engleski

COX-2 rs689466 polymorphism and metabolic syndrome-related parameters among medicated schizophrenia patients

Introduction: Altered dopaminergic neurotransmission and metabolic disturbances, such as weight gain, lipid disturbance, and glucose dysregulation are frequently observed in schizophrenia individuals. Antipsychotic medications have also been causatively linked to metabolic disturbances in schizophrenia. The use of selective cyclooxygenase-2 (COX-2) inhibitors, such as celecoxib, has been reportedly associated with favourable effects on dopaminergic neurotransmission and insulin sensitivity. Functional rs689466 polymorphism (A/G polymorphism) of the COX-2 gene has been extensively investigated in schizophrenia. We previously reported that female smokers with schizophrenia from the Croatian population carrying the COX-2-G allele (COX-2-GG homozygous and COX-2-AG heterozygous) manifested an earlier disease onset. We also found that schizophrenia individuals under antipsychotic treatment carrying the COX-2-G allele manifested higher skin flush response to niacin and that schizophrenia individuals manifesting higher skin flush response to niacin had higher plasma triglyceride levels. Therefore, here we investigated whether metabolic syndrome-related parameters such as body mass index (BMI) and fasting plasma total cholesterol, LDL cholesterol, HDL cholesterol and glucose levels might be influenced by the COX-2 polymorphism among medicated schizophrenia patients. Materials and methods: Genotyping was performed by polymerase chain reaction/restriction fragment length polymorphism analysis for 275 patients (males/females: 143/132). Results: We observed no significant associations between COX-2 polymorphism, BMI, and plasma lipid and glucose levels in any male or female patients (p > 0.05, respectively). Conclusions: Our results indicate that COX-2 polymorphism may not be of relevance in determining metabolic syndrome-related parameters among medicated schizophrenia patients.

antipsychotic agents ; cyclooxygenase-2 ; metabolic syndrome ; schizophrenia

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