Perfil de autoanticuerpos y asociación con patrones inmuno-electroforéticos en pacientes con esclerosis sistémica / Profile of autoantibodies and association with immunoelectrophoretic patterns in patients with systemic sclerosis

Contexto: la esclerodermia es una enfermedad autoinmune, sistémica y mediada por factores genéticos y ambientales; uno de sus marcadores es la presencia de autoanticuerpos con valor clínico, diagnóstico y pronóstico. Métodos: estudio descriptivo, observacional y relacional efectuado en pacientes con diagnóstico de esclerosis sistémica, atendidos en Unidad de Reumatología del Hospital Carlos Andrade Marín entre junio 2014 a mayo 2015. Los datos fueron procesados mediante análisis de correspondencia y cálculo de Chi cuadrado en el paquete estadístico SPSS 22. Resultados: de 80 pacientes estudiados se detectaron anticuerpos anti-topoisomerasa en 18 individuos (22,5%), anti centrómero (n=38, 47,5%), antinucleares (n=13, 16,3%), anti-ribonucleoproteína (n=7, 8,8%) y sin anticuerpos en 4 individuos (5%). Respecto a los patrones inmunoelectroforéticos se determinó el patrón centromérico en 23 sujetos (28,8%), moteado fino y grueso (n=17, 21,3% cada uno), homogéneo (n=8, 10%), nucleolar (n=7, 8,8%) y citoplasmático (n=1, 1,3%); fueron negativos 7 pacientes (8,8%). Mediante la prueba de chi cuadrado se obtuvo un valor de 116,3 de la relación auto-anticuerpos-patrones inmunofluorescencia, con un valor de p= 0,0000. El análisis de correspondencia demostró las siguientes asociaciones: a) anticuerpos antinucleares y patrón nucleolar (p=0,0021), anticuerpos antinucleares y patrón moteado grueso (p= 0,0123), anticuerpos anticentrómero y patrón centromérico (p= 0,0000), anticuerpos anticentrómero y patrón moteado fino (p= 0,0031), anticuerpos anti-topoisomerasa I y patrón homogéneo (p= 0,0001) y anticuerpos anti-ribonucleoproteína y patrón moteado grueso (p= 0,0000). Conclusiones: el perfil de autoanticuerpos en pacientes con esclerosis sistémica tiene una distribución similar a las publicaciones mundiales y relación es estadísticamente significativa con sus patrones inmunoelectroforéticos. (AU)

Introduction: Scleroderma is an autoimmune disease, systemic and mediated by genetic and environmental factors. One of its markers is the presence of autoantibodies with clinical value, diagnosis and prognosis. Subjects and methods: a descriptive, observational and relational study carried out in patients diagnosed with systemic sclerosis who were treated at the Rheumatology Unit of the Hospital Carlos Andrade Marín from June 2014 to May 2015. The data were processed by correspondence analysis and Chi square calculation in the package Statistic SPSS 22 version. Results: anti-topoisomerase antibodies were detected in 18 individuals (22.5%), anti-centromere (n=38, 47.5%), antinuclear antibodies (n=13, 16.3%), anti-ribonucleoprotein (n = 7, 8.8%) and without antibodies in 4 individuals (5%). As regards immune-electrophoretic patterns, the centromeric pattern was determined in 23 subjects (28.8%), fine and thick mottled (n = 17, 21.3% each), homogeneous (n = 8, 10%), nucleolar = 7, 8.8%) and cytoplasmic (n = 1, 1.3%); 7 patients (8.8%) were negative. The chi-square test yielded a value of 116.3 of the autoantibodies-immunofluorescence ratio, with a value of p=0.0000. Correspondence analysis showed the following associations: a) antinuclear antibodies and nucleolar pattern (p= 0.0021), antinuclear antibodies and thick speckle pattern (p=0.0123), anticentromere antibodies and centromeric pattern (p=0.0000) (p=0.0031), anti-topoisomerase I antibodies and homogeneous pattern (p=0.0001) and anti-ribonucleoprotein antibodies and thick speckle pattern (p=0.0000). Conclusion: The profile of autoantibodies in patients with systemic sclerosis has a similar distribution to global publications, and is statistically significant with his immune-electrophoretic patterns. (AU)

Immunohistochemical analysis of paraoxonases-1 and 3 in human atheromatous plaques.

BACKGROUND: The paraoxonase (PON) enzyme family comprising PON1, PON2 and PON3 are antioxidant enzymes that degrade bioactive oxidised lipids and are thus antiatherogenic. MATERIALS AND METHODS: We investigated the localisation of the PON proteins during the development of atherosclerosis by immunohistochemical analysis. RESULTS: In normal aortas, PON1 and PON3 were localised to smooth muscle cells (SMC) and endothelial cells. PON3 staining was stronger than that of PON1. During atherosclerosis development, SMC staining for PON1 and PON3 was greatly reduced, while macrophage staining for both proteins increased with PON1 predominating. Macrophage staining for PON1 and PON3 was significantly and positively related to the amount of aortic inflammation (both P<0·001). CONCLUSIONS: Our data add support to the growing body of evidence for a cellular protective effect of PON1 and PON3 against the proinflammatory/proatherosclerotic effects of lipid peroxidation.