Rheumatoid Arthritis: Bernard-Medina AG

Vázquez-Del MM, Muñoz-Valle JF, Santos A, Bernard-Medina AG, Martínez-Bonilla G, Paczka JA, Ruiz-García H, Orozco-Alcalá J, Orozco-Barocio G, Quezada-Arellano D, Gurrola-Díaz C, Nuño-González P, Best-Aguilera CR, Chávez-Castellanos R, Panduro A. · Instituto de Biología Molecular en Medicina, C.U.C.S., U. de G., México. · Scand J Rheumatol. · Pubmed #11922198 No free full text.

Abstract: OBJECTIVE: To investigate the effect of APO E gene polymorphism over lipid profile, macular toxicity and clinical manifestations in RA and SLE patients treated with chloroquine. MATERIALS AND METHODS: We studied 45 RA and 29 SLE patients treated with chloroquine who were classified based on the therapeutic regime of chloroquine into three groups: A) Cumulative dose of 100-300 g, B) >300 g and C) Never received chloroquine. Clinical evaluation, fasting lipid profile, visual field testing and stereoscopic photos of the retina were performed. APO E genotype was determined by PCR-RFLP. RESULTS: Reduced apo B levels in RA and SLE according to the cumulative dose of chloroquine 2/3 APO E genotype in a subset of SLE patients were observed. Macular toxicity was independent of both APO E genotype and cumulative chloroquine dose. CONCLUSIONS: Reduced apo B levels were observed associated to chloroquine treatment and 2/3 APO E genotype.

Torres-Carrillo N, Torres-Carrillo NM, Martínez-Bonilla GE, Vázquez-Del Mercado M, Palafox-Sánchez CA, Oregón-Romero E, Bernard-Medina AG, Rangel-Villalobos H, Muñoz-Valle JF. · Departamento de Biología Molecular y Genómica, Instituto de Investigación en Reumatología y del Sistema Músculo Esquelético, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico. · Clin Exp Med. · Pubmed #19238514 No free full text.

Abstract: Plasminogen activator inhibitor type 1 (PAI-1) is an inhibitor of plasmin production. Plasmin can directly or indirectly to degrade cartilage and bone matrix. The PAI-1 HindIII polymorphism has been associated with high PAI-1 plasma levels in myocardial infarction patients and control populations. Furthermore, it has been associated with the angiographic extent of coronary artery disease, but their involvement in other diseases is still uncertain. Here, we assessed the relationship between PAI-1 HindIII polymorphism and PAI-1 plasma levels in rheumatoid arthritis (RA). One hundred and twenty-five RA patients and 132 control subjects (CS) were included. Genotypes were identified by the polymerase chain reaction-restriction fragment length polymorphism technique and PAI-1 plasma levels were quantified using an ELISA kit. Not significant differences in genotype and allele frequencies between both studied groups were observed (P > 0.05). RA patients showed lower PAI-1 plasma levels (18.92 +/- 12.94 ng/ml) than CS (23.68 +/- 23.38 ng/ml), without significant difference (P = 0.299). However, in RA patients the C/G genotype carriers showed higher PAI-1 plasma levels (23.00 +/- 13.81 ng/ml) with respect to C/C (16.77 +/- 11.97 ng/ml) and G/G (10.47 +/- 7.07 ng/ml) genotype carriers (P = 0.036). The PAI-1 HindIII polymorphism was not associated with RA susceptibility. However, the C/G genotype is associated with high PAI-1 plasma levels in RA patients.

Oregón-Romero E, Vázquez-Del Mercado M, Ruiz-Quezada SL, Navarro-Hernández RE, Rangel-Villalobos H, Martínez-Bonilla G, Bernard-Medina AG, Armendáriz-Borunda J, García-Bañuelos J, Muñoz-Valle JF. · Instituto de Investigación en Reumatología y del Sistema Músculo Esquelético, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Jalisco, México. · J Investig Med. · Pubmed #18797411 No free full text.

Abstract: BACKGROUND: Rheumatoid arthritis (RA) is characterized by a progressive joint damage mediated mainly by tumor necrosis factor alpha (TNFalpha). We investigated the relationship of TNFalpha-308 and -238 polymorphisms with messenger RNA (mRNA) expression and soluble TNFalpha (sTNFalpha) in 50 RA and 100 healthy subjects (HS). METHODS: Clinical and laboratory assessments were performed. Spanish Health Assessment Questionnaire Disability Index, Spanish version of Arthritis Impact Measurement Scales and Disease Activity Score using 28 joint count indices were applied to RA patients. The TNFalpha-308 and -238 polymorphisms were performed by polymerase chain reaction and restriction fragment length polymorphism techniques. The mRNA expression of TNFalpha was quantified by real-time polymerase chain reaction. The sTNFalpha levels were measured by enzyme-linked immunosorbent assay. RESULTS: The TNFalpha-308 polymorphism showed an increased frequency of guanine (G)/adenine (A) genotype in RA versus HS (P = 0.03; 95% confidence interval, 1.05-8.08; odds ratio, 2.9) and also the A allele was more frequent in RA patients versus HS (P = 0.04; 95% confidence interval, 1.01-7.29; odds ratio, 2.7). The G/G genotype and also the G allele were more frequent in HS. No significant difference was observed in TNFalpha-238 polymorphism. Rheumatoid arthritis patients showed high TNFalpha mRNA expression (1.33-fold). The G/G genotype was associated with high mRNA and sTNFalpha levels in both TNFalpha polymorphisms. The correlation of sTNFalpha levels with C-reactive protein, erythrocyte sedimentation rate, rheumatoid factor, Spanish Health Assessment Questionnaire Disability Index, and Spanish version of Arthritis Impact Measurement Scales, was observed. CONCLUSION: The TNFalpha-308 polymorphism is a susceptibility marker to RA. The G/G genotype is associated with a high mRNA and soluble TNFalpha expression.

Mould-Quevedo J, Peláez-Ballestas I, Vázquez-Mellado J, Terán-Estrada L, Esquivel-Valerio J, Ventura-Ríos L, Aceves-Avila FJ, Bernard-Medina AG, Goycochea-Robles MV, Hernández-Garduño A, Burgos-Vargas R, Shumski C, Garza-Elizondo M, Ramos-Remus C, Espinoza-Villalpando J, Alvarez-Hernández E, Flores-Alvarado D, Rodríguez-Amado J, Casasola-Vargas J, Skinner-Taylor C, Anonymous00077. · Unidad de Investigación en Economía de la Salud, Instituto Mexicano del Seguro Social, México D.F., México. · Gac Med Mex. · Pubmed #18714591 No free full text.

Abstract: OBJECTIVE: To estimate the social costs of rheumatoid arthritis (RA), ankylosing spondylitis (AS), and gout from the patient's perspective. METHODS: We carried out a cross-sectional analysis of the cost and resource utilization of 690 RA, AS, and gout patients from 10 medical centers and private facilities in five cities of Mexico. The information was obtained from the baseline of a dynamic cohort. We estimated out-of-pocket expenses, institutional direct costs, and direct medical costs. RESULTS: The mean (SD) annual out-of-pocket expense (USD) was $610.0 ($302.2) for RA, $578.6 ($220.5) for AS, and $245.3 ($124.0) for gout. Figures correspond to 15%, 9.6%, and 2.5% of the family income. They also represented 26.1%, 25.3%, and 24.4% of the total annual cost per RA, AS, and gout patients, respectively. The expected direct institutional patient/year costs were 1,724.2 for RA, $1,710.8 for AS, and $760.7 for gout. The total patient annual costs were $2,334.3 for RA, $2,289.4 for AS, and $1,006.1 for gout. Most out-of-pocket expenses were used to purchase drugs, pay for laboratory tests, imaging studies, and alternative therapies. CONCLUSIONS: From the patient's perspective, the cost of RA, AS, and gout represents 25% of direct medical costs. The cost of RA is higher than that for AS and gout.