The Risk of Endocrine Dysfunction and Metabolic Disorders Antipsychotics in Patients with Schizophrenia during Therapy with Second-Generation

Background: efficacy of atypical antipsychotics in relation to cognitive functions and negative symptoms of schizophrenia, their better safety profile in relation to extrapyramidal symptoms compared with first-generation antipsychotics, accompanied by the frequent occurrence of endocrine and metabolic disorders, which can lead to both low adherence to therapy and reduction in life expectancy. Early diagnosis of these disorders, as well as the development of therapeutic tactics would minimize manifestations of endocrine and metabolic imbalance. The aim of the study was to assess the risk of occurrence and severity of neuroendocrine dysfunction, metabolic disorders in the treatment of patients with schizophrenia with second-generation antipsychotics. Patients and Methods: 76 inpatient patients (43 men and 33 women) aged 18 to 70 years with a diagnosis of paranoid schizophrenia (ICD-10 F20.0) and a positive response to the courses of therapy (at least 30% reduction of the total score on the PANSS scale) were examined. 3 groups of patients who received monotherapy with one of the atypical antipsychotics of the second generation (quetiapine, olanzapine, risperidone) were formed. The studied drugs were either prescribed for the first time upon admission, or were already prescribed before, and dose adjustments was carried out due to an exacerbation of the condition. The duration of the study was 10 weeks (70 days). Clinical and psychopathological, psychometric (PANSS, UKU), anthropometric, laboratory and statistical methods were used. Results: differences in prolactin levels in the studied respondent patients were established depending on the second-generation antipsychotic used for the course of monotherapy. The index of prolactin level during risperidone monotherapy was M ± m = 1401 ± 91 µm/ml, which was twice the upper limit of the physiological norm (M ± m = 96–637 µm/ml). Manifestations of hyperprolactinemia were less with olanzapine monotherapy (M ± m = 781 ± 52 µm/ml). The lowest prolactin level, which corresponded to the norm, was found in the quetiapine monotherapy group (M ± m = 422 ± 48 µm/ml). Changes in prolactin levels associated with the gender of patients were found in the form of a stable tendency to a more pronounced increase in female patients. The greatest statistically significant weight gain (p < 0.5) was recorded in patients receiving olanzapine monotherapy, slightly less when using risperidone and minimal when taking quetiapine (4.9 ± 1.8 kg 3.3 ± 1.1 kg and 0.8 ± 0.3 kg, respectively). The average value of the atherogenicity coefficient at the end of the courses of monotherapy with olanzapine and risperidone exceeded its normative level (3.8 ± 0.4 and 3.4 ± 0.5, respectively). Conclusions: the changes in the endocrine and metabolic profile confirm the results of previous studies. Regular monitoring of anthropometric and laboratory parameters both before and during antipsychotic therapy is recommended as a secondary prevention.