Examining the independent and joint effects of genomic and exposomic liabilities for schizophrenia across the psychosis spectrum.

AIMS: Psychosis spectrum disorder has a complex pathoetiology characterised by interacting environmental and genetic vulnerabilities. The present study aims to investigate the role of gene-environment interaction using aggregate scores of genetic (polygenic risk score for schizophrenia (PRS-SCZ)) and environment liability for schizophrenia (exposome score for schizophrenia (ES-SCZ)) across the psychosis continuum. METHODS: The sample consisted of 1699 patients, 1753 unaffected siblings, and 1542 healthy comparison participants. The Structured Interview for Schizotypy-Revised (SIS-R) was administered to analyse scores of total, positive, and negative schizotypy in siblings and healthy comparison participants. The PRS-SCZ was trained using the Psychiatric Genomics Consortiums results and the ES-SCZ was calculated guided by the approach validated in a previous report in the current data set. Regression models were applied to test the independent and joint effects of PRS-SCZ and ES-SCZ (adjusted for age, sex, and ancestry using 10 principal components). RESULTS: Both genetic and environmental vulnerability were associated with case-control status. Furthermore, there was evidence for additive interaction between binary modes of PRS-SCZ and ES-SCZ (above 75% of the control distribution) increasing the odds for schizophrenia spectrum diagnosis (relative excess risk due to interaction = 6.79, [95% confidential interval (CI) 3.32, 10.26], p < 0.001). Sensitivity analyses using continuous PRS-SCZ and ES-SCZ confirmed gene-environment interaction (relative excess risk due to interaction = 1.80 [95% CI 1.01, 3.32], p = 0.004). In siblings and healthy comparison participants, PRS-SCZ and ES-SCZ were associated with all SIS-R dimensions and evidence was found for an interaction between PRS-SCZ and ES-SCZ on the total (B = 0.006 [95% CI 0.003, 0.009], p < 0.001), positive (B = 0.006 [95% CI, 0.002, 0.009], p = 0.002), and negative (B = 0.006, [95% CI 0.004, 0.009], p < 0.001) schizotypy dimensions. CONCLUSIONS: The interplay between exposome load and schizophrenia genetic liability contributing to psychosis across the spectrum of expression provide further empirical support to the notion of aetiological continuity underlying an extended psychosis phenotype.

Effect of thought disorders on quality of life in patients with schizophrenia.

OBJECTIVE: The aim of the present study was to investigate the impact of thought disorder on quality of life in patients with schizophrenia. METHODS: Seventy two patients with schizophrenia and 46 healthy subjects were included in the study. World Health Organization Quality of Life Instrument Short Forum (WHOQOL-BREF) was given to patients and healthy subjects to assess quality of life. Thought and Language Index (TLI) for thought disorders, Positive and Negative Syndrome Scale (PANNS) for symptom and Calgary Depression Scale (CDS) for depressive symptoms were administered to the patients. RESULTS: The comparison of quality of life between patients and healthy subjects showed a significant difference except environmental domain. There were no significant correlations between thought disorder and quality of life in patients with schizophrenia. CONCLUSION: The present study revealed that quality of life was lower in patients with schizophrenia compared to healthy subjects. There was no relation between thought disorders and quality of life in schizophrenia. Patients with schizophrenia were aware of their quality of life perception.

Motor axonal polyneuropathy in the course of ulcerative colitis: a case report.

We describe an axonal motor polyneuropathy in a patient with ulcerative colitis. Symptoms of neuropathy occurred during active colitis. Electrophysiological study showed motor axonal degeneration. After treatment with steroid added to mesalazine, the patient had a gastrointestinal recovery and neurological symptoms were improved. Axonal motor polyneuropathy is an unusual extraintestinal manifestation of ulcerative colitis, and is probably associated with an autoimmune process.