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Anorexia Nervosa in Juvenile Systemic Lupus Erythematosus (SLE): A Causality Dilemma

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CHILDREN-BASEL
卷 10, 期 4, 页码 -

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MDPI
DOI: 10.3390/children10040697

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neuropsychiatric lupus; depression; feeding and eating disorder; leptin; mental health; weight loss; body image; pediatric rheumatology; trauma

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This review examined the potential association between juvenile-onset systemic lupus erythematosus (jSLE) and anorexia nervosa (AN). The majority of reported cases showed that AN was diagnosed before jSLE, with a time span of no more than two years between the diagnoses. The stress of chronic disease diagnosis and chronic inflammation associated with AN are likely important factors in the relationship between these two conditions. Further research is needed to increase awareness among clinicians and explore this association.
Juvenile-onset systemic lupus erythematosus (jSLE) is an autoimmune disorder with multifaceted clinical findings in different organ systems. Neuropsychiatric manifestations affect more than half of SLE patients, and there is increasing evidence that anorexia nervosa (AN), a feeding and eating disorder (FED) characterized by significantly reduced energy intake, is among them. Herein, a review of the literature on the potential association between jSLE and AN was performed. Reported clinical cases were identified, and putative pathophysiological mechanisms were sought that could potentially explain the observed relationship between these two pathological entities. Four reports of isolated cases and a case series including seven patients were identified. In this limited patient pool, the diagnosis of AN preceded that of SLE in the majority of cases, whereas in all cases both entities were diagnosed within a time span of two years. Many explanations for the observed relationships have been proposed. AN has been associated with the stress of chronic disease diagnosis; on the other hand, the chronic inflammation associated with AN may contribute to the development/appearance of SLE. Adverse childhood experiences, concentrations of leptin, shared autoantibodies, and genetic traits appear to be important factors in this well-established interplay. In essence, it seems important to increase clinician awareness of the concomitant development of AN and SLE and invite further research on the subject.

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