Influence of inflammatory status in the acute phase of stroke on post-stroke depression |
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| Affiliation: | 1. Division of Brain Injury Outcomes, Johns Hopkins University School of Medicine, Baltimore, MD, USA;2. Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA;3. Division of Neurocritical Care, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Hospital, Baltimore, MD, USA;4. Department of Neurosurgery, University of Chicago Pritzker School of Medicine, Chicago, IL, USA;5. Division of Neurocritical Care, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA;1. The Ottawa Hospital, Ottawa Hospital Research Institute, Department of Psychiatry, School of Public Health and Epidemiology, Brain and Mind Research Institute, University of Ottawa, 75 Laurier Ave. East, Ottawa, ON K1N 6N5, Canada;2. Department of Psychiatry, Western Psychiatric Hospital, School of Medicine, University of Pittsburgh, 3811 O''Hara St., Pittsburgh, PA 15213, USA;3. Department of Statistics, University of Pittsburgh, 230 S. Bouquet St., Pittsburgh, PA 15213, USA;4. Department of Psychiatry and Human Behavior, Warren Alpert Medical School of Brown University, Box G-BH, Providence, RI 02912, USA;5. Department of Health Services, Policy and Practice, Brown University School of Public Health, 121 South Main Street, Providence, RI 02903, USA;6. Department of Psychiatry, University of California San Diego, 4510 Executive Drive, Suite 315, San Diego, CA 92121, USA;7. Departments of Psychiatry, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA;8. Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA;9. Department of Psychiatry, University of Miami, 1120 NW 14th St., Miami, FL 33136, USA;10. Department of Psychiatry, Sunnybrook Health Sciences Centre, University of Toronto Faculty of Medicine, 2075 Bayview Ave., FG-53, Toronto, ON M4N 3M5, Canada;11. Department of Psychiatry, Bradley Hospital, 1011 Veterans Memorial Parkway, East Providence, RI 02915, USA;1. School of Clinical medicine of Weifang Medical College, Weifang, China;2. The Department of Neurology, Affiliated Hospital of Weifang Medical College, Weifang, China;3. The Department of Neurosurgery, Affiliated Hospital of Weifang Medical College, Weifang, China;1. Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Medical College of Soochow University, 199 Renai Road, Industrial Park District, Suzhou, Jiangsu Province, 215123, China;2. Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, USA;3. Department of Epidemiology, School of Public Health, Chongqing Medical University, Chongqing, China;4. Department of Global Health, Ningbo Institute of Life and Health Industry, University of Chinese Academy of Sciences, Ningbo, Zhejiang, PR China;5. Department of Neurology, Kerqin District First People''s Hospital of Tongliao City, Inner Mongolia, China;6. Department of Neurology, Jilin Central Hospital, Jilin, China;7. Department of Neurology, the 88th Hospital of PLA, Taian, Shandong, China;8. Department of Medicine, Tulane University School of Medicine, New Orleans, LA, USA |
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| Abstract: | ![]()
BackgroundThirty percent of stroke patients will suffer from post-stroke depression (PSD). Recent data suggest that inflammation accounts for a substantial amount of depression. Our primary objective was to assess the association between standard inflammation biomarkers in the acute phase of stroke and PSD at three months. The secondary objective was to elaborate a predictive model of PSD from clinical, biological and radiological data.MethodsWe performed a retrospective analysis of a single-centre cohort of stroke patients with a three-month follow-up. Serum levels of C-reactive protein (CRP), fibrinogen, leukocyte count and neutrophil to lymphocyte ratio (NLR) were tested at admission and at peak. Mood was assessed at three months using the depression sub-scale of the Hospital Anxiety and Depression Scale (HADS). Association between inflammation biomarkers and HADS was evaluated with multi-linear regression adjusted on clinical and radiological parameters. Logistic predictive models of PSD at three months, with and without inflammation biomarkers, were compared.ResultsThree hundred and forty-eight patients were included, of whom 20.06% developed PSD. Baseline and peak values of all inflammatory markers were associated with the severity of PSD at three months. Area under the curve for the receiver operating characteristic curve of PSD prediction was 0.746 (CI 95% 0.592–0.803) with selected inflammation biomarkers and 0.744 (CI 95% 0.587–0.799) without.ConclusionMost inflammation biomarkers are weakly associated with PSD, adding negligible value to predictive models. While they suggest the implication of inflammation in PSD pathogenesis, they are useless for the prediction of PSD, underscoring the need for more specific biomarkers. |
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| Keywords: | Depression Stroke Inflammation Biomarkers C-reactive protein |
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