Biomarkers predict hemorrhagic transformation and stroke severity after acute ischemic stroke |
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| Institution: | 1. Comprehensive Stroke Care Program, Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India;2. Achutha Menon Centre for Health Science Studies, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India;3. Department of Biochemistry, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India;1. Department of Haematology, Oslo University Hospital Rikshospitalet, Sognsveien 20, Oslo 0372, Norway;2. Department of Haematology, Akershus University Hospital, Sykehusveien 25, 1478 Nordbyhagen, Lørenskog, Norway;3. Department of Microbiology, Oslo University Hospital Rikshospitalet, Sognsveien 20, Oslo 0372, Norway.;4. Norwegian National Unit for Platelet Immunology, Division of Diagnostics, University Hospital of North Norway, Sykehusveien 38, Tromsø 9019, Norway;5. Department of Immunology and Transfusion Medicine, Oslo University Hospital, Ullevål, Kirkeveien 166, Oslo 0450, Norway;6. Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Klaus Torgårdsvei 3, Oslo 0372, Norway;7. Department of Neurology, Oslo University Hospital Rikshospitalet, Sognsveien 20, Oslo 0372, Norway;8. Department of Radiology and Nuclear Medicine, Oslo University Hospital Rikshospitalet, Sognsveien 20, Oslo 0372, Norway;9. Department of Neurosurgery, Oslo University Hospital Rikshospitalet. Sognsveien 20, Oslo 0372, Norway;1. Department of Neurosurgery, Iwate Medical University, Iwate, Japan;2. Division of Ultrahigh Field MRI, Institute for Biomedical Sciences, Iwate Medical University, Iwate, Japan;1. Medical Student, Jeonbuk National University Medical School, Korea;2. Department of Radiology and Research Institute of Clinical Medicine of Jeonbuk National University-Biomedical Research Institute of Jeonbuk National University Hospital, Korea;1. Department of Clinical Epidemiology, Clinical Research and Education Premotion Division, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashi-cho, Kodaira, Tokyo 187-8551, Japan;2. Department of Psychiatry, Dokkyo Medical University School of Medicine, 880 Kitakobayashi, Mibu, Tochigi 321-0293, Japan;3. Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan;4. Department of Preventive Intervention for Psychiatric Disorders, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashi-cho, Kodaira, Tokyo 187-8551, Japan;1. Department of Neurosurgery, Yantai Affiliated Hospital of Binzhou Medical University, Yantai 264100, China;2. Department of Neurosurgery, Yantai Harbour Hospital, Yantai 264000, China;3. Yantai Comprehensive Health Service Center, Yantai 264000, China;1. Sunshine Coast University Hospital, Birtinya, Queensland, Australia;2. Griffith University, School of Medicine, Birtinya, Australia;3. Stroke and Ageing Research, Department of Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, Australia;4. Peninsula Clinical School, Central Clinical School, Monash University, Frankston, Australia;5. Eastern Health Clinical School, Faculty of Medicine, Nursing and Health Science, Monash University, Box Hill, Australia;6. Florey Institute of Neuroscience and Mental Health, Heidelberg, University of Melbourne, Vic, Australia |
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| Abstract: | ObjectivesHemorrhagic transformation (HT) is a complication occurring in patients with acute ischemic stroke (AIS) either spontaneously or post-thrombolysis leading to significant morbidity and mortality. We assessed circulating matrix metalloproteinase-9 (MMP-9), Claudin-5, and soluble serum stimulation-2 (sST2) in HT and stroke severity in AIS based on their temporal distribution.Materials and methodsWe prospectively enrolled 111 AIS patients within 12 h from onset. Patient demographic, clinical, and imaging details were documented. Follow-up imaging was conducted 24–48 h after admission. Blood samples were taken at three time-points from stroke onset. HT was classified according to the European Co-operative Acute Stroke Study-III(ECASS-III). Stroke severity was assessed using the National Institutes of Health Stroke Scale (NIHSS). Multiple logistic regression and receiver operating characteristic curve were conducted to determine the discriminative capacity.ResultsMean age was 62.3 ± 11.7 years and median baseline NIHSS was 12IQR 8.0–18.0]. HT was detected in 30(27%) patients. Biomarker levels at 12 h were elevated with median MMP-9 concentration of 153.9 ng/mLIQR 110.6–309 ng/mL] indicating a trend toward significant positive correlation with HT(P = 0.05). Claudin-5 levels at 12 h was elevated but was not statistically significant (43.1 pg/mLIQR:26.7–72.6 pg/mL] vs 59.4 pg/mLIQR:24.5–100.8 pg/mL];P = 0.4). Multiple logistic regression indicated Claudin-5 levels at 12 h (OR 9.46;95% CI:1.97–64.6;P = 0.010) and baseline low ASPECTS score(OR 20.3;95% CI:3.46–193; P = 0.003) independently predicted HT. MMP-9 at 12 h was significantly elevated in patients with moderate to severe strokes (P = 0.04).ConclusionsClaudin-5 and low ASPECTS independently predicted HT. MMP-9 was positively correlated with baseline stroke severity. |
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