinically and electrophysiologically for evidence of peripheral neuropathy. Sural nerve biopsies were performed in the involved cases. In all RA patient medications, disease activity, results of blood tests, and X-rays of affected joints were recorded. Twenty-three patients complained of paresthesias in the extremities. Vibration sensations were decreased in 9, and tendon reflexes were decreased or absent in 28 patients. Sixty-two (57.4%) patients had electrophysiologic evidence of neuropathy. Of these 53 (85.5%) patients had pure sensory or sensory motor axonal neuropathy (mononeuritis multiplex, n = 7), while 9 (14.5%) had demyelinating neuropathy (chronic inflammatory demyelinating polyneuropathy, n = 1). Carpal tunnel syndrome was seen in 11 (10.1%) patients (associated with neuropathy in 6). Of 23 sural nerve biopsies available, perineurial thickening (n = 5, amyloid deposits n = 4), perivascular lymphomononuclear cell infiltrate (n = 4), loss of myelin fibers (n = 2), and necrotizing vasculitis (n = 1) were found. Clinically, however, seven patients had evidence of cutaneous vasculitis. Comparing the clinical characteristics of the patients with or without electrophysiological neuropathy, absence of deep tendon jerks (p < 0.005) and presence of extra articular manifestations (p < 0.01) were conspicuous in the neuropathic group. There was no relation of neuropathy with the duration of RA, seropositivity, joint erosions, joint deformities, prior disease-modifying anti-rheumatic drugs or glucocorticoid intake, and 28-joint disease activity score. Neuropathy in RA was mostly subclinical and predominantly axonal. Pathologically, neuropathy secondary to amyloid infiltration was second only to vasculitic neuropathy. Absence of deep tendon jerks and presence of vasculitis were more commonly observed in patients with neuropathy.
17763203 Effects of selective and non-selective cyclo-oxygenase inhibition on endothelial function 2007 Jul OBJECTIVES: Rheumatoid arthritis (RA) is associated with increased cardiovascular disease (CVD) risk that has been attributed to endothelial dysfunction and inflammation. Non-steroidal anti-inflammatory drugs (NSAIDs) and cyclo-oxygenase (COX)-2 inhibitors have been shown in some studies to improve endothelial function in subjects without RA. The aim of this study was to investigate the effects of COX inhibition on endothelial function in patients with RA. METHODS: Patients with RA (n = 37) were randomized to receive a 2-week course of either indomethacin (75 mg bd), rofecoxib (12.5 mg bd), or placebo in a double-blind study. Endothelial function was measured using flow-mediated dilation (FMD) of the brachial artery in response to reactive hyperaemia. Arterial stiffness was also assessed using pulse wave analysis (PWA) through the measurement of the aortic augmentation index (AIx). Measurements of vascular function and inflammatory markers were taken before and at the end of the treatment period. RESULTS: There were no significant differences in changes in FMD, AIx, blood pressure (BP), serum creatinine, erythrocyte sedimentation rate (ESR), or high-sensitivity C-reactive protein (hsCRP) between groups. However, compared with the other treatment groups, there was a tendency for systolic BP to decrease in the placebo group (p = 0.063) and for creatinine to increase in the indomethacin and rofecoxib groups after treatment (p = 0.054). CONCLUSIONS: This study suggests that COX inhibition by indomethacin or rofecoxib do not improve endothelial function in patients with RA.
18799105 Incidence and risk of fatal myocardial infarction and stroke events in rheumatoid arthriti 2008 Jul BACKGROUND: There is substantial evidence of excess cardiovascular morbidity and mortality in rheumatoid arthritis (RA) patients, but the related studies showed important variations in the estimation of the risk. We conducted a meta-analysis to evaluate more accurately the incidence of cardiovascular events, and the excess of cardiovascular risk in a population of RA patients. METHODS: The authors searched for observational studies accounting for the number of myocardial infarction or stroke events, using Medline, and congress abstracts published until February 2006. The populations studied were adults and RA diagnosis was based on the American College of Rheumatology (ACR) criteria. We calculated the incidence of myocardial infarction and cerebrovascular fatal events in RA patients and estimated the cardiovascular risk increase for RA patients compared with the control group. RESULTS: 17 publications and abstracts were identified, 15 were selected for the meta-analysis (two publications were excluded because of the lack of person-years information). The incidence of fatal myocardial infarction was 13.3 for 1000 RA patients-year (IC95%=[13-13.6]). The incidence of fatal cerebrovascular accident was 4.5 for 1000 RA patients-year (IC95%=[4.3-4.7]). Risk of myocardial ischemia in RA patients was about 1.63 compared to the general population (OR=1.63, IC95%=[1.34-2]). No excess was found for the risk of stroke event in RA patients. CONCLUSION: RA patients were reported to present an excess risk of fatal myocardial infarction compared to the general population. The prevention of cardiovascular complications, including management of cardiovascular risk factors and control of systemic inflammation, should be taken into account by the rheumatologist.
17418000 Clustering of cardiovascular risk factors in rheumatoid arthritis: the rationale for using 2007 Jan Atherosclerosis may be more prevalent and more extensive in individuals with rheumatoid arthritis (RA) compared with the general population. Despite the fact that traditional and novel cardiovascular disease (CVD) risk factors are clinically important in these patients, it seems that inflammation--a key feature of RA--plays a crucial role in atherogenesis. Reducing the CVD burden in patients with RA is a more complex process than in the general population, mostly due to inadequate inflammation suppression as well as multiple concomitant drug therapy. Furthermore, there is no current consensus on whether RA patients should be treated as individuals at high-risk for vascular events. Statins have proved their efficacy in reducing CVD events in the general population. Despite the fact that they are not specifically indicated in RA, there is evidence supporting a beneficial effect on CVD risk factors as well as disease activity and progression. The present review considers the traditional and novel as well as the RA-specific CVD risk factors. The current evidence supporting the use of statins in this patient population is also discussed.