期刊论文详细信息
Arthritis Research & Therapy
Autoantibody profile in systemic lupus erythematosus with psychiatric manifestations: a role for anti-endothelial-cell antibodies
Fabrizio Conti1  Cristiano Alessandri1  Daniela Bompane1  Michele Bombardieri1  Francesca Romana Spinelli1  Anna Carlotta Rusconi2  Guido Valesini1 
[1] Cattedra di Reumatologia, Dipartimento di Clinica e Terapia Medica Applicata – Università degli Studi di Roma 'La Sapienza', Rome, Italy
[2] Dipartimento di Scienze Psichiatriche e Medicina Psicologica, Università degli Studi di Roma 'La Sapienza', Rome, Italy
关键词: systemic lupus erythematosus;    psychiatric disorders;    mood disorders;    autoantibodies;    anti-endothelial-cell antibodies;   
Others  :  1101241
DOI  :  10.1186/ar1198
 received in 2004-03-29, accepted in 2004-05-18,  发布年份 2004
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【 摘 要 】

This study was performed to determine the correlation between psychiatric manifestations and several autoantibodies that might participate in the pathogenesis of psychiatric disorders in the course of systemic lupus erythematosus (SLE). Fifty-one unselected outpatients with SLE were enrolled. Psychiatric evaluation was performed according to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition. The prevalence of antibodies against endothelial cells (AECA), cardiolipin, β2 glycoprotein I, Ro, Ro52, La, glial fibrillary acidic protein, ribosomal P protein, dsDNA, and nucleosomes was assessed by experimental and commercial enzyme-linked immunosorbent assays. According to the cutoff value, AECA were present in 11 of 17 (64.7%) SLE patients with psychosis and mood disorders and in 10 of 34 (29.4%) patients without psychiatric manifestations other than anxiety (P = 0.03). Moreover, the AECA binding index was significantly higher in the first group (P = 0.03). Conversely, no significant correlation was found between the presence of the other autoantibodies studied and psychiatric involvement. The results of this study suggest a relationship between AECA and psychosis and mood disorders in SLE, supporting the hypothesis of a biological origin of these disturbances.

【 授权许可】

   
2004 Conti et al.; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.

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