Association of the HTR2A T102C SNP with Weight Gain and Changes in Biochemical Markers in Patients Receiving Antipsychotics

• Published in: International journal of biomedicine Vol. 8; no. 3; pp. 186 - 191
• Main Authors: Tolmachev, Mikhail, Akhmetova, Liliya, Shnayder, Natalia, Ershov, Evgeny, Bugorsky, Alexander, Kravtsov, Vladimir, Taraskina, Anastasia, Andreev, Boris, Yakhin, Kausar, Neznanov, Nikolay, Nasyrova, Regina
• Format: Journal Article
• Language: English
• Published: International Medical Research and Development Corporation 01.09.2018
• Subjects: antipsychotics; HTR2A gene; serotonin receptor 2A; single nucleotide polymorphism; weight gain
• ISSN: 2158-0510; 2158-0529
• DOI: 10.21103/Article8(3)_OA3

The purpose of our research was to study the association of the HTR2A T102C (rs6313) SNP with anthropometric and biochemical markers in patients treated with typical and atypical antipsychotics in monotherapy mode. Materials and methods: One hundred and seventeen white inpatients (95 men and 22 women) with F2 disorders (ICD-10, 1995) were enrolled in the study. All patients were divided into two groups by the antipsychotic class with which they were treated (Group 1 included 40 patients treated with typical antipsychotics; Group 2 included 77 patients treated with atypical antipsychotics) and two subgroups by weight change criteria during the study (Subgroup 1 included patients with weight change >6%; Subgroup 2 included patients with weight change <6%). The following examinations were performed: physical examination, anthropometric measurements (BMI. WC, TC), clinical examination, blood test (ALT, AST, FPG, VLDL-C, LDL-C, HDL-C, total cholesterol, triglycerides, total protein, albumin, creatinine, uric acid, carbamide), and genotyping for the HTR2A T102C (rs6313) SNP. Results: There were no statistically significant differences in the distribution of genotypes of the HTR2A T102C (rs6313) SNP between Group 1 and Group 2 (P>0.05). Kruskal-Wallis one-way analysis of variance between subgroups showed statistically significant differences between carbamide levels in the second visit in Group 2 (P=0.02). A Dunn post hoc test with Bonferroni adjustment showed statistically significant differences between TT and CT genotypes of the HTR2A T102C SNP: carbamide level was greater in TT carriers (P=0.02). The strength of associations and risks between alleles of the HTR2A T102C SNP and antipsychotic-induced weight change were as follows: ORC=0.49; CIC [0.25; 0.95]; RRC=0.58 CIC [0.35; 0.97]; ORT=2.03; CIT [1.05; 3.94]; RRT=1.7 CIT [1.02; 2.81]. Conclusion: Our results of the pilot pharmacogenetic studies show an association of the T allele carriage of the HTR2A T102C SNP with risk of antipsychotic-induced weight gain. The continuation of this study and an increase in the sample size will allow establishing valid pharmacogenetic markers for the risk of antipsychotic-induced weight gain.