Relationship between long-term use of a typical antipsychotic medication by Chinese schizophrenia patients and the bone turnover markers serum osteocalcin and β-CrossLaps

Background: Increasing evidence shows that schizophrenia patients with long-term exposure to antipsychotic medications have decreased bone mass, which suggests that they are at a high risk of osteoporosis. However, the mechanism underlying this remains unclear. In this study, we selected two bone turnover markers to explore whether atypical antipsychotics can affect bone metabolism and identified possible influencing factors.

Methods: A total of 116 schizophrenia patients (18-40years old) participated in the study. The subjects included 31 drug-naive first-episode patients and 85 patients who had undergone atypical antipsychotic monotherapy for at least 6months. A total of 71 subjects were assigned as normal controls. Demographic and physical examination data were analyzed for all subjects. The positive and negative syndrome scale (PANSS) was used to assess psychopathology in schizophrenia patients. Levels of the bone turnover markers osteocalcin and β-CrossLaps were measured. Serum prolactin (PRL), lipid, sex hormone, glucose, insulin, and parathyroid hormone levels were also measured.

Results: The serum β-CrossLaps levels of patients who had been treated with atypical antipsychotics were higher compared with those of drug-naive first-episode patients and normal subjects. Atypical antipsychotics, schizophrenia, age, gender, and body mass index, as well as serum levels of PRL, triglyceride, high-density lipoprotein cholesterol, glucose, and testosterone, were significantly associated with serum osteocalcin and β-CrossLaps levels. Serum insulin was only positively associated with serum osteocalcin, whereas estradiol was only negatively associated with serum β-CrossLaps.

Conclusion: Patients who had been treated with atypical antipsychotics had accelerated bone resorption. Our findings uncover a link between atypical antipsychotics and bone metabolism, possibly through abnormalities in glucose and lipid metabolism and insulin resistance.