Key result
Electroconvulsive therapy did not significantly change serum S100B levels, and post-ECT S100B change was not associated with clinical effect (rho = 0.14, p = 0.54).
Why the study?
Recent research suggests S100B may be a biomarker of response to ECT, prompting investigation into its utility as a depression biomarker, predictor of ECT response, and indicator of potential ECT-induced neural distress.
Does electroconvulsive therapy alter serum S100B levels or is S100B a predictor of ECT response in patients with depression?
Observational (n=22)
Does electroconvulsive therapy alter serum S100B levels or is S100B a predictor of ECT response in patients with depression?
Serum S100B does not appear to be a useful biomarker for depression state or ECT response, and ECT does not cause neural distress as measured by S100B.
Answers are grounded in this paper and cite their sources.
S100B does not appear useful as an ECT biomarker in depression; this cohort study leaves open its validity and needs prospective confirmation.
Objective: S100B is a glial cell protein with bimodal function. In low concentrations, it exerts neurotrophic effects, but higher levels reflect neuronal distress. Recent research suggests that this molecule may be a biomarker of response to electroconvulsive therapy (ECT). We examined the effect of ECT on serum S100B and its utility as 1) a biomarker of a depressive state and 2) a predictor of ECT response. We also wanted to ensure that ECT does not cause a marked serum S100B elevation, indicating neural distress. Methods: We measured serum S100B in 22 in-patients treated with ECT due to depression. Depression severity was assessed using 17-item Hamilton Rating Scale for Depression (HAMD-17). The data were collected before an ECT series, within 1 week after the series (post-ECT), and at a 6-month follow-up. Changes in serum S100B and clinical outcomes were tested using a linear mixed model. A relationship between serum S100B and the clinical outcomes was examined using Spearman’s and partial correlation. Results: Serum S100B did not change significantly immediately after an ECT series or 6 months later. The post-ECT serum S100B change was not associated with the clinical effect (rho = 0.14, n = 22, p = 0.54). The baseline serum S100B did not predict the clinical effect when controlling for age (r = 0.02, n = 22, df = 19, p = 0.92). Conclusion: The study neither supports serum S100B as a state marker of depression nor a predictor of ECT response. No evidence for ECT-related neural distress was found.
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Gbyl et al. (2022) conducted an observational in depression (n=22). Electroconvulsive therapy (ECT) was evaluated on Association between post-ECT serum S100B change and clinical effect (rho 0.14, p=0.54). Electroconvulsive therapy did not significantly change serum S100B levels, and post-ECT S100B change was not associated with clinical effect (rho = 0.14, p = 0.54).
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