Introduction

Metabolic disturbances are common in patients maintained on neuroleptics. These abnormalities significantly increase the physical comorbidity and mortality rates due to cardiovascular disease. We hypothesized that 5-HT receptor genes polymorphisms have associations with drug-induced metabolic syndrome development in schizophrenic patients.

Objectives

To investigate the role of polymorphic variants of serotonin receptors genes in the development of antipsychotic-induced metabolic syndrome.

Methods

467 patients with schizophrenia receiving long-term antipsychotic therapy were investigated. The mean age was 40.0±11.6 years. The standard phenol-chloroform method for DNA isolation was used. Genotyping was carried out on eight SNP’s of genes HTR1A, HTR2A, HTR3A and HTR2C with the MassARRAY^® Analyzer 4 (Agena Bioscience™) using the set SEQUENOM Consumables iPLEX Gold 96 on the base The Core Facility "Medical Genomics", Tomsk NRMC.

Results

The prevalence of metabolic syndrome was 26.1%. In the study sample, there were significantly more women with metabolic syndrome (56.6%) than men (43.4%) (p=0.002). The majority of patients with metabolic disturbances were aged >40 years (62.3%), versus 40.9% in the group without metabolic disorders (p<0.001). The duration of the disease was statistically significantly higher in the group of patients with metabolic syndrome (p=0.003). We did not find statistically significant associations of polymorphic variants of the studied genes with the development of the drug-induced metabolic syndrome.

Conclusions

Our results do not demonstrate any significant association between allelic variants of serotonin receptor genes and metabolic syndrome in patients with schizophrenia.

Conflict of interest. The authors declare no conflict of interest.

Supported by Grant of RSF 19-75-10012.

Introduction

Medication is primary tactics in schizophrenia treatment. First and second generation antipsychotics (FGA and SGA respectively) affect on core symptoms. Unfortunately, it causes side effects. Metabolic syndrome one of them and includes large number of affections like body mass index changes, lipidemias, hypertension and others.

Objectives

To study the role of polymorphic variants FTO gene in metabolic syndrome in schizophrenia patients.

Methods

We were investigated 480 patients. Main criteria for inclusion in study was using antipsychotics, verified diagnosis of schizophrenia and metabolic syndrome. Mean age was 42,1±1,4 years. The metabolic syndrome was assessment based on clinical data. Standard phenol-chloroform protocol for DNA isolation was used. Genotyping was carried out on six SNP’s of FTO gene with real-time PCR. Statistical analysis was carried out with R 3.6.2 with basic functions and SNPassoc package.

Results

The distribution of genotypes for variants rs7185735 and rs9939609 was not in according to Hardy-Weinberg equilibrium (a p-value less than 0.05) and excluded from further analysis. Patients with schizophrenia were divided into two groups: patients with metabolic syndrome and patients without it. We did not identify any statistically significant associations between genotypes and alleles of FTO gene and metabolic syndrome.

Conclusions

We did not find any associations of alleles and genotypes of FTO gene with metabolic syndrome in schizophrenia patients from Siberia region. Metabolic syndrome needs more further studies with larger number of samples and different populations.

Conflict of interest. The authors declare no conflict of interests.

Supported by Grant of RSF 19-75-10012.

Introduction

Metabolic syndrome (MS) is an often co-occurring condition that occurs during antipsychotic therapy and impairs social functioning

Objectives

We tried to conduct a self - evaluation of social adaptation in patients with schizophrenia and MS

Methods

We examined 150 patients with schizophrenia receiving antipsychotic therapy at the clinics of Mental Health Research Institute. The study was supported by a grant from the Russian Science Foundation 18-15-00011. The IDF criteria were used to diagnose metabolic syndrome. We used «The social adaptation self - evaluation scale» (SASS).

Results

63 patients (42%) had MS and 87 patients (58%) did not. In the subgroup of patients with MS, 59 people (93.65%) had disabilities or were unemployed, in the group without MS - 82 (94.26%) patients. There were no statistically significant differences between the groups (p ≥ 0.05). In the patients with schizophrenia and concomitant MS, the median SSAS scores was 35 [29; 39], which corresponds mainly to a high level of self - evaluation of social adaptation. At the same time, in patients with schizophrenia and without MS, on the contrary, the self - evaluation of social adaptation was 30 [23; 38] points (p = 0.03914). Perhaps this is due to the great attention from relatives and doctors of general somatic practice and the primary medical network in connection with the risk of developing severe somatic pathology.

Conclusions

Patients with MS can give a higher assessment of social adaptation, despite a objectively low social status.

Introduction

Schizophrenia is associated with lower life expectancy due to cardiovascular disease. Metabolic syndrome (MetS) occupies an important place among the main problems. Indicators of hormones regulating metabolism may be appealing candidates as biomarkers of metabolic side-effects. Certain role belongs to genetic factors that might be the basis of sensitivity to development of MetS.

Objectives

The aim is to study polymorphisms of leptin gene (LEP) and serum leptin concentration in schizophrenia patients with metabolic syndrome.

Methods

After obtaining informed consent, patients with schizophrenia (ICD-10: F20) were included: 91 patients for biochemical research and 463 patients for genotyping. Patients were divided into two groups: 46 (119) with MetS; 45 (344) without it. Concentration of leptin was measured on an analyzer MAGPIX (Luminex, USA). Determination of 4 polymorphisms (rs2167270, rs3828942, rs10954173, rs4731426) of LEP was performed by PCR. Differences were considered significant at p<0.05.

Results

The leptin concentration is significantly (p<0.001) higher in MetS (13511.5 [7392.5; 28278.75] pg/ml) compared to patients without MetS (6662 [2131.5; 11380] pg/ml). Significant differences were found in the distribution of rs3828942 (GG:GA:AA): 25.9%:44%:30.2% in MetS and 31.2%:52.6%:16.2% without MetS (χ²=10.545, p=0.005). The genotype AA and the allele A have a predisposing effect on the development of MetS (OR₁=2.247, C.I:1.248-4.046; OR₂=1.475, C.I:1.093-1.991, χ²=6.49, p=0.01).

Conclusions

A number of features are observed in patients with MetS, which impair the functioning of patients. These investigations should aim to optimize the approach to assess the risk of MetS.

The study was supported by grants from the RSF 19-75-10012 (genetic research) and 18-15-00011 (determination of leptin concentration)