RESUMEN
OBJECTIVE: To determine the ability of the revised version of the Childhood Health Assessment Questionnaire (CHAQ), the VASCHAQ, to detect clinical change over time in pediatric patients with juvenile idiopathic arthritis (JIA). We studied the relative responsiveness of the VASCHAQ as compared to the original CHAQ-30 and revised CHAQ-38, as well as the parent-patient, physician-patient, and physician-parent concordance. METHODS: The CHAQ-38 and VASCHAQ were administered to 30 parents and patients (if older than 8 years) with any subtype of JIA before and after the start of a new treatment. The standardized response means (SRM) were calculated for the VASCHAQ, the original CHAQ-30, and the CHAQ-38. Comparisons of SRM were made using the relative SRM. Parent-patient, physician-patient, and physician-parent concordances were assessed by calculating a series of intraclass correlation coefficients. RESULTS: Twenty-seven parents and 21 patients completed questionnaires at both visits. All questionnaires demonstrated large responsiveness; however, the VASCHAQ was found to be about 25% more responsive than both the original CHAQ-30 and CHAQ-38. CONCLUSION: The VASCHAQ was moderately more responsive than the CHAQ-30 and CHAQ-38 in both parent and patient groups and should be considered for use in studies evaluating change in function over time.
Asunto(s)
Artritis Juvenil/diagnóstico , Estado de Salud , Encuestas y Cuestionarios , Adolescente , Niño , Preescolar , Evaluación de la Discapacidad , Progresión de la Enfermedad , Femenino , Humanos , Masculino , Examen Físico , Calidad de Vida , Evaluación de Síntomas , Adulto JovenRESUMEN
Lipid peroxidation has been implicated in the pathogenesis of a number of diseases, including neurodegenerative disorders. Evidence that antioxidants can affect the clinical course of neurodegenerative diseases is limited. In the present study, we examined the ability of five common antioxidants or antioxidant combinations, alpha-tocopherol, gamma-tocopherol, ascorbic acid, GSH ethyl ester, and a combination of ascorbate and alpha-tocopherol, to modulate lipid peroxidation in peroxidizing rat cerebral synaptosomes, a well-characterized model of oxidant injury. In these studies, we quantified isoprostanes (IsoPs) derived from arachidonic acid as an index of whole tissue oxidation and neuroprostanes (NeuroPs) formed from docosahexaenoic acid as a marker of selective neuronal peroxidation. We report that these various antioxidants displayed markedly different capacities to inhibit IsoP and NeuroP formation with the most potent effects on IsoPs observed for ascorbate, GSH ethyl ester, and the alpha-tocopherol-ascorbate combination. alpha-Tocopherol was slightly less potent and gamma-tocopherol significantly less effective. The concentration-response relationships were significantly different for NeuroP formation with the antioxidants being significantly less potent than for IsoP generation. In particular, alpha-tocopherol did not inhibit NeuroP formation at concentrations up to 100 microM. We also determined that tocopherols, in particular alpha-tocopherol, act in vitro as reducing agents to convert IsoP and NeuroP endoperoxides to reduced F-ring compounds, a finding we have observed previously in vivo in brain. These studies are of importance because they have further defined the role of antioxidants to modulate the formation of lipid peroxidation products in peroxidizing brain tissue. In addition, they suggest that alpha-tocopherol may not be a particularly effective agent to inhibit oxidant stress in the terminal compartment of neurons in the central nervous system.