The status of serum cortisol before and after treatment of schizophrenia and its correlation to disease severity and improvement: A longitudinal study

Abstract

Background: Hypothalamic–pituitary–adrenal axis functioning, with cortisol as its major output hormone, has been presumed to play a key role in the development of psychopathology of schizophrenia. Objective: We examined the association of serum cortisol with disease severity and improvement in schizophrenia patients in Jimma, Ethiopia. Method: A total of 34 newly diagnosed schizophrenics were included in this study. Data on demographic, behavioral, clinical state, serum cholesterol level, and antipsychotic usage were obtained at baseline and after 8 weeks. The Positive and Negative Syndrome Scale was used to assess psychotic symptoms severity. A paired sample t-test was used to compare baseline and post-treatment values. Linear regression was used to assess associations. Result: Post-treatment serum cortisol level was significantly lower than its baseline value ( p = 0.001). There was also a significant positive and negative psychotic symptoms decrease after treatment (baseline positive psychotic vs post-treatment positive psychotic symptoms: t(33) = 6.24 (95% confidence interval = 7.03,13.84, p = 0.000) and (baseline negative psychotic vs post-treatment negative psychotic symptoms: t(33) = 4.21 (95% confidence interval = 3.82, 10.99, p = 0.000). At baseline, neither positive nor negative subscore on the Positive and Negative Syndrome Scale showed an association with serum cortisol level ( B = −0.016, p = 0.794 and B = −0.032, p = 0.594). However, serum cortisol level showed strong associations with post-treatment positive sub scores and negative sub scores ( B = 0.167, p = 0.007) and ( B = 0.144, p = 0.010) on the Positive and Negative Syndrome Scale. Conclusion: We found a significant decrease in serum cortisol level after antipsychotics treatment and that was associated with improvement in psychotic symptoms in schizophrenics in Jimma, Ethiopia.

The Association between Serum Cortisol and Folate Levels and Positive and Negative Symptoms in Patients with first episode of Schizophrenia: A Case-Control Study

“…In the Woldesenbet et al study, at baseline, no association was observed between serum cortisol levels in schizophrenia patients and PANSS positive and negative sub-scores. However, after treatment with antipsychotics, serum cortisol levels showed a strong association with PANSS positive and negative subscores (31). In the present study, no association was observed between serum cortisol levels and PANSS scores.…”

“…According to the results of Woldesenbet et al, serum cortisol levels were signi cantly lower in schizophrenia patients after treatment with antipsychotics compared to their baseline values. However, due to limitations related to assessing the effect of medication, it is essential to approach these ndings cautiously (31). Yildirim et al evaluated serum cortisol levels in patients with schizophrenia, comparing them with control relatives and control volunteers.…”

Psychotropic Drug Effects on Steroid Stress Hormone Release and Possible Mechanisms Involved

“…Treatment with various antipsychotic drugs (risperidone, haloperidol, chlorpromazine, olanzapine) was used in patients newly diagnosed with schizophrenia for 8 weeks. Post-treatment serum cortisol concentrations were significantly lower than those at the baseline [84].…”

Association of Blood Metabolomics Biomarkers with Brain Metabolites and Patient-Reported Outcomes as a New Approach in Individualized Diagnosis of Schizophrenia

“…A similarly low cortisol value was recorded in a patient after aripiprazole, but during polytherapy with lamotrigine and sertraline. Likewise, Woldesenbent et al, in their study on the impact of antipsychotic treatment on the cortisol level in a group of patients with newly diagnosed schizophrenia, observed a significant decrease the initial blood cortisol concentration after treatment [32]. Glutamate, the anionic form of glutamic acid, is the main excitatory neurotransmitter in the brain, the homeostasis of which is regulated by glutamate transporters [33].…”