Longitudinal relationship between Personal and Social Performance (PSP) and anxiety symptoms in schizophrenia.

BACKGROUND: We aimed to examine the longitudinal relationship between the personal and social functioning and anxiety symptoms in patients with schizophrenia. For this purpose, we confirmed the validity of the anxiety subscale of the Symptom-Checklist-90-Revised (SCL-90-R) and then applied the latent growth modeling method for longitudinal causal relationships. METHODS: Five hundred and seventy-eight patients diagnosed with schizophrenia were evaluated and 369 patients were included in the study at baseline. After conducting Rasch model analyses for the validation of the anxiety subscale in the SCL-90-R, we applied latent growth model to determine the causal relationship between the PSP and the anxiety symptoms. RESULTS: The validity of the anxiety subscale of the SCL-90-R was confirmed based on the Rasch rating model, where the criteria for Infit, Outfit, item difficulty, and point-measure correlations were satisfied. The results from the latent growth model showed that the intercept and slope (rate of change) of the PSP negatively predicted the slope of anxiety symptoms along the longitudinal trajectory. Together with previous studies examining the predictive role of anxiety symptoms on quality of life, our longitudinal findings lend evidence for bidirectional effects between quality of life and anxiety symptoms. The transactional nature of the relationship between anxiety symptoms and quality of life warrant further investigation using a longitudinal cross-lagged design. CONCLUSION: The anxiety subscale of the SCL-90-R may be utilized by clinicians and researcher to make inferences about quality of life in addition to assessing anxiety symptoms in patients with schizophrenia.

The effects of long-term clozapine add-on therapy on the rehospitalization rate and the mood polarity patterns in bipolar disorders.

OBJECTIVE: We investigated the effect long-term clozapine add-on therapy has on rehospitalization rate and mood polarity patterns in patients with bipolar disorders. METHOD: Clinical data from medical records of 51 patients with bipolar disorder (DSM-IV) treated with clozapine add-on for more than 6 months at the Refractory Bipolar Disorders Clinic of Seoul National University Hospital were retrospectively analyzed. Patients had been registered from 1995 to 2004. Rehospitalization rates were compared before and after clozapine add-on. The clinical polarity of episodes resulting in hospitalizations was also compared. Twenty-seven bipolar patients treated with clozapine add-on for more than 3 years were further analyzed for long-term stability. RESULTS: The number of hospital days per year was reduced in 90.2% of patients after clozapine add-on. Total number and duration of hospitalizations per year decreased, and the effect size of clozapine add-on was substantially large (Wilcoxon z = -5.48, p < .01 for number of hospitalizations/year; Wilcoxon z = -5.32, p < .01 for hospital days/year; r = -0.54 and -0.53, respectively). Significant reductions were found in the number and duration of hospitalizations associated with manic, depressive, and hypomanic episodes. Number and duration of hospitalizations associated with mixed episodes did not show significant changes. The long-term efficacy of clozapine add-on was supported by continuous reduction in hospital days per year in the 27 selected patients. CONCLUSION: Long-term clozapine add-on therapy was effective in reducing the number and duration of rehospitalizations of bipolar patients resistant to conventional treatment. A significant reduction was found in rehospitalizations associated with manic, depressive, and hypomanic episodes, whereas mixed episode-associated rehospitalizations did not show significant changes.

No association found between 158 Val/Met polymorphism of the COMT gene and schizophrenia with minor physical anomalies.

The catechol-O-methyl transferase (COMT) gene has been a promising candidate in genetic research on schizophrenia because of its function in dopamine metabolism and its location on chromosome 22q11.2, which may be implicated in both schizophrenia and velocardiofacial syndrome (VCFS). To explore the possible genetic contribution of COMT to the development of schizophrenia, we focused on the subgroup of patients with schizophrenia characterized by minor physical anomalies as a phenotype and the 158 Val/Met polymorphism as a genotype. Since some physical anomalies are found in both schizophrenia and VCFS, schizophrenia patients with minor physical anomalies could represent the putative subgroup of schizophrenia linked to a disruption in neurodevelopment. Genotyping for the 158 Val/Met (472 G>A) polymorphism in the COMT gene was done for 239 patients with schizophrenia and 248 normal controls. Our analysis did not yield any significant between-group differences in terms of either allele or genotype frequency. We also could not find any association between the COMT gene and the schizophrenia subgroup with minor physical anomalies, although there was a significant difference in Waldrop total scores between the patients with schizophrenia and the normal controls. Analyses of subgroups based on other clinical variables also did not reveal significant differences. Overall, this study does not support the hypothesis that the 158 Val/Met polymorphism in the COMT gene is associated with schizophrenia in Koreans.