Multimodal Psychotherapeutic Inpatient Therapy of Depression Is Successful in Patients With High Cytokine Production

Bibliographic Data

ID15518823
AuthorsEva M J Peters (0000-0003-2423-527X, Justus-Liebig-Universität Gießen, corresponding author), Melanie Neusetzer (Justus-Liebig-Universität Gießen), Secil Akinci (Justus-Liebig-Universität Gießen), Aysenur Murat (Justus-Liebig-Universität Gießen), Sabine Treuherz (Justus-Liebig-Universität Gießen), Matthias Rose (0000-0001-5233-3139, Charité - Universitätsmedizin Berlin), Frank Leweke (Justus-Liebig-Universität Gießen), Falk Leichsenring (0000-0002-3808-0072, Justus-Liebig-Universität Gießen), Melanie L Conrad (0000-0002-8811-5536, Charité - Universitätsmedizin Berlin), Johannes Kruse (0000-0001-7159-9610, Justus-Liebig-Universität Gießen)
Year2020
Volume11
Pages571636-571636
Publication date2020-11-02
Open AccessYes
TypeARTICLE
VenueFrontiers in Psychiatry (JOURNAL)
Journal identifiersISSN: 1664-0640 • E-ISSN: 1664-0640
PublisherFrontiers Media (PUBLISHER • CH)
DOI10.3389/fpsyt.2020.571636
PMID33240126
OpenAlexW3096760613
LanguageEN
Citations received1
References cited72

Objective: In experimental settings, systemically elevated inflammation markers interfere with major depression treatment. In German healthcare, compulsory national health insurance covers treatment of a wide variety of depressive disorders, if it follows evidence-based medicine guidelines combining recommended therapies. To date, little is known about the relevance of immune system cytokine production with regard to real-world clinical care for patients with moderate depression. Methods: Seventy three patients with moderate depression subjected to multimodal psychotherapeutic inpatient therapy (mPT) following a psychodynamic concept at a German university hospital were included. As a primary outcome, mPT success, evidenced by delta HADS "depression," was analyzed according to tumor necrosis factor alpha (TNFα) production by peripheral blood mononuclear cells (PBMC) after phytohemagglutinin (PHA) challenge at baseline. Secondary outcomes addressed the inflammatory response and mental health comparing high and low TNFα-producers. Results: First, higher PBMC TNFα production at baseline predicted a better mPT-outcome ( R 2 0.162, p = 0.014). Second, patients with high TNFα (hTNF) at baseline produced significantly more acute inflammatory cytokines [interleukin (IL)1β, IL6), TH1/TH2 cytokines [interferon gamma (IFNγ), IL4] as well as eotaxin and IL2 compared to low TNFα producers (lTNF) (Cohen's ds between -0.532 and -1.013). Demographic data, diagnosis subtype-distribution, medication, systemic inflammation markers [C-reactive protein (CRP), high mobility group box 1 (HMGB1), leptin], anxiety and depression (HADS) did not differ. From baseline to mPT-discharge, HADS "depression" decreased in both hTNF (11.31 to 5.47, p = 0.001, d = 1.184) and lTNF patients (11.50-7.92, p = 0.001, d = -0.765), while PBMC cytokine production decreased significantly in hTNF (Cohen's ds between -0.304 and -0.345) with a significant group by time interaction for TH1/TH2 ratio. At the end of therapy, comparison of TNF groups revealed significantly lower depression-scores in hTNF compared to lTNF patients (5.47 compared to 7.92, p = 0.035, d = 0.504). Conclusions: Our study demonstrates successful treatment of depression in a clinical care setting using multimodal psychotherapy based on a psychodynamic concept following guideline recommendation. The greatest improvement in patient depression was linked to the highest production of TNFα by PBMCs at baseline. Our study contributes to the definition of patient subpopulations with differing cytokine responses that are related to succesful treatment of depression

Anxiety · Cytokine · Depression (economics · Hospital Anxiety and Depression Scale · Inflammation · Peripheral blood mononuclear cell · Psychiatry · Tumor necrosis factor alpha · Health, psychology, and well-being · Medicine · Stress Responses and Cortisol · Tryptophan and brain disorders · Immunology · Internal Medicine

Tools

Open DOIOpen Access