Hostname: page-component-cd9895bd7-7cvxr Total loading time: 0 Render date: 2024-12-26T03:45:53.241Z Has data issue: false hasContentIssue false

Serum S100B protein after electroconvulsive therapy in patients with depression

Published online by Cambridge University Press:  07 March 2022

Krzysztof Gbyl*
Affiliation:
Center for Neuropsychiatric Depression Research (CNDR), Mental Health Center Glostrup, Glostrup, Denmark Institute of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Niklas Rye Jørgensen
Affiliation:
Department of Clinical Biochemistry, Rigshospitalet-Glostrup, Glostrup, Denmark Institute of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Poul Videbech
Affiliation:
Center for Neuropsychiatric Depression Research (CNDR), Mental Health Center Glostrup, Glostrup, Denmark Institute of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
*
Author for correspondence: Krzysztof Gbyl, Email: krzysztof.gbyl@regionh.dk

Abstract

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.

Type
Original Article
Copyright
© The Author(s), 2022. Published by Cambridge University Press on behalf of Scandinavian College of Neuropsychopharmacology

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Agelink, MW, Andrich, J, Postert, T, Würzinger, U, Zeit, T, Klotz, P and Przuntek, H (2001) Relation between electroconvulsive therapy, cognitive side effects, neuron specific enolase, and protein S-100. Journal of Neurology, Neurosurgery & Psychiatry 71(3), 394396.CrossRefGoogle ScholarPubMed
Ambrée, O, Bergink, V, Grosse, L, Alferink, J, Drexhage, HA, Rothermundt, M, Arolt, V and Birkenhäger, TK (2016) S100B serum levels predict treatment response in patients with melancholic depression. International Journal of Neuropsychopharmacology 19(3), 19.CrossRefGoogle Scholar
Anand, N and Stead, LG (2005) Neuron-specific enolase as a marker for acute ischemic stroke: a systematic review. Cerebrovascular Diseases 20(4), 213219.CrossRefGoogle ScholarPubMed
Andrade, C and Bolwig, TG (2014) Electroconvulsive therapy, hypertensive surge, blood-brain barrier breach, and amnesia. The Journal of ECT 30(2), 160164.CrossRefGoogle ScholarPubMed
Arts, B, Peters, M, Ponds, R, Honig, A, Menheere, P and Os, Jvan (2006) S100 and impact of ECT on depression and cognition. The Journal of ECT 22(3), 206212.Google ScholarPubMed
Bjørnshauge, D, Hjerrild, S and Videbech, P (2019) Electroconvulsive therapy practice in the Kingdom of Denmark. The Journal of ECT 35(4), 258263.Google ScholarPubMed
Carlier, A, Boers, K, Veerhuis, R, Bouckaert, F, Sienaert, P, Eikelenboom, P, Vandenbulcke, M, Stek, ML, van Exel, E, Dols, A and Rhebergen, D (2019) S100 calcium-binding protein B in older patients with depression treated with electroconvulsive therapy. Psychoneuroendocrinology 110, 104414.CrossRefGoogle ScholarPubMed
Carney, S, Cowen, P, Geddes, J, Goodwin, G, Rogers, R, Dearness, K, Tomlin, A, Eastaugh, J, Freemantle, N, Lester, H, Harvey, A, Scott, A (2003) Efficacy and safety of electroconvulsive therapy in depressive disorders: a systematic review and meta-analysis. The Lancet 361(9360), 799808.Google Scholar
Cheng, F, Yuan, Q, Yang, J, Wang, W and Liu, H (2014) The prognostic value of serum neuron-specific enolase in traumatic brain injury: systematic review and meta-analysis. PLoS ONE 9(9), e106680.Google ScholarPubMed
Dassan, P, Keir, G and Brown, MM (2009) Criteria for a clinically informative serum biomarker in acute ischaemic stroke: a review of S100B. Cerebrovascular Diseases 27(3), 295302.CrossRefGoogle ScholarPubMed
van Diermen, L, van den Ameele, S, Kamperman, AM, Sabbe, BCG, Vermeulen, T, Schrijvers, D and Birkenhäger, TK (2018) Prediction of electroconvulsive therapy response and remission in major depression: meta-analysis. The British Journal of Psychiatry 212(2), 7180.Google ScholarPubMed
Ercole, A, Thelin, EP, Holst, A, Bellander, BM and Nelson, DW (2016) Kinetic modelling of serum S100b after traumatic brain injury. BMC Neurology 16(1), 93.CrossRefGoogle ScholarPubMed
Gbyl, K, Rostrup, E, Raghava, JM, Andersen, C, Rosenberg, R, Larsson, HBW and Videbech, P (2020) Volume of hippocampal subregions and clinical improvement following electroconvulsive therapy in patients with depression. Progress in Neuro-Psychopharmacology and Biological Psychiatry 104, 110048.CrossRefGoogle ScholarPubMed
Gbyl, K, Rostrup, E, Raghava, JM, Carlsen, JF, Schmidt, LS, Lindberg, U, Ashraf, A, Jørgensen, MB, Larsson, HBW, Rosenberg, R, Videbech, P (2019) Cortical thickness following electroconvulsive therapy in patients with depression – a longitudinal MRI study. Acta Psychiatrica Scandinavica 140(3), 205216.CrossRefGoogle ScholarPubMed
Gbyl, K, Støttrup, MM, Raghava, JM, Jie, SX and Videbech, P (2021) Hippocampal volume and memory impairment after electroconvulsive therapy in patients with depression. Acta Psychiatrica Scandinavica 143(3), 238252.CrossRefGoogle ScholarPubMed
Hamilton, M (1960) A rating scale for depression. Journal of Neurology, Neurosurgery & Psychiatry 23(1), 5662.CrossRefGoogle ScholarPubMed
Hunsberger, J, Austin, DR, Henter, ID and Chen, G (2009) The neurotrophic and neuroprotective effects of psychotropic agents. Dialogues in clinical neuroscience 11(3), 333348.CrossRefGoogle ScholarPubMed
Ingebrigtsen, T and Romner, B (2002) Biochemical serum markers of traumatic brain injury. The Journal of Trauma: Injury, Infection, and Critical Care 52(4), 798808.Google ScholarPubMed
Jang, B-S, Kim, H, Lim, S-W, Jang, K-W and Kim, D-K (2008) Serum S100B levels and major depressive disorder: its characteristics and role in antidepressant response. Psychiatry Investigation 5(3), 193198.CrossRefGoogle ScholarPubMed
Jelovac, A, Kolshus, E and McLoughlin, DM (2013) Relapse following successful electroconvulsive therapy for major depression: a meta-analysis. Neuropsychopharmacology 38(12), 24672474.CrossRefGoogle ScholarPubMed
Jiang, H, Veldman, ER, Tiger, M, Ekman, C-J, Lundberg, J and Svenningsson, P (2021) Plasma levels of brain-derived neurotrophic factor and S100B in relation to antidepressant response to ketamine. Frontiers in Neuroscience 15, 698633.CrossRefGoogle Scholar
Kranaster, L, Janke, C, Mindt, S, Neumaier, M and Sartorius, A (2014) Protein S-100 and neuron-specific enolase serum levels remain unaffected by electroconvulsive therapy in patients with depression. Journal of Neural Transmission 121(11), 14111415.CrossRefGoogle ScholarPubMed
Kroksmark, H and Vinberg, M (2018) Does S100B have a potential role in affective disorders? A literature review. Nordic Journal of Psychiatry 72(7), 19.CrossRefGoogle ScholarPubMed
Maier, H, Helm, S, Toto, S, Moschny, N, Sperling, W, Hillemacher, T, Kahl, KG, Jakubovski, E, Bleich, S, Frieling, H, Neyazi, A (2018) S100B, homocysteine, vitamin B12, folic acid, and procalcitonin serum levels in remitters to electroconvulsive therapy: a pilot study. Disease Markers 2018, 18.Google ScholarPubMed
Michetti, F, D’Ambrosi, N, Toesca, A, Puglisi, MA, Serrano, A, Marchese, E, Corvino, V and Geloso, MC (2019) The S100B story: from biomarker to active factor in neural injury. Journal of Neurochemistry 148(2), 168187.CrossRefGoogle ScholarPubMed
O’Leary, LA and Mechawar, N (2021) Implication of cerebral astrocytes in major depression: a review of fine neuroanatomical evidence in humans. Glia 69(9), 20772099.CrossRefGoogle ScholarPubMed
Palmio, J, Huuhka, M, Laine, S, Huhtala, H, Peltola, J, Leinonen, E, Suhonen, J and Keränen, T (2010) Electroconvulsive therapy and biomarkers of neuronal injury and plasticity: serum levels of neuron-specific enolase and S-100b protein. Psychiatry Research 177(1-2), 97100.Google ScholarPubMed
Schroeter, M, Sacher, J, Steiner, J, Schoenknecht, P and Mueller, K (2013) Serum S100B represents a new biomarker for mood disorders. Current Drug Targets 14(11), 12371248.CrossRefGoogle ScholarPubMed
Schroeter, ML, Abdul-Khaliq, H, Diefenbacher, A and Blasig, IE (2002) S100B is increased in mood disorders and may be reduced by antidepressive treatment. NeuroReport 13(13), 16751678.CrossRefGoogle ScholarPubMed
Thelin, EP, Nelson, DW and Bellander, B-M (2017) A review of the clinical utility of serum S100B protein levels in the assessment of traumatic brain injury. Acta Neurochirurgica 159(2), 209225.CrossRefGoogle ScholarPubMed
Tural, U, Irvin, MK and Iosifescu, DV (2021) Correlation between S100B and severity of depression in MDD: a meta-analysis. The World Journal of Biological Psychiatry, 18. doi: 10.1080/15622975.2021.2013042.CrossRefGoogle ScholarPubMed
Zachrisson, OCG, Balldin, J, Ekman, R, Naesh, O, Rosengren, L, Ågren, H and Blennow, K (2000) No evident neuronal damage after electroconvulsive therapy. Psychiatry Research 96(2), 157165.CrossRefGoogle ScholarPubMed
Supplementary material: PDF

Gbyl et al. supplementary material

Table S1

Download Gbyl et al. supplementary material(PDF)
PDF 29.4 KB