Sleep Problems, Suicidal Ideation, and Psychopathology in First-Episode Psychosis.

BACKGROUND AND HYPOTHESIS: Insomnia occurs frequently in the clinical course of schizophrenia. A growing literature has found associations between insomnia, suicidal ideation and behavior, and psychopathology in schizophrenia. We explored associations between sleep problems, suicidal ideation, and psychopathology in a cohort of patients with first-episode psychosis. STUDY DESIGN: We performed a secondary analysis of data for n = 403 subjects with data from the Recovery After an Initial Schizophrenia Episode study using regression models. STUDY RESULTS: The prevalence of sleep problems and suicidal ideation at baseline was 57% and 15%, respectively. After controlling for potential confounders, in the study baseline sleep problems were associated with increased odds of suicidal ideation with evidence of a dose-dependent relationship (OR = 2.25, 95% CI 1.15-4.41, P = .018). Over 24 months, sleep problems at any time point were associated with an over 3-fold increased odds of concurrent suicidal ideation (OR = 3.21, 95% CI 1.45-7.14, P = .004). Subjects with persistent sleep problems were almost 14 times more likely to endorse suicidal ideation at least once over the study than those without sleep problems (OR = 13.8, 95% CI 6.5-53.4, P < .001). Sleep problems were also a predictor of higher Positive and Negative Syndrome Scale total (ß = 0.13-0.22), positive (ß = 0.14-0.25), and general (ß = 0.16-0.27) subscale scores at baseline and multiple follow-up visits (P < .01 for each). CONCLUSIONS: Sleep problems are highly prevalent and associated with suicidal ideation and greater psychopathology in first-episode psychosis. Formal assessment and treatment of insomnia appear relevant to the clinical care of patients with psychosis as a predictor of suicidal ideation and symptom severity.

Transforming growth factor-ß signaling in systemic sclerosis.

Systemic sclerosis (SSc) is a complex, multiorgan autoimmune disease of unknown etiology. Manifestation of the disease results from an interaction of three key pathologic features including irregularities of the antigen-specific immune system and the non-specific immune system, resulting in autoantibody production, vascular endothelial activation of small blood vessels, and tissue fibrosis as a result of fibroblast dysfunction. Given the heterogeneity of clinical presentation of the disease, a lack of universal models has impeded adequate testing of potential therapies for SSc. Regardless, recent research has elucidated the roles of various ubiquitous molecular mechanisms that contribute to the clinical manifestation of the disease. Transforming growth factor ß (TGF-ß) has been identified as a regulator of pathological fibrogenesis in SSc. Various processes, including cell growth, apoptosis, cell differentiation, and extracellular matrix synthesis are regulated by TGF-ß, a type of cytokine secreted by macrophages and many other cell types. Understanding the essential role TGF-ß pathways play in the pathology of systemic sclerosis could provide a potential outlet for treatment and a better understanding of this severe disease.