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Craniomandibular disorders in rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. A clinical study.

Sixty-one subjects with rheumatoid arthritis, 61 with psoriatic arthritis, 61 with ankylosing spondylitis, and 61 healthy controls were examined with regard to subjective symptoms and clinical signs of craniomandibular disorders (CMD). The frequencies of most subjective and clinical variables were higher in all three disease groups than in the control group. Subjects with rheumatoid arthritis and psoriatic arthritis showed more frequent and severe signs and symptoms than subjects with ankylosing spondylitis. It is concluded that subjective symptoms and clinical signs of CMD are common in rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis and are mainly caused by the respective general joint disease. None of the signs and symptoms is pathognomonic for rheumatoid arthritis, psoriatic arthritis, or ankylosing spondylitis.

Adult↗

Radiographic changes in the temporomandibular joint of patients with rheumatoid arthritis, psoriatic, arthritis, and ankylosing spondylitis.

Sixty-one subjects with rheumatoid arthritis, 61 with psoriatic arthritis, 61 with ankylosing spondylitis, and 77 healthy controls were examined using orthopantomography to determine the frequency of radiographic changes in the condyle of the temporomandibular joint. Radiographic changes were found significantly more often in subjects with rheumatoid arthritis (66%), psoriatic arthritis (38%), and ankylosing spondylitis (30%) than in controls (12%). Subjects with rheumatoid arthritis also had significantly more radiographic changes, especially cortical erosions and subcortical cysts, than subjects with psoriatic arthritis or ankylosing spondylitis. It may be concluded that rheumatoid arthritis is a more severe disease than psoriatic arthritis or ankylosing arthritis regarding temporomandibular joint involvement.

Adult↗

Quantification of radiological damage in inflammatory arthritis: rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis.

Quantification of radiological damage in inflammatory arthritis is important. It has proven its value in clinical trials, but its use in clinical practice is becoming more important as well. Scoring methods for rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis are available. These differ in the joints and features assessed. This results in differences in the scoring range, but also in the method of performance. The various methods for the three diseases are detailed in this chapter. Most information is available for rheumatoid and for this disease the relationship between radiological damage and long-term outcome is summarised.

Arthritis, Psoriatic↗

Synovial fluid levels of anti-cyclic citrullinated peptide antibodies and IgA rheumatoid factor in rheumatoid arthritis, psoriatic arthritis, and osteoarthritis.

OBJECTIVE: To assess the levels of anti-cyclic citrullinated peptide (anti-CCP) and IgA rheumatoid factor (IgA-RF) in synovial fluids of patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), and osteoarthritis (OA). METHODS: Knee effusions of 29 patients with RA (23 women, 6 men; mean +/- SD age 60 +/- 15 years), 20 with PsA (6 women, 14 men; mean age 51 +/- 12 years), and 19 with OA (9 women, 10 men; mean age 73 +/- 11.8 years) were aspirated, tested for white blood cell (WBC) counts, centrifuged, and stored at -20 degrees . Sera of 22, 11, and 12 of these patients with RA, PsA, and OA, respectively, were similarly stored. IgG anti-CCP and IgA-RF were detected by enzyme-linked immunosorbent assay. Erythrocyte sedimentation rate and C-reactive protein levels were used as measures of disease activity. RESULTS: Mean levels of synovial fluid anti-CCP and IgA-RF were significantly increased in RA joint effusions compared with PsA and OA (anti-CCP: 150 +/- 134, 34 +/- 29, and 24 +/- 26 units, respectively [P < 0.003]; IgA-RF: 76 +/- 77, 15.7 +/- 10, and 18 +/- 20 units, respectively). No significant difference was noted between OA and PsA. A significant correlation was found between synovial fluid anti-CCP and serum anti-CCP and IgA-RF. In patients with RA, a significant correlation was found between synovial fluid WBC counts and IgA-RF (P = 0.03) and serum IgA-RF (P = 0.008), but not between synovial fluid and serum anti-CCP levels. In RA patients, C-reactive protein correlated with serum IgA-RF. CONCLUSION: Anti-CCP and IgA-RF were significantly increased in synovial fluid of RA in comparison with PsA and OA patients.

Aged↗

Anemia, serum vitamin B12, and folic acid in patients with rheumatoid arthritis, psoriatic arthritis, and systemic lupus erythematosus.

OBJECTIVE: Although anemia is frequent in inflammatory rheumatic diseases, data regarding vitamin B12 status is scarce. The purpose of this study was to analyze the incidence and nature of B12 and folic acid (FA) deficiencies in a cohort of rheumatic patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), and systemic lupus erythematosus (SLE). METHODS: Levels of B12, FA, and parameters of anemia were recovered or examined in 276 outpatients. In those with recent findings of low serum B12 levels, further studies of serum homocysteine (Hcy) and urine methylmalonic acid (MMA) levels were performed. RESULTS: The incidence of anemia was high: 49%, 46%, and 35%, in RA, SLE, and PsA, respectively. Low levels of serum B12 were also frequent (24%), with almost similar occurrence in the three disease groups. Deficiency in FA was rare (<5%). Mean levels of both vitamins did not differ significantly among the three groups. No correlation between serum B12 levels and anemia was found. In the 15 patients with recently detected low B12 levels, Hcy and MMA were evaluated before and following B12 therapy. In ten of them, baseline Hcy levels were high, while MMA was increased in one patient only. Response to B12 administration, i.e., a decrease in Hcy and/or MMA levels, was noticed in four patients only, suggesting that only 26% of the low-serum-B12 patients had true B12 deficiency. CONCLUSIONS: The incidences of anemia and decreased serum B12 levels were high in these three groups of rheumatic patients. However, true tissue deficiency seems to be much rarer.

Adult↗

Mig, GRO alpha and RANTES messenger RNA expression in lining layer, infiltrates and different leucocyte populations of synovial tissue from patients with rheumatoid arthritis, psoriatic arthritis and osteoarthritis.

To investigate lymphocyte and monocyte recruitment-specific chemokine expression in synovial tissues from patients with rheumatoid arthritis (RA), psoriatic arthritis (PA) and osteoarthritis (OA), synovial membranes and cytocentrifuge preparations of 7 RA, 8 PA and 10 OA patients were examined by in situ hybridisation with antisense probes of Mig, GRO alpha and RANTES and by immunohistochemistry. Patients' local disease activity (swelling and tenderness) in order to was graded and histological evaluation was performed compare these data with their chemokine expression profiles. Mig and RANTES hybridisation signals were detected in the synovial lining layer and in cellular infiltrates, whereas GRO alpha expression was localised exclusively in the lining layer of PA and RA. Cytological analysis revealed Mig and GRO alpha mRNA mainly in monocytic cells expressing KIM6, while RANTES mRNA was demonstrated predominantly in lymphocytic cells expressing CD3. In OA synovial membranes, significantly fewer hybridisation signals were present than in RA and PA synovial membranes. Patients with PA and RA had mild to severe local disease activity, whereas OA patients showed only mild disease activity. Histologically, PA and RA inflammatory scores ranged from 1 to 5, while OA synovium was consistently graded 1. Therefore, we conclude that the differential expression of Mig, GRO alpha and RANTES in resident and in inflammatory cells has an important role in regulating leucocyte traffic in inflammatory arthropathies. The diverse leucocyte specificity of Mig, GRO alpha and RANTES may thus regulate the recruitment of different leucocyte populations, as detected in PA and RA. Therefore, the pattern of cellular infiltration in human synovitis and the corresponding clinical signs of inflammation basically reflect the localisation and expression intensity of chemokines, which may be an important target for future disease modulation.

Adult↗

Spotlight on etanercept in rheumatoid arthritis, psoriatic arthritis and juvenile rheumatoid arthritis.

Etanercept (Enbrel) is a subcutaneously administered biological response modifier that binds and inactivates tumour necrosis factor-alpha, a proinflammatory cytokine. In patients with early active rheumatoid arthritis, etanercept 25mg twice weekly was associated with a more rapid improvement in disease activity and a significantly greater cumulative response than methotrexate over 12 months of treatment in a randomised, double-blind trial. In addition, etanercept recipients showed a slower rate of radiographic progression and a more rapid improvement in quality of life than methotrexate recipients. The efficacy of etanercept was maintained at 3 years' follow-up. Etanercept was also significantly better than placebo at reducing disease activity in patients who had an inadequate response to previous treatment with disease-modifying antirheumatic drugs (DMARDs) in several well controlled trials. At study end (after 3 or 6 months' treatment), the percentage of patients achieving an American College of Rheumatology 20% (ACR20) response with etanercept (25mg or 16 mg/m(2) twice weekly) was 59-75% as monotherapy and 71% in combination with methotrexate; corresponding placebo response rates were 11-14% and 27%, respectively. Response has been maintained in patients who continued treatment for up to 5 years. In patients with psoriatic arthritis, etanercept 25mg twice weekly significantly reduced disease activity and improved skin lesions in two double-blind, placebo-controlled, 12- to 24-week trials. In the 24-week study, ACR20 response rates (50 vs 13%), psoriatic arthritis response rates (70 vs 23%) and the median improvement in skin lesions (33 vs 0%) were significantly greater in etanercept than in placebo recipients. In patients with polyarticular-course juvenile rheumatoid arthritis, etanercept resulted in improvements in all measures of disease activity and was significantly more effective than placebo at reducing disease flare. Eighty percent of patients receiving etanercept achieved a > or =30% reduction in disease activity over 7 months of treatment, and this was maintained for up to 2 years in a trial extension. Etanercept was generally well tolerated in children and adults in clinical trials; the most commonly occurring adverse effects included injection site reactions, infection, headache, rhinitis and dizziness. In conclusion, etanercept has emerged as an important new treatment option in inflammatory arthritis. Etanercept provides rapid and sustained improvements in disease activity in patients with early and DMARD-refractory rheumatoid arthritis and has been shown to inhibit radiographic progression in those with early disease. Well controlled studies have also demonstrated the efficacy of etanercept in patients with psoriatic arthritis or polyarticular-course juvenile rheumatoid arthritis.

Antirheumatic Agents↗

Etanercept: an updated review of its use in rheumatoid arthritis, psoriatic arthritis and juvenile rheumatoid arthritis.

Etanercept is a subcutaneously administered biological response modifier that binds and inactivates tumour necrosis factor-alpha, a proinflammatory cytokine. In patients with early active rheumatoid arthritis, etanercept 25mg twice weekly was associated with a more rapid improvement in disease activity and a significantly greater cumulative response than methotrexate over 12 months of treatment in a randomised, double-blind trial. In addition, etanercept recipients showed a slower rate of radiographic progression and a more rapid improvement in quality of life than methotrexate recipients. The efficacy of etanercept was maintained at 3 years' follow-up. Etanercept was also significantly better than placebo at reducing disease activity in patients who had an inadequate response to previous treatment with disease-modifying antirheumatic drugs (DMARDs) in several well controlled trials. At study end (after 3 or 6 months' treatment), the percentage of patients achieving an American College of Rheumatology 20% (ACR20) response with etanercept (25mg or 16 mg/m(2) twice weekly) was 59 to 75% as monotherapy and 71% in combination with methotrexate; corresponding placebo response rates were 11 to 14% and 27%, respectively. Response has been maintained in patients who continued treatment for up to 5 years. In patients with psoriatic arthritis, etanercept 25mg twice weekly significantly reduced disease activity and improved skin lesions in two double-blind, placebo-controlled, 12- to 24-week trials. In the 24-week study, ACR20 response rates (50 vs 13%), psoriatic arthritis response rates (70 vs 23%) and the median improvement in skin lesions (33 vs 0%) were significantly greater in etanercept than in placebo recipients. In patients with polyarticular-course juvenile rheumatoid arthritis, etanercept resulted in improvements in all measures of disease activity and was significantly more effective than placebo at reducing disease flare. Eighty percent of patients receiving etanercept achieved a >or=30% reduction in disease activity over 7 months of treatment, and this was maintained for up to 2 years in a trial extension. Etanercept was generally well tolerated in children and adults in clinical trials; the most commonly occurring adverse effects included injection site reactions, infection, headache, rhinitis and dizziness. In conclusion, etanercept has emerged as an important new treatment option in inflammatory arthritis. Etanercept provides rapid and sustained improvements in disease activity in patients with early and DMARD-refractory rheumatoid arthritis and has been shown to inhibit radiographic progression in those with early disease. Well controlled studies have also demonstrated the efficacy of etanercept in patients with psoriatic arthritis or polyarticular-course juvenile rheumatoid arthritis.

Adolescent↗

High prevalence and distinct patterns of metabolic syndrome in rheumatoid arthritis, psoriatic arthritis, and axial spondyloarthritis: a population-based study.

INTRODUCTION: Metabolic syndrome (MetS) in inflammatory arthritis (IA) directly impacts its management and associated morbidity and mortality. MetS is a well-recognised comorbidity in PsA, but the epidemiology across IA is unclear. This study aimed to characterise the prevalence of MetS across rheumatoid arthritis (RA), psoriatic arthritis (PsA) and axial spondyloarthritis (axSpA) compared to controls. METHODS: We performed a cross-sectional analysis of half a million individuals from the UK Biobank, aged 40 to 69 years, who were collected between 2006 and 2010. Participants with RA, PsA, and axSpA were identified using ICD-10 codes and/or read codes. MetS was defined according to adapted National Cholesterol Education Program Adult Treatment Panel III criteria. Statistical analysis included ANOVA and chi-squared test for between-group difference and logistic regression for odds of MetS, adjusted for age, sex, CRP and smoking status. RESULTS: The prevalence of MetS was highest in RA (43.4%), followed by PsA (42.3%), axSpA (37.1%) and controls (31.8%). Hypertension was prevalent across all IAs (~&#x2009;80%), as was hypertriglyceridaemia. Elevated waist circumference and dysglycaemia were more prevalent in RA and PsA compared to axSpA. The adjusted odds of comorbid MetS were elevated in RA (OR 1.15; 95% CI 1.07, 1.24; p&#x2009;<&#x2009;0.001) and PsA (OR 1.31; 95% CI 1.13, 1.52; p&#x2009;<&#x2009;0.001) compared to controls, but decreased in axSpA (OR 0.82; 95% CI 0.70, 0.96; p&#x2009;=&#x2009;0.012). CONCLUSION: RA and PsA, but not axSpA, are associated with an increased odds of MetS. Holistic management strategies that address both IA and MetS are essential for improving mortality and morbidity.

Humans↗

Cardiovascular disease and risk factors in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis.

OBJECTIVE: To compare the prevalence of cardiovascular diseases and their risk factors between patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS) and control subjects. METHODS: Data for patients continuously enrolled in an integrated outcomes database between January 1, 2001, and December 31, 2002, with International Classification of Diseases, 9th Revision codes of 714.x (RA), 696.0 (PsA), or 720.0 (AS) were evaluated in this cross-sectional comparative study. Control groups were established for each patient group (1:4 ratio) by matching on the basis of age, sex, geographic region, and length of time in plan. Age- and sex-adjusted prevalence of cardiovascular comorbidities and risk factors were calculated; the prevalence ratio of the comorbidities and risk factors for the patient groups compared with the control population were estimated. Use of selected cardiovascular medications was also compared between patient and control groups. RESULTS: The RA, PsA, and AS cohorts comprised 28,208, 3066, and 1843 patients, respectively. The prevalence ratio of ischemic heart disease (1.5, 1.3, 1.2), atherosclerosis (1.9, 1.4, 1.5), peripheral vascular disease (2.4, 1.6, 1.6), congestive heart failure (2.0, 1.5, 1.8), cerebrovascular disease (1.6, 1.3, 1.7), type II diabetes (1.4, 1.5, 1.2), hyperlipidemia (1.2, 1.2, 1.2), and hypertension (1.3, 1.3, 1.3) were higher in patients than controls. For RA, PsA, and AS, use of angiotensin-converting enzyme inhibitors, calcium channel blockers, diuretics, nitrates/vasodilators, anticoagulants, and antihyperlipidemia agents was significantly higher in patients than controls. CONCLUSION: Cardiovascular diseases and their risk factors were more common in patients with RA, PsA, and AS than in matched controls.

Arthritis, Psoriatic↗

Characterization of changes in IgG associated oligosaccharide profiles in rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis using fluorophore linked carbohydrate electrophoresis.

OBJECTIVE: To investigate fluorophore linked carbohydrate electrophoresis (FCE) as a method of analyzing serum immunoglobulin G (IgG) oligosaccharides in healthy individuals and those with rheumatic disease and compare with lectin binding assays of carbohydrate composition. METHODS: IgG was isolated from patients with rheumatoid arthritis (RA) (n = 21), ankylosing spondylitis (AS) (n = 20), psoriatic arthritis (PsA) (n = 20), and healthy adults (n = 36). IgG oligosaccharides were released enzymatically, fluorescently labelled using 8 aminonaphthalene-136 trisulfonic acid; and identification of the oligosaccharide bands was by stepwise enzymatic degradation. Comparison of FCE was made with lectin binding analysis in which the lectins Ricinus communis (RCA1) and Bandeiraea simplicifolia (BSII) were used to detect galactose (Gal) and N-acetylglucosamine (GlcNAc), respectively. RESULTS: Each disease could be differentiated from healthy adults on the basis of Band 1 asialodigalacto core fucosylated oligosaccharide (gf2) intensity (p = 0.001), but not from each other. Reduced levels of different sugars were associated with specific diseases: reduced gf2 with RA (p < 0.001), PsA (p < 0.001) and AS (p < 0.02), reduced Band 5 disialo-digalacto core fucosylated (a2f) oligosaccharide with AS (p < 0.001), reduced Band 6 disialo-digalacto (a2) oligosaccharide with AS (p < 0.001) and PsA (p = 0.021). All diseases were associated with a significant increase in Band 4 asialo-agalacto core fucosylated oligosaccharide (g0f) (p < 0.001). In RA, FCE band intensities correlated with sugar quantity when identified using lectin binding analysis (p < 0.003). In contrast, there was no correlation between the same bands in healthy individuals. CONCLUSION: FCE is an accurate method of analyzing IgG associated oligosaccharides and reveals unique band patterns or sugar prints associated with healthy adults and patients with RA, PsA, and AS, and comparison with lectin binding analysis suggests undetected RA glycoprotein structural differences. FCE has potential in the early diagnosis and differentiation of rheumatic diseases.

Adult↗

Immunolocalization of adhesion molecules in psoriatic arthritis, psoriatic and normal skin.

Adhesion molecule expression in synovial membrane obtained from patients with psoriatic arthritis (PA) has previously been compared with rheumatoid arthritis (RA). Although expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) was similar in both psoriatic and rheumatoid synovium, in contrast, little or no endothelial leucocyte adhesion molecule-1 (ELAM-1) was observed in psoriatic synovium. In the present study, the expression of ICAM-1, ELAM-1 and VCAM-1 was examined in the involved and uninvolved skin from patients with PA (n = 15), patients with psoriasis (Ps) but no arthritis (n = 5) and in normal skin (n = 4). ICAM-1 was intensely expressed on endothelium and keratinocytes of involved skin from patients with Ps with or without arthritis. There was constitutive expression of ICAM-1 on endothelium only in uninvolved and normal skin. In contrast, ELAM-1 expression was restricted to endothelial cells; it was widespread and intense in involved skin, but was minimal in uninvolved and normal skin. VCAM-1 was expressed on endothelium, and also on some dendritic cells in involved psoriatic skin. There was minimal VCAM-1 staining on endothelial cells in uninvolved and normal skin. In conclusion, in involved psoriatic skin from patients with and without arthritis ICAM-1, ELAM-1 and VCAM-1 expression is up-regulated on vascular endothelium, and ICAM-1 is expressed on keratinocytes. However, ELAM-1 and VCAM-1 expression seen in dermal vessels is not found in psoriatic synovial vessels. These differences suggest a mechanism for controlling cellular traffic in Ps and in PA.

Adult↗

Interleukin 2 and interleukin 2 inhibitors in human serum and synovial fluid. II. Mitogenic stimulation, interleukin 2 production and interleukin 2 receptor expression in rheumatoid arthritis, psoriatic arthritis and Reiter's syndrome.

Peripheral blood and synovial fluid (SF) mononuclear cells from 30 patients with rheumatoid arthritis (RA) were hyporesponsive to mitogenic stimulation with plant lectins and CD3 antibodies, due to depressed interleukin 2 (IL-2) production and IL-2 receptor upregulation. In contrast, in the seronegative arthritis patient group only SF mononuclear cells were hyporesponsive to mitogenic stimulation and there were no significant differences in IL-2 production or IL-2 receptor upregulation as compared with control subjects. No significant correlations were observed between IL-2 inhibitor levels and mitogenic responses, IL-2 production and IL-2 receptor upregulation on peripheral blood and SF mononuclear cells but an inverse correlation was noted between SF mitogenic responses and the expression of selected activation markers. We conclude that IL-2 abnormalities appear to be most pronounced in RA compared with other inflammatory arthritides and that these changes do not appear to be directly related to serum or SF IL-2 inhibitor levels.

Arthritis↗

Current concepts in psoriatic arthritis.

Psoriatic arthritis is an inflammatory arthropathy associated with psoriasis and characterized by absence of rheumatoid factor. Any form of psoriasis can be complicated by joint inflammation. Four groups have been identified: pauciarticular psoriatic arthritis, psoriatic spondylitis, symmetrical polyarticular psoriatic arthritis and arthritis mutilans. The etiology of psoriatic arthritis remains unclear. Genetic, immunologic and environmental factors are thought to be important in the development of the disease. The role of cytokines and adhesion molecules in the mechanism of joint destruction is highlighted, and recent therapeutic strategies are discussed.

Arthritis, Psoriatic↗