scholarly journals Disease Activity in Disease Modifying Anti-Rheumatic Drug (DMARD) Naïve Rheumatoid Arthritis Patients in A Subset of Karachi Population

Background: Rheumatoid arthritis (RA) is a progressive inflammatory disease affecting the joints with a marked impact upon functional capacity of the patient. The working ability of RA patients can be preserved if the disease modifying antirheumatic drug (DMARD) therapy is initiated early in the course of disease. The objective of our study was to compare the disease activity variables in DMARD-naïve seropositive rheumatoid arthritis (SPRA) and seronegative rheumatoid arthritis (SNRA) patients and to determine correlations between the disease activity variables in RA. Methods: A cross-sectional study recruited n=90 patients from Rheumatology Clinic from May 2020 to October 2020. The rheumatoid factor (RF), anti-cyclic citrullinated peptide levels (ACCP), erythrocyte sedimentation rates (ESR) were clinically measured. Disease activity variables including the tender joint count (TJC), swollen joint count (SJC), health assessment questionnaire-disability index (HAQ-DI) and disease activity score of 28 joints (DAS28) were consistently calculated. Patients were divided into seropositive RA group and seronegative RA group, based on RF and ACCP. Chi squared test and Pearson correlation were applied, p≤0.05 was considered statistically significant. Results: High HAQ-DI and DAS28-ESR scores were found in SPRA than in the SNRA patients and were statistically significant (p=0.000, p=0.054). TJ-28 and SJ-28 counts were higher in SPRA but were not statistically significant. There was a significant correlation of DAS28 with TJ-28 (r=0.816, p-value = 0.000), with SJ-28(r=0.801, p-value = 0.000) and HAQ-DI (r=0.517, p-value = 0.000). Conclusion: Evaluation of inflammatory markers and functional disability was found significant (p=0.000) in determining the disease activity compared to presence of autoantibodies in DMARD naïve RA patients. Keywords: Disease Modifying Antirheumatic Drug; Arthritis; Rheumatoid Factor; Autoimmune Diseases.

Author(s):  
Małgorzata Łączna ◽  
Damian Malinowski ◽  
Agnieszka Paradowska-Gorycka ◽  
Krzysztof Safranow ◽  
Violetta Dziedziejko ◽  
...  

Abstract Aim Leflunomide is a disease-modifying antirheumatic drug used in therapy for rheumatoid arthritis (RA). Previous studies indicated that oestrogens and androgens may affect the response to leflunomide in RA patients. The synthesis of androgens is regulated by cytochrome CYB5A. The aim of this study was to examine the association between the CYB5A gene rs1790834 polymorphism and the response to leflunomide in women with RA. Methods The study included 111 women diagnosed with RA. Leflunomide was administered in monotherapy at a dose of 20 mg/day. All patients underwent a monthly evaluation for 12 months after the initiation of treatment with leflunomide. Results After 12 months of therapy, the changes in individual disease activity parameters, such as: DAS28, ESR, CRP and VAS, were not statistically significantly different between rs1790834 genotypes in the Kruskal–Wallis test. Conclusions The results of our study suggest lack of statistically significant association between the CYB5A gene rs1790834 polymorphism and the response to leflunomide in women with RA.


2020 ◽  
Vol 39 (7) ◽  
pp. 1271-1278 ◽  
Author(s):  
Rafael Mendonça da Silva Chakr ◽  
João Cláudio de Oliveira Santos ◽  
Laura da Silva Alves ◽  
Nicole Pamplona Bueno Andrade ◽  
Aline Ranzolin ◽  
...  

2009 ◽  
Vol 36 (9) ◽  
pp. 1885-1891 ◽  
Author(s):  
TRINE BAY LAURBERG ◽  
JAN FRYSTYK ◽  
TORKELL ELLINGSEN ◽  
IB T. HANSEN ◽  
ANETTE JØRGENSEN ◽  
...  

Objective.Rheumatoid arthritis (RA) is a systemic chronic inflammatory joint disease, whereas osteoarthritis (OA) is a local joint disease with low-level inflammatory activity. The pathogenic role of the adipocytokine adiponectin is largely unknown in these diseases. We hypothesized (1) that plasma adiponectin concentrations differ in healthy controls and patients with early disease-modifying antirheumatic drug (DMARD)-naive RA, chronic RA, and OA; (2) that changes in adiponectin are observed during methotrexate (MTX) treatment of chronic RA; and (3) that adiponectin correlates to disease activity measures in RA.Methods.Plasma adiponectin was analyzed with a validated in-house immunoassay. We measured adiponectin in healthy controls (n = 45) and patients with early DMARD-naive RA (n = 40), chronic RA (n = 74), and OA (n = 35). In a subgroup of patients with chronic RA (n = 31), the longitudinal effect of MTX treatment on adiponectin (Week 0 vs Week 28) was investigated.Results.Adiponectin differed significantly between healthy controls (mean 4.8 ± SD 2.7 mg/l) and the 3 groups, with 8.9 ± 4.8 mg/l in early RA, 11.6 ± 5.6 mg/l in chronic RA, and 14.1 ± 6.4 mg/l in OA. Longitudinally, MTX treatment increased adiponectin significantly from 9.7 ± 4.5 mg/l at Week 0 to 11.0 ± 4.5 mg/l at Week 28 in chronic RA. No correlations to disease activity measures were found.Conclusion.Both early DMARD-naive and chronic RA were associated with higher plasma adiponectin compared to healthy controls, but lower plasma adiponectin than OA. Adiponectin increased 13% during MTX treatment. In patients with RA and OA body mass index, age, sex, and disease activity measures failed to explain the findings.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 555.1-555
Author(s):  
A. Fazaa ◽  
H. Boussaa ◽  
K. Ouenniche ◽  
S. Miladi ◽  
M. Sellami ◽  
...  

Background:Fatigue is a significant issue in rheumatoid arthritis (RA) with no accepted evidence-based management guidelines. Several studies suggested that biologic Disease Modifying Anti-Rheumatic Drugs (bDMARDs) have a direct role on fatigue in RA.Objectives:This study aimed to compare fatigue between patients treated with bDMARDs and conventional synthetic Disease Modifying Anti-Rheumatic Drugs (cs DMARDs).Methods:We conducted a longitudinal study including patients with RA (ACR/EULAR 2010). Patients with other acute or chronic diseases that may induce fatigue (such as cancer, infection or depression) were excluded. Demographic data and the following disease-related parameters were collected: pain Visual Analog Scale (VAS), Global Patient Assessment (GPA), tender joint count (TJC), swollen joint count (SJC), Erythrocyte Sedimentation Rate (ESR), C Protein Reactive (CRP), Disease Activity Score 28 (DAS28), Health Assessment Questionnaire (HAQ) and DMARDs used. Fatigue was assessed at baseline (T0), at 6 months (T6) and at 12months (T12) using the Functional Assessment of Chronic Illness Therapy – Fatigue (FACIT-F) which is a short 13-item questionnaire validated in RA. The score FACIT-F ranges between 0 and 52. Fatigue was considered mild if the FACIT-F score was ≥40, moderate if 20≤FACIT-F<40 and severe if 0≤FACIT-F<20. A p value inferior to 0.05 was considered significant.Results:We included 100 RA patients (84 women and 16 men) with a mean age of 49.5±10 years old [18-65]. The mean disease duration was 87.3 months [1-360]. The mean pain VAS was 49 cm [0-100] and the mean GPA was 47.8 cm [0-100]. The mean TJC and SJC were 5.3 [0-36] and 1 [0-9] respectively. The mean levels of ESR and CRP were 38.1 mm [10-120] and 10.8 mg/l [2-61] respectively. The mean DAS28 ESR was 3.68 [1.90-8.33] and the mean HAQ score was 0.90 [0-2.75].Eighty-three percent of patients used csDMARDs: Methotrexate (n=96), sulphasalazine (n=28), leflunomide (n=21), and hydroxychloroquine (n=12). bDMARDs were prescribed in 17% of patients: Rituximab (n=10), Infliximab (n=9), and Etanercept (n=5).At baseline, the mean FACIT-F score was 27.1 [0-51]. Moderate fatigue was noted in 57% of cases and severe fatigue in 26% of cases. Patients on csDMARDs had a lower FACIT-F score when compared to patients on bDMARDs (26.89 versus 28.41), but the difference was not statistically significant (p=0.630).The mean FACIT-F score was 27.41 in bDMARDs patients versus 29.80 in csDMARDs patients (p=0.497) at T6, and 32.35 versus 33.65 respectively at T12 (p=0.695).The mean delta FACIT-F was 2.18 in bDMARDs patiens versus 2.73 in csDMARDs patients between T6 and T0 (p=0.815), and 3.94 versus 7.2 respectively between T12 and T0 (p=0.807).When considering all patients, a significant positive correlation was noted between delta FACIT-F and delta DAS28 at T6 (r=0.418, p<0.001) and at T12 (r=0.338, p<0.001).Conclusion:RA patients treated with bDMARDs didn’t show significant improvement of fatigue in comparison with those treated with csDMARDs. Further studies are needed to determine if biologics improve fatigue, and whether the improvement results from a direct action on fatigue or indirectly through reduction in disease activity.Disclosure of Interests:None declared


2020 ◽  
Vol 79 (11) ◽  
pp. 1414-1422 ◽  
Author(s):  
Sven Plein ◽  
Bara Erhayiem ◽  
Graham Fent ◽  
Sarah Horton ◽  
Raluca Bianca Dumitru ◽  
...  

ObjectivesTo determine whether patients with early rheumatoid arthritis (ERA) have cardiovascular disease (CVD) that is modifiable with disease-modifying antirheumatic drug (DMARD) therapy, comparing first-line etanercept (ETN) + methotrexate (MTX) with MTX strategy.MethodsPatients from a phase IV ERA trial randomised to ETN+MTX or MTX strategy±month 6 escalation to ETN+MTX, and with no CVD and maximum one traditional risk factor underwent cardiovascular magnetic resonance (CMR) at baseline, years 1 and 2. Thirty matched controls underwent CMR. Primary outcome measure was aortic distensibility (AD) between controls and ERA, and baseline to year 1 AD change in ERA. Secondary analyses between and within ERA groups performed. Additional outcome measures included left ventricular (LV) mass and myocardial extracellular volume (ECV).ResultsEighty-one patients recruited. In ERA versus controls, respectively, baseline (geometric mean, 95% CI) AD was significantly lower (3.0×10−3 mm Hg−1 (2.7–3.3) vs 4.4×10−3 mm Hg−1 (3.7–5.2), p<0.001); LV mass significantly lower (78.2 g (74.0–82.7), n=81 vs 92.9 g (84.8–101.7), n=30, p<0.01); and ECV increased (27.1% (26.4–27.9), n=78 vs 24.9% (23.8–26.1), n=30, p<0.01). Across all patients, AD improved significantly from baseline to year 1 (3.0×10−3 mm Hg−1 (2.7–3.4) to 3.6×10–3 mm Hg−1 (3.1–4.1), respectively, p<0.01), maintained at year 2. The improvement in AD did not differ between the two treatment arms and disease activity state (Disease Activity Score with 28 joint count)-erythrocyte sedimentation rate-defined responders versus non-responders.ConclusionWe report the first evidence of vascular and myocardial abnormalities in an ERA randomised controlled trial cohort and show improvement with DMARD therapy. The type of DMARD (first-line tumour necrosis factor-inhibitors or MTX) and clinical response to therapy did not affect CVD markers.Trial registration numberISRCTN: ISRCTN89222125; ClinicalTrials.gov: NCT01295151.


2014 ◽  
Vol 41 (2) ◽  
pp. 216-226 ◽  
Author(s):  
Edward C. Keystone ◽  
Andrew Anisfeld ◽  
Sarika Ogale ◽  
Jenny N. Devenport ◽  
Jeffrey R. Curtis

Objective.To evaluate whether patients with rheumatoid arthritis who did not respond sufficiently to tocilizumab (TCZ) plus disease-modifying antirheumatic drug (DMARD) treatment by Week 8 responded at later timepoints when continuing to take their original dose of TCZ.Methods.In this posthoc analysis of data from phase III randomized controlled trials of inadequate responders (IR) to DMARD or tumor necrosis factor-α inhibitors (anti-TNF), percentages of patients meeting early response criteria were calculated by randomized treatment arm (TCZ 4 mg/kg, 8 mg/kg, or placebo in combination with DMARD). Percentages of patients achieving certain disease activity thresholds at later timepoints were calculated for patients who had/had not achieved response by Week 8.Results.In DMARD-IR early nonresponders, 29.0%, 17.2%, and 3.7% of TCZ 8 mg/kg-randomized, TCZ 4 mg/kg-randomized, and placebo-randomized patients, respectively, achieved 28-joint Disease Activity Score (DAS28) ≤ 3.2 by Week 24. Among anti-TNF-IR patients without early response, 26.5%, 8.5%, and 1.9% of TCZ 8 mg/kg-randomized, TCZ 4 mg/kg-randomized, and placebo-randomized patients, respectively, achieved DAS28 ≤ 3.2 at Week 24.Conclusion.A substantial number of DMARD-IR patients taking TCZ 4 or 8 mg/kg and anti-TNF-IR patients taking TCZ 8 mg/kg who failed to respond by 8 weeks benefited from continued TCZ treatment in combination with DMARD. In contrast, the anti-TNF-IR patients without early responses who continued to take TCZ 4 mg/kg were unlikely to experience a cumulative benefit. ClinicalTrials.gov registration numbers: NCT00106548, NCT00106574, NCT00106535, NCT00106522.


2015 ◽  
Vol 42 (10) ◽  
pp. 1752-1760 ◽  
Author(s):  
Mark C. Genovese ◽  
Elizabeth Hsia ◽  
Stanley M. Belkowski ◽  
Caly Chien ◽  
Tara Masterson ◽  
...  

Objective.To assess the efficacy and safety of JNJ-40346527, a selective inhibitor of colony-stimulating factor-1 (CSF-1) receptor kinase that acts to inhibit macrophage survival, proliferation, and differentiation in patients with active rheumatoid arthritis (RA) despite disease-modifying antirheumatic drug (DMARD) therapy.Methods.In this randomized, double-blind, placebo-controlled, parallel group study, adults were randomized (2:1) to receive oral JNJ-40346527 100 mg or placebo twice daily through Week 12. Patients with RA had disease activity [≥ 6 swollen/≥ 6 tender joints, C-reactive protein (CRP) ≥ 0.8 mg/dl] despite DMARD therapy for ≥ 6 months. The primary endpoint was change from baseline at Week 12 in the 28-joint Disease Activity Score with CRP (DAS28-CRP). Pharmacokinetic/pharmacodynamic analyses were also performed, and safety was assessed through Week 16.Results.Ninety-five patients were treated (63 JNJ-40346527, 32 placebo); 8 patients discontinued treatment (6 JNJ-40346527, 2 placebo) through Week 12. Mean improvements in DAS28-CRP from baseline to Week 12 were 1.15 for the JNJ-40346527 group and 1.42 for the placebo group (p = 0.30); thus, a statistically significant difference was not observed for the primary endpoint. Pharmacokinetic exposure to JNJ-40346527 and its active metabolites was above the projected concentration needed for pharmacologic activity, and effective target engagement and proof of activity were demonstrated by increased levels of CSF-1 and decreased CD16+ monocytes in JNJ-40346527–treated, but not placebo-treated, patients. Thirty-seven (58.7%) JNJ-40346527–treated and 16 (50.0%) placebo-treated patients reported ≥ 1 adverse event (AE); 1 (1.6%) JNJ-40346527–treated and 3 (9.4%) placebo-treated patients reported ≥ 1 serious AE.Conclusion.Although adequate exposure and effective peripheral target engagement were evident, JNJ-40346527 efficacy was not observed in patients with DMARD-refractory active RA. ClinicalTrials.gov identifier: NCT01597739. EudraCT Number: 2011-004529-28.


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