CONTEXT: Human and animal studies have suggested an underlying inflammatory mechanism for a variety of neuropsychiatric disorders, including schizophrenia. To date, most available reports focused on adult patients. OBJECTIVE: We wished to test the hypothesis that the first psychotic episode in youth is associated with inflammation. PATIENTS: We studied patients admitted to a pediatric inpatient psychiatric unit. Patients (n=80) had new-onset psychosis diagnosed using DSM-IV TR criteria for Psychosis NOS, Schizophreniform Disorder or Schizoaffective Disorder. Patients were matched for age, race and gender with inpatient controls without psychosis within the same unit (n=66). We also compared these values to normal pediatric hematologic values. To study the role of inflammation in youth with psychosis, we collected serum samples of 28 children presenting with first-episode psychosis and compared their serum cytokine and S100B levels to eight healthy controls. MAIN OUTCOME MEASURES: In this study, we measured serum markers of systemic inflammation. RESULTS: Leukocyte counts revealed a statistically significant increase in absolute monocytes compared to patients without psychosis (0.61 ± 0.282 k/ml vs. 0.496 ± 0.14 k/ml; p<0.01) and lymphocytes (2.51 ± 0.84 k/ml vs. 2.24 ± 0.72 k/ml; p<0.05) in patients with psychosis. All other hematologic values were similar between the groups. In addition, psychosis was characterized by increased serum levels of S100B, a peripheral marker of blood-brain barrier (BBB) damage. Several inflammatory mediators (e.g., TNF-α, IL-1β, IL-6, IL-5, IL-10, and IFN-γ) were elevated in children with psychosis. CONCLUSIONS: These results strongly support a link between systemic inflammation, blood-brain barrier disruption and first-episode psychosis in pediatric patients.
CONTEXT: Human and animal studies have suggested an underlying inflammatory mechanism for a variety of neuropsychiatric disorders, including schizophrenia. To date, most available reports focused on adult patients. OBJECTIVE: We wished to test the hypothesis that the first psychotic episode in youth is associated with inflammation. PATIENTS: We studied patients admitted to a pediatric inpatient psychiatric unit. Patients (n=80) had new-onset psychosis diagnosed using DSM-IV TR criteria for Psychosis NOS, Schizophreniform Disorder or Schizoaffective Disorder. Patients were matched for age, race and gender with inpatient controls without psychosis within the same unit (n=66). We also compared these values to normal pediatric hematologic values. To study the role of inflammation in youth with psychosis, we collected serum samples of 28 children presenting with first-episode psychosis and compared their serum cytokine and S100B levels to eight healthy controls. MAIN OUTCOME MEASURES: In this study, we measured serum markers of systemic inflammation. RESULTS: Leukocyte counts revealed a statistically significant increase in absolute monocytes compared to patients without psychosis (0.61 ± 0.282 k/ml vs. 0.496 ± 0.14 k/ml; p<0.01) and lymphocytes (2.51 ± 0.84 k/ml vs. 2.24 ± 0.72 k/ml; p<0.05) in patients with psychosis. All other hematologic values were similar between the groups. In addition, psychosis was characterized by increased serum levels of S100B, a peripheral marker of blood-brain barrier (BBB) damage. Several inflammatory mediators (e.g., TNF-α, IL-1β, IL-6, IL-5, IL-10, and IFN-γ) were elevated in children with psychosis. CONCLUSIONS: These results strongly support a link between systemic inflammation, blood-brain barrier disruption and first-episode psychosis in pediatric patients.
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