Psychiatry Research EG

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by systemic inflammation, autoantibody production, and immune dysregulation, and it may lead to significant neurological and psychiatric morbidities during childhood [1,2]. Children have more severe presentations and often have early nervous system involvement [3,4]. The American College of Rheumatology developed a standardized nomenclature system for the neuropsychiatric syndromes of SLE (NPSLE) for the purposes of classification and reporting. It includes three subsets of manifestations: psychiatric disorders, cognitive deficits, and acute confusion. Anxiety, mood disorder, and psychosis are included in the term ‘psychiatric disorders’ [5]. Controversy exists concerning the factors responsible for psychiatric manifestations in patients with SLE, which have been attributed to the pathophysiology of the disease (including antibodies, vasculitis, thrombosis, hemorrhage, and cytokine-mediated damage) [6], iatrogenic effects of corticosteroids, [7] and psychosocial stressors related to chronic disease [8]. One hundred and sixteen autoantibodies were described in patients with SLE. These include autoantibodies that target nuclear antigens, cytoplasmic antigens, cell membrane antigens, phospholipid-associated antigens, blood cells, endothelial cells, nervous system antigens, plasma proteins, matrix proteins, and miscellaneous antigens [9]. Several autoantibodies have been implicated in the pathogenesis of neuropsychiatric SLE (NPSLE), including antiribosomal P protein, antineuronal, and antiphospholipid (aPL) [10–12]. Various pathogenic mechanisms for these antibodies have been proposed, such as binding to epitopes on the cell membrane surface, intracellular penetration, inhibition of protein synthesis, production of proinflammatory cytokines, and cell apoptosis [13]. The roles of autoantibodies have been extensively examined in adult patients with SLE with neuropsychiatric syndromes. To our knowledge, no studies have assessed associations between these autoantibodies and isolated psychiatric disorders in juvenile SLE in Egypt. Hence, our study aimed first to report the prevalence of psychiatric disorders in pediatric patients with SLE. Next, we aimed to determine the associations between aPL, antineuronal, and antiribosomal P antibodies and psychiatric disorders. Finally, we planned to assess the value of these antibodies in the early prediction of psychiatric disorders in juvenile patients with SLE