Evaluation of a simple articular index for joint tenderness in rheumatoid arthritis.

Ritchie, David A.; Boyle, J A; McInnes, J M; Jasani, M K; Dalakos, Theodore G.; Grieveson, Phillida; Buchanan, W. Watson

doi:10.1136/ard.28.2.196-a

Cited by 44 publications

(41 citation statements)

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“…Eight control examinations were planned (at baseline, on day 15, and at months 1, 2, 4, 6, 9, and 12). Eficacy monitoring was based on clinical parameters (number of tender and swollen joints, duration of morning stiffness, grip strength, pain assessment using a 100-mm visual analog scale (31), Ritchie articular index score [32], and Lee functional index score [33]), and on laboratory parameters (ESR, Creactive protein [CRP] levels, and rheumatoid factor as assayed at baseline and at months 6 and 12). Safety monitoring was based on evaluation of blood pressure and measurements of hemoglobin, differential leukocyte counts, platelets, transaminases, total bilirubin, alkaline phosphatase, serum creatinine, blood urea nitrogen, electrolytes, uric acid, and urinalysis.…”

Section: Methodsmentioning

confidence: 99%

Slow progression of joint damage in early rheumatoid arthritis treated with cyclosporin a

Pasero

Priolo

Marubini

et al. 1996

Arthritis & Rheumatism

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Objective. To evaluate the ability of low‐dose cyclosporin A (CsA) to control radiologic disease progression, and to assess the clinical efficacy and tolerability of CsA, compared with conventional disease‐modifying antirheumatic drugs (DMARDs), in patients with early active rheumatoid arthritis (RA). Methods. In this long‐term, multicenter, prospective, open, blinded end point, randomized trial, 361 consenting patients with early (< 4 years since diagnosis) active RA were enrolled. Of the eligible patients, 167 were treated with CsA at 3 mg/kg/day, and 173 with DMARDs. The decision to use conventional antirheumatic drugs as controls was based on the fact that joint erosion could be expected to occur after 1 year regardless of the type of DMARD being used. The possibility of switching therapies in both groups was intended to keep the largest possible number of patients in the study. Results. Blinded evaluation of hand and foot radiographs after 12 months of treatment showed that CsA led to a significant (P < 0.001) delay in the mean ± SD progression in the eroded joint count (1.3 ± 3.1 versus 2.4 ± 3.0 for the control group) and in the joint damage score (3.6 ± 8.9 versus 6.9 ± 9.1 for the control group), both measured by the Larsen‐Dale method. When only the patients without erosion at baseline were considered (37 in the CsA‐treated group and 54 in the control group), erosion appeared in only 10.8% of the CsA‐treated patients, but in 51.8% of the controls (P = 0.00005). Low‐dose CsA was as effective as traditional DMARDs in controlling clinical symptoms. Maintenance on the initially prescribed treatment regimen (“survival on treatment”) was also better at 12 months with CsA than with DMARDs (89.2% versus 77.5%; P = 0.002). The tolerability of CsA was acceptable. Conclusion. These 12‐month results suggest that low‐dose CsA decreases the rate of further joint damage in previously involved joints as well as the rate of new joint involvement in previously uninvolved joints, in patients with early RA.

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Section: Methodsmentioning

confidence: 99%

Slow progression of joint damage in early rheumatoid arthritis treated with cyclosporin a

Pasero

Priolo

Marubini

et al. 1996

Arthritis & Rheumatism

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“…Criteria were ranked at the outset of the study, in order of importance for evaluation. The following features were assessed at baseline and after 3,6,9, and 12 months: physician's global assessment of disease activity (0-4 scale, 0 = symptom-free and 4 = very severe), patient's global assessment of disease activity (0-10-cm visual analog scale, 0 = symptom-free and 10 = very severe), physician's and patient's assessment of pain (0-4 scale, 0 = no pain and 4 = very severe), duration of morning stiffness (in minutes), grip strength (in mm Hg; mean of 3 measurements), Ritchie articular index for pain (22) (60 joints; scored 0-3 for each joint, 0 = no pain and 3 = very severe), number of painful joints and number of swollen joints (maximum of 60 each), and concomitant medications (NSAIDs and/or DMARDs).…”

Section: Methodsmentioning

confidence: 99%

Long‐term effect of omega‐3 fatty acid supplementation in active rheumatoid arthritis

Geusens

Wouters

Nijs

et al. 1994

Arthritis & Rheumatism

235

108

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Objective. To study the long-term effects of supplementation with omega-3 fatty acids (03) in patients with active rheumatoid arthritis.Methods. Ninety patients were enrolled in a 12-month, double-blind, randomized study comparing daily supplementations with either 2.6 gm of 03, or 1.3 gm of 0 3 + 3 gm of olive oil, or 6 gm of olive oil.Results. Significant improvement in the patient's global evaluation and in the physician's assessment of pain was observed only in those taking 2.6 gdday of d. The proportions of patients who improved and of those who were able to reduce their concomitant antirheumatic medications were significantly greater with 2.6 gmlday of 03.Conclusion. Daily supplementation with 2.6 gm of 0 3 results in significant clinical benefit and may reduce the need for concomitant antirheumatic medication.

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“…However, this conclusion may be flawed, because of the inappropriate manner in which studies were combined and because of Approx, approximately; NSAID, non-steroidal anti-inflammatory drugs. *Based on the summation of a number of quantitative evaluations of the pain experienced by the patient when the joints were subjected to pressures when exerted over the articular margin or in some instances on movement of the joint (106) .…”

Section: Trials Of N-3 Pufa In Rheumatoid Arthritismentioning

confidence: 99%

Session 3: Joint Nutrition Society and Irish Nutrition and Dietetic Institute Symposium on ‘Nutrition and autoimmune disease’ PUFA, inflammatory processes and rheumatoid arthritis

Calder

2008

Proc. Nutr. Soc.

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Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease manifested by swollen and painful joints, bone erosion and functional impairment. The joint lesions are characterised by infiltration of T lymphocytes, macrophages and B lymphocytes into the synovium and by synovial inflammation involving eicosanoids, cytokines and matrix metalloproteinases. In relation to inflammatory processes, the main fatty acids of interest are the n-6 PUFA arachidonic acid, which is the precursor of inflammatory eicosanoids such as PGE2 and leukotriene B4, and the n-3 PUFA EPA and DHA, which are found in oily fish and fish oils. Eicosanoids derived from the n-6 PUFA arachidonic acid play a role in RA, and the efficacy of non-steroidal anti-inflammatory drugs in RA indicates the importance of pro-inflammatory cyclooxygenase pathway products of arachidonic acid in the pathophysiology of the disease. EPA and DHA inhibit arachidonic acid metabolism to inflammatory eicosanoids. EPA also gives rise to eicosanoid mediators that are less inflammatory than those produced from arachidonic acid and both EPA and DHA give rise to resolvins that are anti-inflammatory and inflammation resolving. In addition to modifying the lipid mediator profile, n-3 PUFA exert effects on other aspects of immunity relevant to RA such as antigen presentation, T-cell reactivity and inflammatory cytokine production. Fish oil has been shown to slow the development of arthritis in an animal model and to reduce disease severity. Randomised clinical trials have demonstrated a range of clinical benefits in patients with RA that include reducing pain, duration of morning stiffness and use of non-steroidal anti-inflammatory drugs.

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Evaluation of a simple articular index for joint tenderness in rheumatoid arthritis.

Cited by 44 publications

References 0 publications

Slow progression of joint damage in early rheumatoid arthritis treated with cyclosporin a

Slow progression of joint damage in early rheumatoid arthritis treated with cyclosporin a

Long‐term effect of omega‐3 fatty acid supplementation in active rheumatoid arthritis

Session 3: Joint Nutrition Society and Irish Nutrition and Dietetic Institute Symposium on ‘Nutrition and autoimmune disease’ PUFA, inflammatory processes and rheumatoid arthritis

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