Association Between Acute Inflammatory Cells and Mutation in ICAM-1 Gene With Injury Severity and Outcome Among Traumatic Cerebral Hemorrhagic Contusion

急性炎症细胞与ICAM-1基因突变和创伤性脑出血挫伤的损伤严重程度及预后之间的关联

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Abstract

BACKGROUND: Acute inflammation in the brain after trauma is mediated by acute inflammatory cells (neutrophils) that contributes to ischemic brain damage, neurological deterioration, and poor outcome. Migration of neutrophils to brain is mediated by intercellular adhesion molecule-1 (ICAM-1). The aim was to determine an association between neutrophils counts, ICAM-1 level and mutation in ICAM-1 gene with injury severity and patient's outcome. METHODS: Cross-sectional study was conducted for ninety Sudanese patients presented with traumatic cerebral hemorrhagic contusion to the National Center for Neurological Sciences, Khartoum, Sudan from December 2015 to January 2018. Non-Sudanese patients, and hemorrhagic contusion associated with other type of brain bleeding were excluded in this study. Moreover, 90 apparently healthy individuals were participated as control. RESULTS: Most patients were males (93.3%), their ages ranged from 25 to 44 years, 11.1% of the patients had severe brain injury, 22.2% had brain edema and the mortality rate was 8.9%. Circulatory levels of leukocytes, neutrophil and ICAM-1 among patients who sustained trauma were significantly elevated compared with controls (p = 0.000). The high level of leukocytes and neutrophils counts were significantly associated with ICAM-1pg/mL circulatory level. High levels of leukocytes, neutrophils, and ICAM-1 were documented in severe brain injuries, whereas. high level of ICAM-1 was observed among patients admitted with brain edema. Leukocytes and neutrophils counts were significantly associated with patient outcome. High level of ICAM-1 (304.88 pg/mL) was observed among patients with poor outcome compared to survivals (263.93 pg/mL). The highest circulatory level of ICAM-1 (280.75 pg/mL) was observed among patient having adenine-adenine (AA) mutant homozygous alleles, followed by (272 pg/mL) for guanine-guanine (GG) homozygous alleles, then (245.12 pg/mL) for guanine-adenine (GA) heterozygous alleles. CONCLUSIONS: Mutation in ICAM-1 gene and increased levels of leukocytes, neutrophils and ICAM-1 constitutes important markers for injury severity and patient's outcome.

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