Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/48630
Título: Factors involved in the progress of preclinical atherosclerosis associated with systemic lupus erythematosus: A 2-year longitudinal study
Autores/as: Rua-Figueroa, I.
Arencibia-Mireles, O.
Elvira, M.
Erausquin, C.
Ojeda, S.
Francisco, F.
Naranjo, A. 
Rodríguez-Gallego, C. 
Garcia-Laorden, I.
Rodríguez-Perez, J. 
Rodríguez-Lozano, C.
Clasificación UNESCO: 32 Ciencias médicas
3205 Medicina interna
Palabras clave: Atherosclerosis
Systemic lupus erythematosus
Fecha de publicación: 2010
Publicación seriada: Annals of the rheumatic diseases 
Resumen: Objectives To assess the changes in carotid intima-media thickness (IMT) and the associated risks factors in patients with low severity systemic lupus erythematosus (SLE). Methods Common carotid IMT measurements were obtained by ultrasound from 101 patients with SLE at an interval of 2 years. Cardiovascular risk factors, disease activity, accumulated damage, severity (Katz index) and biochemical parameters (including high sensitivity C-reactive protein, interleukin 6, C3a, C4a, C5a and homocysteine) were also assessed. Multiple linear regression was used to assess the effect of these variables on the end IMT measurement (eIMT) adjusted to the baseline measurement (bIMT). Results The cohort comprised 94.1% women, with a mean age at entry of 41.5 years and a mean disease duration of 12.1 years. An increase of 0.078 mm in IMT was detected over 2 years, from a mean bIMT of 0.37 mm to a mean eIMT of 0.44 mm (p<0.001). When adjusted for the bIMT, multiple linear regression identified bIMT, age at diagnosis, homocysteine, C3 and C5a as risk factors for IMT progression. Conclusions IMT significantly increases over 2 years in patients with SLE. Age, baseline IMT, C3, C5a anaphylatoxin and homocysteine are all associated risk factors, supporting a role for complement and homocysteine in the early stages of premature SLE-associated atherosclerosis.
URI: http://hdl.handle.net/10553/48630
ISSN: 0003-4967
DOI: 10.1136/ard.2008.104349
Fuente: Annals of the Rheumatic Diseases[ISSN 0003-4967],v. 69, p. 1136-1139 (Junio 2010)
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