Rheumatoid Arthritis: Ho M

Galarraga B, Ho M, Youssef HM, Hill A, McMahon H, Hall C, Ogston S, Nuki G, Belch JJ. · Vascular and Inflammatory Diseases Research Unit, University Division of Medicine and Therapeutics, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK. · Rheumatology (Oxford). · Pubmed #18362100 links to  free full text

Abstract: OBJECTIVES: Dose-dependant gastrointestinal and cardiovascular side-effects limit the use of NSAIDs in the management of RA. The n-3 essential fatty acids (EFAs) have previously demonstrated some anti-inflammatory and NSAID-sparing properties. The objective of this study was to determine whether cod liver oil supplementation helps reduce daily NSAID requirement of patients with RA. METHODS: Dual-centre, double-blind placebo-controlled randomized study of 9 months' duration. Ninety-seven patients with RA were randomized to take either 10 g of cod liver oil containing 2.2 g of n-3 EFAs or air-filled identical placebo capsules. Documentation of NSAID daily requirement, clinical and laboratory parameters of RA disease activity and safety checks were done at 0, 4, 12, 24 and 36 weeks. At 12 weeks, patients were instructed to gradually reduce, and if possible, stop their NSAID intake. Relative reduction of daily NSAID requirement by >30% after 9 months was the primary outcome measure. RESULTS: Fifty-eight patients (60%) completed the study. Out of 49 patients 19 (39%) in the cod liver oil group and out of 48 patients 5 (10%) in the placebo group were able to reduce their daily NSAID requirement by >30% (P = 0.002, chi-squared test). No differences between the groups were observed in the clinical parameters of RA disease activity or in the side-effects observed. CONCLUSIONS: This study suggests that cod liver oil supplements containing n-3 fatty acids can be used as NSAID-sparing agents in RA patients.

Blake DR, Robson P, Ho M, Jubb RW, McCabe CS. · Royal National Hospital for Rheumatic Diseases, Bath BA1 1RL, UK. · Rheumatology (Oxford). · Pubmed #16282192 links to  free full text

Abstract: OBJECTIVES: To assess the efficacy of a cannabis-based medicine (CBM) in the treatment of pain due to rheumatoid arthritis (RA). METHODS: We compared a CBM (Sativex) with placebo in a randomized, double-blind, parallel group study in 58 patients over 5 weeks of treatment. The CBM was administered by oromucosal spray in the evening and assessments were made the following morning. Efficacy outcomes assessed were pain on movement, pain at rest, morning stiffness and sleep quality measured by a numerical rating scale, the Short-Form McGill Pain Questionnaire (SF-MPQ) and the DAS28 measure of disease activity. RESULTS: Seventy-five patients were screened and 58 met the eligibility criteria. Thirty-one were randomized to the CBM and 27 to placebo. Mean (S.D.) daily dose achieved in the final treatment week was 5.4 (0.84) actuations for the CBM and 5.3 (1.18) for placebo. In comparison with placebo, the CBM produced statistically significant improvements in pain on movement, pain at rest, quality of sleep, DAS28 and the SF-MPQ pain at present component. There was no effect on morning stiffness but baseline scores were low. The large majority of adverse effects were mild or moderate, and there were no adverse effect-related withdrawals or serious adverse effects in the active treatment group. CONCLUSIONS: In the first ever controlled trial of a CBM in RA, a significant analgesic effect was observed and disease activity was significantly suppressed following Sativex treatment. Whilst the differences are small and variable across the population, they represent benefits of clinical relevance and show the need for more detailed investigation in this indication.

Shayan K, Ho M, Edwards V, Laxer R, Thorner PS. · Division of Pathology, The Hospital for Sick Children, 555 University Avenue, Toronto, ON M5G 1X8, Canada. · Pediatr Dev Pathol. · Pubmed #15702367 No free full text.

Abstract: At least 25 families with camptodactyly-arthropathy-coxa vara-pericarditis (CACP syndrome) have been reported, with descriptions of a distinctive synovial pathology based largely on light microscopy. Although described as "proliferative," with numerous multinucleated giant cells, the natures of proliferating cells and giant cells have not been determined. To clarify the pathogenesis of this disorder, we studied 3 patients who had CACP syndrome and underwent synovial biopsy. Cells in the biopsies were studied by immunohistochemistry and electron microscopy. Giant cells were identified as macrophage in origin based on CD68 expression and electron microscopic features of macrophages. Most cells in the synovium were CD68 positive, in keeping with macrophages. The degree of proliferation in synovial biopsies was estimated by MIB1 immunostaining, which showed that up to 30% of cells were cycling compared with fewer than 10% in control synovial biopsies. None of the giant cells was cycling. By double immunostaining, proliferating cells were determined to be fibroblastic synoviocytes rather than macrophages. Thus the proliferative synovitis in this CACP syndrome can be more accurately thought of as hypercellularity by infiltrating macrophages with a contribution by proliferating fibroblastic synoviocytes. The synoviocyte proliferation is likely a response to the underlying genetic mutations involving the proteoglycan-4 (or CACP) gene. The encoded protein normally acts as a lubricant and possibly controls cell proliferation. Loss of one or another of these functions may be a possible mechanism that leads to synoviocyte proliferation in this disease, but the exact pathophysiology leading to this change requires further study.

Alkaabi JK, Ho M, Levison R, Pullar T, Belch JJ. · University Department of Medicine, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK. · Rheumatology (Oxford). · Pubmed #12595625 links to  free full text

Abstract: OBJECTIVE: To measure the extent of subclinical atherosclerosis in patients with rheumatoid arthritis (RA) compared with controls, and to evaluate any potential vascular risk factors. METHODS: Forty RA patients were compared with an age- and sex-matched control group. Non-invasive vascular tests, i.e. carotid duplex scanning [measuring common carotid artery intima-media thickness (IMT)], ankle-brachial blood pressure index (ABPI) and QT dispersion on ECG (QTD), were performed. Traditional risk factors such as high blood pressure, blood sugar, lipids and steroid usage were assessed. RESULTS: The average IMT (S.E.) in RA patients was 0.73 (0.03) mm, compared with 0.62 (0.03) mm in the control group (P=0.01, Mann-Whitney). Ten out of 40 RA patients (25%) had an ABPI < 1.0 compared with 1/40 (2.5%) in the control group (P=0.007, Fisher's). QTD was higher in RA patients; mean (S.E.) 55 (2.70) ms compared with 40 (2.50) ms in the control group (P < 0.001, t-test). There were no significant differences in the prevalence of high blood pressure, diabetes or lipid profiles. However, patients on steroids had a higher mean QTD (S.E.): 63.5 (4) compared with 48 (2.7) ms in those patients who had not received long-term steroids (P=0.003, t-test). CONCLUSION: RA patients have an increased risk of subclinical vascular disease as was shown by a higher prevalence of carotid disease, peripheral arterial disease and increased QTD. Among traditional risk factors we found a history of steroid usage to be one of the potential risk factors.

Ho M, Pullar T. · No affiliation provided · Rheumatology (Oxford). · Pubmed #10888715 links to  free full text

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