Association between the IL10 rs1800896 Polymorphism and Tardive Dyskinesia in Schizophrenia
- Affiliations
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- 1Department of Psychiatry, Chungnam National University College of Medicine, Daejeon, Republic of Korea
- 2Department of General Surgery, Korea University College of Medicine, Seoul, Republic of Korea
- 3Department of Psychiatry, Gyeongsang National University School of Medicine, Jinju, Republic of Korea
- 4Department of Psychiatry, Seoul Metropolitan Eunpyeong Hospital, Seoul, Republic of Korea
- 5Chronobiology Institute, Korea University, Seoul, Republic of Korea
- 6Department of Psychiatry, Korea University College of Medicine, Seoul, Republic of Korea
Abstract
Objective
Interleukin-10 (IL-10) is a major immunoregulatory cytokine and its gene plays a fundamental role in anti-inflammatory and immunosuppressive activity. This study aimed to examine the association between the IL10 gene promoter -1082G/A polymorphism (rs1800896) and tardive dyskinesia (TD) in schizophrenia.
Methods
Two hundred and eighty unrelated Korean schizophrenic patients participated in this study (105 TD and 175 non-TD patients). TD was diagnosed using the Research Diagnostic Criteria for TD and Abnormal Involuntary Movement Scale (AIMS). Genotyping was performed by RT-PCR and high-resolution melting curve analysis.
Results
The distributions of genotypic frequencies did not differ between patients with and without TD (χ2=4.33, p=0.115). However, allelic frequencies of the two groups were different (χ2=4.45, p=0.035); the A allele frequency was higher in TD. The total AIMS scores of the three genotypes were not different (F=1.33, p=0.266). However, the total AIMS scores of the A allele carrier and the A allele non-carrier were significantly different (t=5.79, p<0.001). Logistic regression analaysis showed that IL10 -1082G/A genotype significantly predicts presence of TD (p=0.045) after adjusting for covariates such as age and treatment duration.
Conclusion
This finding suggests that the A allele of rs1800896 may be associated with TD development following a low IL-10 function.