Cortisol, DHEA and DHEA-S during exposure therapy in patients with obsessive-compulsive disorder – secretion patterns and prediction of treatment response

• Published in: Psychiatry research 2020-09, Vol.291, p.113288-113288, Article 113288
• Main Authors: Kellner, Michael, Yassouridis, Alexander, Adel, Fred, Muhtz, Christoph, Jelinek, Lena, Wiedemann, Klaus
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Biomarkers - analysis; Biomarkers - chemistry; Biomarkers - metabolism; Cortisol; Dehydroepiandrosterone; Dehydroepiandrosterone - analysis; Dehydroepiandrosterone - metabolism; Dehydroepiandrosterone sulfate; Dehydroepiandrosterone Sulfate - analysis; Dehydroepiandrosterone Sulfate - metabolism; Exposure therapy; Female; HPA axis; Humans; Hydrocortisone - analysis; Hydrocortisone - metabolism; Implosive Therapy - trends; Male; Middle Aged; Obsessive-compulsive disorder; Obsessive-Compulsive Disorder - metabolism; Obsessive-Compulsive Disorder - psychology; Obsessive-Compulsive Disorder - therapy; Predictive Value of Tests; Saliva - chemistry; Saliva - metabolism; Stress; Treatment Outcome; Young Adult
• ISSN: 0165-1781; 1872-7123
• DOI: 10.1016/j.psychres.2020.113288

•During the first session of exposure therapy in patients with obsessive-compulsive disorder the adrenocortisol stress hormones cortisol, DHEA and DHEA-S did not increase despite considerable subjective distress.•Only DHEA-S was elevated before the start of exposure therapy, possible due to anticipatory anxiety.•Cortisol, DHEA or DHEA-S profiles did not predict treatment response one month later. The cortisol response in patients with obsessive-compulsive disorder (OCD) during exposure with response prevention (ERP), a stressful but very effective psychotherapeutic treatment, has shown contradictory findings in three prior studies with low sample sizes. In a larger cohort of 51 patients with OCD we repeatedly measured subjective units of distress (SUD) and the adrenocortical stress hormones cortisol, dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) in saliva during the very first session of ERP and on the day before. Expectedly, SUD were increased on the ERP day before the session and further rose during ERP, but salivary cortisol and DHEA were statistically indistinguishable from the comparison condition. Interestingly, DHEA-S was significantly elevated throughout the ERP versus the comparison day, but did not further increase in acute response to ERP. According to an explorative analysis in a subsample, hormone levels on the comparison or the ERP day did not predict anti-OCD treatment response one month later. These results corroborate our prior findings of cortisol non-response despite considerable subjective stress in ERP. The role of DHEA-S in anticipatory anxiety and the effects of augmentative cortisol therapy in ERP need further study.