Levels In Rheumatoid Arthritis Patients Research Articles

English

Rheumatoid arthritis is a chronic systemic autoimmune disorder causing inflammation of the synovial joints leading to joint destruction as well as a variety of extra articular features. In this present study, serum Adenosine deaminase and Alkaline phosphatase levels were studied in patients of rheumatoid arthritis. Thirty patients in the age group of 30-60 years of both sexes and equal number of age and sex matched healthy controls were included in this study. In rheumatoid arthritis patients, serum Adenosine deaminase levels were high, the mean serum Adenosine deaminase levels were 60 ± 9.55 and in controls the mean Adenosine deaminase levels were 21 ± 3.04. The p value was significant at p < 0.001. We conclude that serum Adenosine deaminase can be used as a marker for cell mediated immunity to monitor disease activity in rheumatoid arthritis. Serum Alkaline phosphatase was found to be raised in rheumatoid arthritis, the mean serum Alkaline phosphatase levels were 291.63 ± 35.84 in patients of rheumatoid arthritis when compared to healthy controls (196.73 ± 32.71).The p value was significant at p<0.001. The present study has focused on investigating the serum total Alkaline phosphatase levels in Rheumatoid Arthritis Patients and The findings have indicated a raised serum Alkaline phosphatase in patients of rheumatoid arthritis when compared to healthy controls thereby suggesting the role of serum Alkaline phosphatase as a marker of disease activity in rheumatoid arthritis.

Serum Copper as a Marker of Disease Activity in Rheumatoid Arthritis.

Copper is an important trace element for normal growth and development of the body. It is also essential for maturation of collagen tissues. The purpose of the study was to estimate the serum copper levels in rheumatoid arthritis patients and to see its association with the various parameters of disease activity. The study was carried out among 50 diagnosed rheumatoid arthritis patients (25 each of active disease & remission patients) and 50 age and sex matched controls. Fasting blood sample was collected for estimation of serum copper, haemoglobin level and ESR in the subjects. Mean serum copper level in the case group was found to be significantly higher than that of the control group (p-value<0.001). This increase of copper level was more in active disease than those with remission (p-value < 0.0001). A significant positive correlation was found between serum copper level and ESR, serum copper level and morning stiffness and a negative correlation was found between serum copper level and haemoglobin level in rheumatoid arthritis patients. In rheumatoid arthritis patients, serum copper level may be used as an additional biochemical marker for estimation of disease activity.

Biochemical markers for early detection of cardiovascular disorders in rheumatoid arthritis

Background The mechanism of accelerated atherosclerosis accompanied with rheumatoid arthritis (RA) remains unclear. Aim The aim of this study was to investigate the association between fetuin-A, asymmetric dimethylarginine (ADMA), advanced oxidation protein products (AOPPs), and accelerated atherosclerosis in patients with RA, for early detection of cardiovascular disorders. Patients and methods This study was carried out on 60 participants: 40 RA patients and 20 healthy volunteers of similar age and sex. Assessment of Disease Activity for 28-Joint Indices Score and ultrasonographic examinations of carotid intimal thickness and stiffness parameter β were carried out. In addition, lipid profile, serum high-sensitivity C-reactive protein, ADMA, fetuin-A, and AOPPs levels were measured in all participants. Results There was a significant increase in serum ADMA and AOPP levels in RA patients compared with controls. Serum fetuin-A levels were lower in RA patients than in controls. There was a positive correlation between serum ADMA levels and serum erythrocyte sedimentation rate, high-sensitivity C-reactive protein, rheumatoid factor, Disease Activity for 28-Joint Indices Score, carotid intima-media thickness, stiffness index β, total cholesterol, low-density lipoprotein cholesterol, triglyceride levels, and total cholesterol/high-density lipoprotein cholesterol and low-density lipoprotein cholesterol/high-density lipoprotein cholesterol ratios. Conclusion Low levels of fetuin-A, in RA, suggest its possible contribution in the pathophysiology of endothelial dysfunctions, subsequently causing increase in arterial stiffness. An increase in ADMA and AOPPs in RA patients, together with dyslipidemia, suggests their possible involvement in the physiology and pathophysiology of vascular diseases in RA. These findings open new avenues for further studies on the physiology of cardiovascular diseases in RA that may lead to a better treatment of these diseases.

The relationships between serum sclerostin, bone mineral density, and vascular calcification in rheumatoid arthritis.

Recent data indicate that the secreted glycoprotein sclerostin may be involved in vascular calcification (VC). The objective of the study was to establish whether serum sclerostin levels are associated with VC in patients with rheumatoid arthritis (RA). This was a cross-sectional study. The study was conducted with ambulatory care. We compared 75 RA patients with 75 age- and gender-matched control participants. Coronary artery calcification (CAC) and abdominal aortic calcification (AAC) scores were evaluated by computed tomography. Serum sclerostin levels (determined with an ELISA) were assessed. A statistical analysis was performed to identify the determinants of serum sclerostin and VC. AAC and CAC were more prevalent and more severe in patients with RA than in controls. Higher levels of AAC (P = .02) and a higher lumbar bone mineral density (BMD; P = .03) were identified as independent determinants of higher serum sclerostin levels in RA patients, whereas male gender (P = .03), higher lumbar BMD (P < .0001), and low estimated glomerular rate (P < .001) were identified as determinants in controls. In RA patients, a multivariate logistic regression analysis indicated that older age [P < .01, with an odds ratio (OR) per year 1.10] and male gender (P = .02, OR 6.79) were independent determinants of CAC and that older age (P < .001, OR 1.16) were independent determinants of AAC. In controls, the independent determinants were older age (P < .01, OR 1.19), hypertension (P < .01, OR 7.31), and lumbar BMD (P = .03, OR per 30 mg/cm(2) increment of 1.14) for CAC and older age (P = .01, OR 1.11) for AAC. Serum sclerostin levels were significantly and independently associated with AAC in RA patients.

Undercarboxylated osteocalcin may be an attractive marker of teriparatide treatment in rheumatoid arthritis patients

Dear Editor, Elderly rheumatoid arthritis (RA) patients suffer from osteoporosis resulting in fragility fractures [1]. Therapy with lowdose glucocorticoids, which are often used to treat RA, suppresses bone strength. However, evidence regarding the effects of treatment for osteoporosis in RA patients remains limited. Ebina and colleagues [2] conducted an 18-month prospective trial of daily teriparatide (TPTD) in patients with RA and postmenopausal osteoporosis. Their findings showed the advantage of TPTD in the RA patients, compared to that observed in the subjects with primary osteoporosis, and identified available predictors of TPTD treatment in the setting of RA. Their findings provide several significant messages for clinicians. In the current article, I would like to discuss this topic from the point of view of a marker of bone formation, undercarboxylated osteocalcin (ucOC). It has previously been reported that the serum ucOC level is elevated by TPTD treatment in RA patients [3]. In addition, serum ucOC level and daily glucocorticoid dose are inversely correlated in RA patients treated with teriparatide [3]. The serum ucOC levels in RA patients receiving more than 10 mg per day of prednisolone are often undetectable on an electrochemiluminescence immunoassay. We recently administered TPTD treatment in a small number of RA patients and followed the BMD and serum ucOC levels for 48 weeks (n= 34, mean age 74.6 years). Based on our preliminary data, the percent change from baseline in the LS BMD at 48 weeks positively correlated with the absolute change from baseline in ucOC at 24 weeks (rs=0.389, p=0.025). These results are consistent with the observations noted by Ebina and colleagues [2]. Therefore, we agree with the suggestion that the serum ucOC level has the potential to be a useful predictor of TPTD treatment in RA patients. Nevertheless, it is unknown whether the ucOC level is a suitable biomarker for TPTD treatment in all types of glucocorticoid-induced osteoporosis (GIO). As noted above, high-dose prednisolone treatment may make the serum ucOC level undetectable. Therefore, further research is needed to clarify the relationship between ucOC and TPTD treatment in RA and GIO patients.

Vitamin D status in rheumatoid arthritis patients: relation to clinical manifestations, disease activity, quality of life and fibromyalgia syndrome.

To assess vitamin D levels in rheumatoid arthritis (RA) patients and to find their relation to clinical parameters, fibromyalgia syndrome (FMS), quality of life (QoL) and disease activity. The study included 63 RA patients and 62 controls. Clinical examination and laboratory investigations were performed. For patients, the Disease Activity Score (DAS-28), QoL index, Health Assessment Questionnaire II (HAQ II) and Modified Larsen score were calculated. 25-OH-vitamin D was measured in patients and controls. The patients' mean age was 41.59±9.69years and disease duration 5.89±3.67years. The level of vitamin D in RA patients was significantly lower (23.11±12.71ng/mL) than that in the controls (32.59±13.06ng/mL) (P=0.005) being deficient in 50.8%, insufficient in 23.8% and normal in 25.4%. The RA patients with FMS (n=33) had significantly lower levels of vitamin D (19.08±10.59ng/mL) than those without (27.55±13.51ng/mL) (P=0.008). The difference was significant on comparing those receiving hydroxychloroquine (17.39±7.84ng/mL) to those not (31.85±13.85ng/mL) (P<0.001). Vitamin D significantly correlated with QoL index (r=0.58, P<0.001) and negatively with HAQ II (r=-0.36, P=0.004) and BMI (r=-0.39, P=0.001). Special attention is required regarding vitamin D levels in RA patients with FMS and decreased QoL. Vitamin D should be corrected and supplementation considered among the RA management armamentarium.

Increased plasma IL-17F levels in rheumatoid arthritis patients are responsive to methotrexate, anti-TNF, and T cell costimulatory modulation.

The aims of this study are to compare plasma levels of IL17A, A/F, and F biomarkers in RA patients versus controls, and to determine responsiveness to methotrexate (MTX), anti-TNFs, and abatacept. We selected plasma samples from RA cohorts consisting of a cross-sectional RA cohort (N = 78) not receiving DMARDs at the time of sampling, as well as from longitudinal drug start cohorts (N = 71 patients) with pre/post samples including anti-TNF, abatacept, and MTX-treated patients. We assayed IL-17A, IL-17F, and IL17-A/F using a highly sensitive immunoassay system. Plasma levels of IL-17A, IL-17A/F, and IL-17F were all significantly increased in RA versus controls. The difference was largest in IL-17F, with median IL-17F levels in RA patients being approximately 18-fold higher than controls (81 pg/mL in RA vs. 4.4 pg/mL in controls, p < 0.001). Among the forms of IL-17, only IL-17F was decreased after therapy in the MTX cohort (p = 0.006), abatacept cohort (p < 0.001), and anti-TNF cohorts (p = 0.02), whereas IL-17A and IL-17A/F were not significantly decreased for any of the three drug cohorts. Synovial fluid analysis demonstrated higher IL-17F levels in RA (p = 0.016) than healthy controls. These results suggest a specific role for IL-17F in human RA pathogenesis and as a therapeutic target.

The correlation between ferritin level and acute phase parameters in rheumatoid arthritis and systemic lupus erythematosus.

In this study, we evaluated the relationship between ferritin levels and disease activation in rheumatoid arthritis (RA) patients. We included 44 patients with RA, 20 patients with systemic lupus erythematosus (SLE), 25 patients with infection, 22 patients with malignancy, and 20 healthy control subjects. Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), whole blood count, and serum iron parameters were determined in all cases. The joint findings in RA patients were recorded, and disease activity score (DAS) was calculated. In SLE patients, antinuclear antibody (ANA) and anti-dsDNA titers and C3 and C4 complement levels were determined. SLE disease activity index (SLEDAI) score was calculated. Serum ferritin levels in the RA, SLE, and control groups were lower than those in the infection and malignancy groups (p<0.05). The ferritin levels in the RA group did not differ significantly from the SLE and control groups. In RA patients, serum ferritin level had a positive correlation with ESR, CRP, RF, platelet count, and DAS score and had a negative correlation with hematocrit (all p values <0.05). In SLE patients, on the other hand, serum ferritin had a positive correlation with ANA, anti-dsDNA, and SLEDAI (all p values <0.05). According to DAS, ferritin level in inactive RA patients was lower than that in active RA patients. When transferrin saturation was considered, iron deficiency anemia was a quite frequent finding in both active and inactive RA patients. Interestingly, we observed that ferritin level in RA patients was similar to the control group; however, it was a good parameter of disease activation. This is because a reduction in storage iron and resultant iron deficiency anemia are very common in RA patients.

FRI0078 European Pilot Study on Vitamin D Serum Levels and Disease Activity in Rheumatoid Arthritis Patients

BackgroundSeveral studies have demonstrated low 25(OH)D3 serum levels, which could influence pathogenesis and clinical outcomes of immune-mediated diseases such as rheumatoid arthritis (RA) (1,2).ObjectivesIn order to investigate the necessity to...

SAT0198 Relation of Doppler Ultrasound Synovitis versus Clinical Synovitis with Changes in Native Complement Component Levels in Rheumatoid Arthritis Patients Treated with Biologic Disease-Modifying Antirheumatic Drugs

BackgroundThe complement system not only forms part of the innate immunity but also contribute in modulating the adaptive responses [1]. There are evidence suggesting increased level of complement as acute...

AB0070 The Importance of Gliostatin as an Indicator of Disease Activity in Patients with Rheumatoid Arthritis

BackgroundGliostatin (GLS) plays an important role in joint destruction in rheumatoid arthritis (RA). GLS not only has an enzymatic activity as a thymidine phosphorylase but also has angiogenic and arthritogenic...

FRI0292 Efficacy of A Conjugated Pneumococcus Vaccine in Rheumatoid Arthritis Patients Treated with Etanercept

BackgroundStreptococcus pneumoniae is the most common cause of pneumonia. Prevenar 13, a conjugated vaccine has been developed and has been widely used int he adult population due to its high...

AB0270 Serum Sclerostin Level among Egyptian Rheumatoid Arthritis Patients: Relation to Bone Mineral Density, Disease Activity and Radiological Grading

BackgroundBone loss in rheumatoid arthritis (RA) is caused by increased bone resorption, however, there is no increased bone formation1. The Wnt pathway is important in the control of bone formation...

AB0086 IL - 17 Levels with Vitamin D Repletion in Rheuamtoid Arthritis

BackgroundIncreasing scientific evidence implicates a pathogenic role of Th17 cells and associated cytokines in rheumatoid arthritis (RA). Vitamin D may have suppressive effect on Th17 cells. In vitro studies show...

FRI0291 Effects of Tnf-Inhibitors (INFLIXIMAB) on CD147 Expression and MMP-3 Level in Rheumatoid Arthritis Patients

BackgroundTumor necrosis factor (TNF) antagonists are highly effective for the treatment of rheumatoid arthritis (RA), but their mechanisms of action are not completely clear. Increased expression of CD147 on monocytes/macrophages...

AB1022 Involvement of Wrist Extensor Tendons and Joints in Rheumatoid Arthritis Assessed by Ultrasonography

ObjectivesTendinopathy involving the extensor tendons of the wrist is frequent in patients with rheumatoid arthritis (RA) and is common reason of pain in wrist interfering with wrist joints synovitis. Aim...

IL-6 inhibition improves nitric oxide in rheumatoid arthritis

Aim To investigate the serum nitrite levels in patients with active rheumatoid arthritis (RA) after treatment with tocilizumab, an IL-6 antagonist, and to correlate between inflammatory disease activity measures and endothelial dysfunction. Materials and methods Eleven anti-IL-6-naive RA patients with high disease activity (DAS28 &gt;5.1) were investigated. Inflammatory disease activity (DAS28 and HAQ-DI scores, ESR and CRP), serum nitrite concentration and flow mediated dilation (FMD) of the brachial artery were measured before and after 12 weeks of therapy with tocilizumab 8mg/kg intravenous infusion every 4 weeks. Serum nitrite levels and FMD were also estimated in 10 age- and sex- matched healthy controls. Results Serum nitrite levels in RA patients at baseline were significantly higher when compared to healthy volunteers (P &lt;0.01). Level of serum nitrite significantly decreased (P &lt;0.001), inflammatory disease activity measures and FMD significantly improved (P &lt;0.001) after treatment. There was a significant correlation of serum nitrite with FMD, CRP, and DAS 28 both at baseline (P &lt;0.05) and after 12 weeks therapy (P &lt;0.05). Conclusion Nitrite production is enhanced to a greater extent in patients with RA compared to controls. Reduction in nitrite level after treatment is associated with the improvement in disease activity and endothelial dysfunction. Serum nitrite level may serve as a good predictor of both inflammatory disease activity and response to therapy in RA.

Increased serum GP88 (Progranulin) concentrations in rheumatoid arthritis.

GP88 (Progranulin; PGRN) is a secreted glycosylated protein with important functions in several processes, including immune response and cancer growth. Recent reports have shown that PGRN is a therapeutic target for rheumatoid arthritis (RA) because of its capability to bind with tumor necrosis factor receptor (TNFR). However, the serum PGRN level in RA patients has not been investigated. We used enzyme-linked immunosorbent assay (ELISA) to quantify the serum levels of PGRN in 417 healthy subjects, 56 patients with RA and 31 patients with osteoarthritis (OA). In RA patients, we also measured the serum TNF-α and sTNFR concentration. Immunohistochemical staining of PGRN was performed using synovectomy tissue of RA patients. The serum PGRN normal range was established as 40.1 ± 8.7 ng/ml. PGRN levels were not influenced by sex or age. A significant increase in serum PGRN levels was observed in RA (50.2 ± 11.1 ng/ml) and OA (45.4 ± 6.6 ng/ml) groups compared to those in age-matched healthy controls (40.4 ± 9.9 ng/ml) (p<0.05, Tukey). Further, PGRN levels in the synovial fluid of RA patients (68.4 ± 3.4 ng/ml) were found to be significantly higher than those in OA patients (35.9 ± 16.8 ng/ml). Immunohistochemical staining of PGRN revealed that the highest positive signal was detected in macrophages. Circulating PGRN in RA patients was weakly associated with TNF-α and sTNFR 2 concentration. Furthermore, PGRN/TNF-α ratio was correlated the stage of the disease in RA patients. The concentrations of serum PGRN in RA were found to be significantly higher than those in age-matched healthy controls, although it remains to be clarified how blood PGRN is related to the pathogenesis of RA. Our results showed that the serum PGRN may be a useful approach to monitor the disease activity in RA patients.

Weighting with the Lansbury articular index improves the correlation of ultrasound score with serum matrix metalloproteinase-3 level in rheumatoid arthritis patients

Objective. To determine whether weighting improves the correlation of ultrasound (US) score with serum matrix metalloproteinase-3 (MMP-3) level in rheumatoid arthritis (RA).Methods. As ultrasound examination was performed on 100 RA patients, and the severity of synovial effusion and synovial hypertrophy and the blood flow were semi-quantitatively graded from 0 to 3 by using the gray-scale (GS) and power Doppler (PD) modes. We then calculated the sums of the scores of the 28 joints of each patient in the 2 modes, that is, the GS28 and PD28 scores, as well as the respective scores weighted using the Lansbury articular index (LAI, shoulder and elbow, × 12; wrist, × 8; and knee, × 24)—Lans GS28 and Lans PD28 scores.Result. The Lans PD28 score showed a higher correlation with MMP-3 (r = 0.591; 95% confidence interval, 0.446–0.705, p < 0.0001) than the existing measures. The scores of the large joints—the knee, shoulder, and elbow—correlated well with the serum MMP-3 level.Conclusion. Weighting with the LAI can improve the correlation of US findings with serum MMP-3 level. Bidirectional approach based on both serum MMP-3 level and US scores can further improve the assessment of disease activity in RA patients.

Osteoprotegerin (OPG) and Matrix Gla protein (MGP) in rheumatoid arthritis patients: Relation to disease activity

BackgroundImbalanced Matrix Gla protein (MGP) and Osteoprotegerin (OPG) levels occur in inflammatory diseases. Aim of the workThe aim of the present study was to evaluate serum MGP and OPG levels in Rheumatoid Arthritis (RA) patients and study their relation to the disease activity. Patients and methodsForty-five female RA patients and 45 age and sex-matched healthy controls were included in this study. Disease activity score 28-C-reactive protein (DAS28-CRP) was used for the assessment of disease activity. High-sensitivity C-reactive protein (hs-CRP), erythrocyte sedimentation rate (ESR), MGP and OPG were measured in patients and controls. The associations of MGP and OPG with DAS28-CRP and the other laboratory and clinical variables were analyzed. ResultsRA patients had significantly higher serum OPG levels (408.3±520.9pg/ml) and hs-CRP (2.8±1.9mg/l) than the control (92.5±86.3pg/ml and 0.9±1.5mg/l respectively) (p<0.001 each). There was no significant difference in MGP levels between the patients and control (p=0.3). The correlation of OPG and MGP with DAS28-CRP in the patients was insignificant (p=0.4 and p=0.8 respectively). Age positively correlated with OPG (r=0.32, p=0.02), but not with MGP concentration (r=0.05, p=0.64) in the RA patients. ConclusionsThe significant elevation of the OPG level in RA patients may through light on its possible role in the pathogenesis of this disease and could be considered as a future therapeutic target. The significant correlation with age suggests that OPG may be an important mediator especially in elderly RA cases.