Rheumatoid Arthritis: Mugnier B

Poullin P, Announ N, Mugnier B, Guis S, Roudier J, Lefèvre P. · No affiliation provided · Joint Bone Spine. · Pubmed #15797486 No free full text.

This publication has no abstract.

Mugnier B, Roudier J. · No affiliation provided · Joint Bone Spine. · Pubmed #15050192 No free full text.

This publication has no abstract.

Mugnier B, Bouvenot G. · Service de rhumatologie, hôpital de la Conception, Marseille, France. · Rev Med Interne. · Pubmed #11075394 No free full text.

Abstract: INTRODUCTION: Current slow-acting anti-rheumatic drugs available for rheumatoid arthritis can fail for certain severe cases; some are used empirically. Improvements in our knowledge of its pathogenesis and advances in molecular biology have made it possible to develop partially selective immunotherapy approaches. CURRENT KNOWLEDGE AND KEY POINTS: Tumor necrosis factor-alpha (TNF-alpha) is a critical inflammatory mediator in rheumatoid arthritis and may therefore be a useful target for specific immunotherapy. This article summarizes clinical studies using anti-TNF-alpha antibodies. It appears that there is good evidence for both safety and beneficial effects of anti-TNF-alpha antibodies in short-term treatment of rheumatoid arthritis. FUTURE PROSPECTS AND PROJECTS: It remains to be determined whether specific blockade of a single inflammatory mediator may be useful in long-term management. Therapeutic strategies aimed at concomitantly interfering with multiple pathogenic pathways are currently under investigation.

Mugnier B, Balandraud N, Darque A, Roudier C, Roudier J, Reviron D. · INSERM EMI 9940, Hôpital La Conception, APHM, and Etablissement Français du Sang-Alpes-Méditerranée, Marseille, France. · Arthritis Rheum. · Pubmed #12847678 links to  free full text

Abstract: OBJECTIVE: To test whether the G-to-A polymorphism at position -308 in the promoter of the tumor necrosis factor alpha (TNFalpha) gene influences response to infliximab therapy in patients with rheumatoid arthritis (RA). METHODS: We genotyped 59 RA patients by polymerase chain reaction and subdivided them into two groups: those with the A/A or A/G genotype and those with the G/G genotype. We compared the groups' clinical responses to infliximab treatment after 22 weeks, using the Disease Activity Score in 28 joints (DAS28). RESULTS: We found that 42% of patients in the A/A and A/G group and 81% of patients in the G/G group had improvement of at least 1.2 in the DAS28 score (P = 0.0086). The average improvement in the DAS28 score was 1.24 in the A/A and A/G patients and 2.29 in the G/G patients (P = 0.029). CONCLUSION: These data suggest that patients with a TNFalpha -308G/G genotype are better infliximab responders than are patients with A/A or A/G genotypes. TNFalpha -308 genotyping may be a useful tool for predicting response to infliximab treatment.

Guis S, Balandraud N, Bouvenot J, Auger I, Toussirot E, Wendling D, Mattei JP, Nogueira L, Mugnier B, Legeron P, Landt O, Serre G, Roudier J, Roudier C. · INSERM UMR 639 and Assistance Publique Hôpitaux de Paris, Hôpital de la Conception, Marseille, France. · Arthritis Rheum. · Pubmed #18050183 links to  free full text

Abstract: OBJECTIVE: To determine whether the -308 A/G tumor necrosis factor alpha (TNFalpha) gene polymorphism can predict the outcome of etanercept therapy in 86 patients with rheumatoid arthritis (RA), as already observed in patients treated with infliximab. METHODS: Eighty-six RA patients treated with etanercept were genotyped for -308 A/G TNFalpha gene polymorphism by polymerase chain reaction and melting curve analysis, using specific gene primers and probes. Patients were subdivided into group A (G/A genotype) and group G (G/G genotype). We compared clinical responses to etanercept between groups A and G after 6 months, using the Disease Activity Score in 28 joints (DAS28). After 12-month treatment, 48 of 86 patients were evaluated again. RESULTS: Of 86 patients, 18 (21%) belonged in group A and 68 (79%) belonged in group G. After 6-month treatment, 55.6% of patients in group A and 82.4% of patients in group G had DAS28 improvement >1.2 (P = 0.027 by chi-square). The mean +/- SD DAS28 improvement was 1.69 +/- 1.31 in group A and 2.23 +/- 1.19 in group G (P = 0.098 by t-test). After 1-year treatment 48 patients were tested again: 10 (21%) belonged in group A and 38 (79%) belonged in group G. Forty percent of patients in group A and 87% in group G had DAS28 improvement >1.2 (P = 0.005 by chi-square). The mean +/- SD DAS28 improvement was 1.334 +/- 1.37 in group A and 2.29 +/- 1.47 in group G (Mann-Whitney U test = 115, P = 0.0057). CONCLUSION: RA patients with a -308 G/G TNFalpha genotype respond to etanercept better than patients with a -308 A/G genotype.

Mugnier B, Poullin P, Lefevre P, Roudier J. · Hôpital de la Conception, Marseille, France. · Arthritis Rheum. · Pubmed #14558061 links to  free full text

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Balandraud N, Meynard JB, Auger I, Sovran H, Mugnier B, Reviron D, Roudier J, Roudier C. · INSERM EMI9940, and Hôpital La Conception, Marseilles, France. · Arthritis Rheum. · Pubmed #12746895 links to  free full text

Abstract: OBJECTIVE: To determine whether patients with rheumatoid arthritis (RA) have elevated Epstein-Barr virus (EBV) load in their peripheral blood mononuclear cells (PBMCs) and whether it is correlated with the HLA-DR genes they express, we developed an accurate EBV DNA quantitative assay using real-time polymerase chain reaction (PCR) with fluorescent probes. METHODS: We studied the EBV DNA load in the PBMCs of 84 patients with RA, 69 normal controls, and 22 patients with rheumatic conditions other than RA. A 214-bp segment from the long internal repeat of EBV was amplified from 500 ng of PBMC DNA (150,000 cells) and quantified by real-time PCR with fluorescent probes. RESULTS: We demonstrated that in patients with RA, the EBV DNA load in PBMCs is increased almost 10-fold compared with that in normal controls. The EBV load is stable over time and is not obviously influenced by disease-modifying antirheumatic drugs or HLA-DR. CONCLUSION: Patients with RA have elevated EBV load in their peripheral blood.

Mugnier B, Roudier J. · No affiliation provided · Arthritis Rheum. · Pubmed #15593229 links to  free full text

This publication has no abstract.