High Prevalence of Personality Disorders in Skin-restricted Lupus Patients.

Psychiatric and personality disorders have been extensively documented in patients with systemic lupus erythematosus (SLE). However, the prevalence of personality disorders in skin-restricted lupus (SRL) patients remains unknown. The aim of this study was to assess the prevalence of personality disorders in SRL outpatients and to examine the associated factors. We evaluated 60 SRL outpatients and 118 controls matched for sex, age and education level. On the basis of the Personality Diagnostic Questionnaire 4+, 38% of patients vs 20% of controls fulfilled the criteria for at least one personality disorder (OR 2.2 [95% CI 1.01-4.6], p = 0.048). Only one patient with a personality disorder had specialised mental health care. Late lupus onset and more frequent past treatments by thalidomide were associated factors. This study evidences a high prevalence of personality disorders in SRL patients and shows that most SRL patients with personality disorder do not receive specialised mental health care.

Metabolic and psychiatric effects of acyl coenzyme A binding protein (ACBP)/diazepam binding inhibitor (DBI).

Acyl coenzyme A binding protein (ACBP), also known as diazepam binding inhibitor (DBI) is a multifunctional protein with an intracellular action (as ACBP), as well as with an extracellular role (as DBI). The plasma levels of soluble ACBP/DBI are elevated in human obesity and reduced in anorexia nervosa. Accumulating evidence indicates that genetic or antibody-mediated neutralization of ACBP/DBI has anorexigenic effects, thus inhibiting food intake and inducing lipo-catabolic reactions in mice. A number of anorexiants have been withdrawn from clinical development because of their side effects including an increase in depression and suicide. For this reason, we investigated the psychiatric impact of ACBP/DBI in mouse models and patient cohorts. Intravenously (i.v.) injected ACBP/DBI protein conserved its orexigenic function when the protein was mutated to abolish acyl coenzyme A binding, but lost its appetite-stimulatory effect in mice bearing a mutation in the γ2 subunit of the γ-aminobutyric acid (GABA) A receptor (GABAAR). ACBP/DBI neutralization by intraperitoneal (i.p.) injection of a specific mAb blunted excessive food intake in starved and leptin-deficient mice, but not in ghrelin-treated animals. Neither i.v. nor i.p. injected anti-ACBP/DBI antibody affected the behavior of mice in the dark-light box and open-field test. In contrast, ACBP/DBI increased immobility in the forced swim test, while anti-ACBP/DBI antibody counteracted this sign of depression. In patients diagnosed with therapy-resistant bipolar disorder or schizophrenia, ACBP/DBI similarly correlated with body mass index (BMI), not with the psychiatric diagnosis. Patients with high levels of ACBP/DBI were at risk of dyslipidemia and this effect was independent from BMI, as indicated by multivariate analysis. In summary, it appears that ACBP/DBI neutralization has no negative impact on mood and that human depression is not associated with alterations in ACBP/DBI concentrations.