Rheumatoid Arthritis: Villa AR

Pascual-Ramos V, Contreras-Yañez I, Cabiedes-Contreras J, Rull-Gabayet M, Villa AR, Vázquez-Lamadrid J, Mendoza-Ruiz JJ. · Early Arthritis Clinic, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico. · Ultrasound Q. · Pubmed #19276959 No free full text.

Abstract: To investigate if serial clinical and ultrasound evaluations differ between early rheumatoid arthritis patients who do or do not develop erosive disease and to identify predictors of erosions. METHODS: Patients with at least 7 consecutive 2-monthly clinical and 3 consecutive 6-monthly ultrasound evaluations were included. Ultrasound (gray scale and power Doppler) assessed synovitis, power Doppler-positive synovitis (PD+) and power Doppler-negative synovitis (PD-) in each of 14 joints of the dominant hand. After 1 and 2 years, erosive disease was defined according to digitized radiography. Areas under the curve (AUCs) for serial assessments were calculated. Multivariate logistic regression analysis was performed. RESULTS: Seventy-one and 38 patients completed 1- and 2-year consecutive assessments. After 2 years (21.5 +/- 6.2 months), 13 patients developed erosions. At baseline, nonerosive patients had shorter duration of symptoms to RA diagnosis, lower number of the American College of Rheumatology (ACR) classification criteria, lesser synovitis and PD+ synovitis than erosive patients. At follow-up, erosive and nonerosive patients showed similar AUC for clinical, serological, and treatment parameters; erosive patients had higher AUCs for synovitis and PD+ synovitis than nonerosive patients. In the multivariate model, the amount of PD+ synovitis (odds ratio, 1.3; 95% confidence interval, 1.11-1.51; P = 0.001) and more ACR classification criteria (odds ratio, 2.3; 95% confidence interval, 1.05-5.02; P = 0.04), both at baseline, predicted erosive disease. CONCLUSIONS: Serial Power Doppler ultrasonography-assessed synovitis was greater in patients who developed erosions than in those who did not. More power Doppler positive (hypervascular) synovitis and more ACR classification criteria, both at baseline, were the only predictors of erosions.

Pascual-Ramos V, Contreras-Yáñez I, Villa AR, Cabiedes J, Rull-Gabayet M. · Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Vasco de Quiroga 15-Colonia Sección XVI-Tlalpan, México City 14000, México. · Arthritis Res Ther. · Pubmed #19228421 links to  free full text

Abstract: INTRODUCTION: Aggressive treatment with disease-modifying antirheumatic drugs (DMARDs) plays a major role in improving early rheumatoid arthritis (RA) patient outcomes. Persistence and adherence with medication occurs variably (20% to 70%). The objectives of the study were to determine medication persistence (MP) in early RA patients over 13 consecutive visits each 2 months apart, to investigate the relationship between MP and disease activity, disability and structural damage, and to identify baseline prognosticators. METHODS: Charts from 75 patients of an early RA cohort were reviewed. At each visit, a rheumatologist interviewed patients regarding therapy, scored disease activity with the 28-joint disease activity score (DAS28) and disability with the health assessment questionnaire (HAQ), and recorded comorbidities and treatment. A complete medical history was obtained at baseline. MP was defined as the duration of time from initiation to discontinuation of at least one DMARD and/or corticosteroids for at least 1 week and was reported as a dichotomous variable at consecutive evaluations. Structural damage was defined by detection of new erosions on radiography. Descriptive statistics, Student's t test, the chi-squared test, and logistic regression analyses were used. RESULTS: The proportion of MP patients decreased from 98% at 2 months to 34% at 2 years. MP patients (n = 32) had similar DAS28 to non-MP patients (n = 53) at initial visits, lower DAS28 and greater DAS28 improvements at follow-ups (P < or = 0.05 at visits 4, 6, 7 and 9) and reached sustained remission (> or = 3 consecutive visits with DAS28 < 2.6) more frequently (82.8% versus 46.5%, P = 0.003) and earlier (7.7 +/- 4.6 versus 13.6 +/- 5.7 months, P = 0.001) than non-MP patients. MP patients had similar baseline HAQ scores, but lower HAQ scores at follow-up (P < or = 0.05 at visits 3, 5, 6, 7, 9, 10 and 13). More non-MP patients developed erosive disease than MP patients (26.8% versus 17.9%, P = 0.56). Older age at baseline was associated with therapy discontinuation (odds ratio = 1.1, 95% confidence interval = 1.007 to 1.103, P = 0.02). CONCLUSIONS: Discontinuation of DMARDs was frequent and progressive in an early RA cohort. Patients with persistence on therapy were younger, had lower disease activity and disability during follow-up, and reached sustained remission more frequently and earlier than patients without it. MP should intentionally be evaluated during follow-up of early RA patients, as it seems to play a major role in outcome.

Villa AR, Kraus A, Jiménez-Corona A, Sandino S, Velázquez-González A, Granados J, Alarcón-Segovia D. · The Clinical Epidemiology Unit. · J Clin Rheumatol. · Pubmed #19078467 No free full text.

Abstract: ABSTRACT: Relationships between autoimmune rheumatic diseases and malignant neoplasms have been discussed, but there is no study of the different rheumatic diseases examining the risk of developing cancer. Our study has examined probabilities for developing malignancy among patients with connective tissue diseases seen in a single institution. Patients with autoimmune rheumatic disease and malignancy were compared with patients with the same autoimmune rheumatic diseases without malignancy. All cases identified through record-linkage from 1964 to 1996 were selected. Four controls per case were randomly selected from a pool of 3228 patients. The rheumatic diseases considered were rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), primary Sjögren's syndrome (pSS), dermatomyositis-polymyositis (DM-PM), and systemic sclerosis (Scl). The statistical analysis was conducted by conditional logistic regression, testing rheumatic disease as main effect. We identified 72 cases and 288 controls. Fifty-three of the cases had solid tumors, and 19 had lymphoproliferative neoplasms. The risk of developing a malignancy was considerably higher in DM-PM than in SLE (odds ratio [OR] = 17.5, 95% confidence interval [CI] 4.1-75.7), in pSS than in SLE (OR = 5.7, 95% CI 2.2-15.1), and in Scl than in SLE (OR = 5.4, 95% CI 1.6-18.0). These risks persisted after controlling for rheumatic disease duration, the time the disease was active, and anti-rheumatic treatment. RA had an OR of 1.8 (95% CI 0.9-3.4) with respect to SLE. This is the first study which describes the magnitude of risks among rheumatic diseases associated with the probability of developing a malignant neoplasm whether lymphoproliferative or solid. The risks in this series depend on the primary rheumatic disease, with DM-PM, pSS, and Scl all having greater risk than SLE.

Alarcón-Segovia D, Alarcón-Riquelme ME, Cardiel MH, Caeiro F, Massardo L, Villa AR, Pons-Estel BA, Anonymous00344. · University of Uppsala, Uppsala, Sweden. · Arthritis Rheum. · Pubmed #15818688 links to  free full text

Abstract: OBJECTIVE: To determine whether there is familial aggregation of systemic lupus erythematosus (SLE) and/or other autoimmune diseases in SLE patients and to identify clinical differences between patients with and those without familial autoimmunity. METHODS: We interviewed members of the Grupo Latinoamericano de Estudio del Lupus Eritematoso (GLADEL) inception cohort of 1,214 SLE patients to ascertain whether they had relatives with SLE and/or other autoimmune diseases. Identified relatives were studied. Familial aggregation was tested using reported highest and intermediate population prevalence data for SLE, rheumatoid arthritis (RA), or all autoimmune diseases, and studies were performed to identify the genetic model applicable for SLE. RESULTS: We identified 116 first-, second-, or third-degree relatives with SLE, 79 with RA, 23 with autoimmune thyroiditis, 3 with scleroderma, 1 with polymyositis, and 16 with other autoimmune diseases, related to 166 of the 1,177 SLE patients in the GLADEL cohort who agreed to participate. Forty-two SLE patients had 2 or more relatives with an autoimmune disease. We found a lambda(sibling) of 5.8 and 29.0 for SLE and of 3.2-5.3 for RA, when comparing with their reported high or intermediate population prevalence, respectively. We also found familial aggregation for autoimmune disease in general (lambda(sibling) = 1.5) and determined that for SLE, a polygenic additive genetic model, rather than a multiplicative one, is applicable. CONCLUSION: In SLE there is familial aggregation of SLE, RA, and autoimmune disease in general. A polygenic additive model applies for SLE. American Indian-white Mestizo SLE patients and those with higher socioeconomic level were more likely to have familial autoimmunity.