| 林洪，王文浩，郑雪峰，胡连水，李君，黄巍.血清CCCK-18增高与硬膜外血肿并脑疝患者术后继发大面积脑梗死的相关性分析[J].神经损伤功能重建,2019,14(10):502-505 |
| 血清CCCK-18增高与硬膜外血肿并脑疝患者术后继发大面积脑梗死的相关性分析 |
| Correlation Analysis of Serum CCCK-18 Elevation and Postoperative Massive CerebralInfarction Secondary to Traumatic Epidural Hematoma and Concurrent Cerebral Herniation |
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| DOI： |
| 中文关键词: 硬膜外血肿 脑疝 CCCK-18 继发性脑梗死 去骨瓣减压术 |
| 英文关键词: epidural hematoma cerebral herniation caspase-cleaved cytokeratin 18 secondary cerebral infarction decompressive
craniectomy |
| 基金项目:福建省自然科学基
金（No.2015J05119） |
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| 中文摘要: |
| 目的：分析血清中Caspase酶切割细胞角蛋白18的裂解产物CCCK-18与单纯硬膜外血肿并脑疝患者
术后继发性脑梗死发生发展的关系，评价CCCK-18对继发性脑梗死的早期预测能力及临床决策价值。方 法：回顾性分析206例单纯硬膜外血肿并脑疝患者术前血清CCCK-18浓度与术后继发性脑梗死占位体积的
潜在关系。结果：术后继发脑梗死49例（23.78%），其中占位体积＞20 mL 32例（15.53%）纳入大面积脑梗死
组；占位体积＜20 mL 17例（8.25%）纳入小面积脑梗死组，无脑梗死157例（76.21%）纳入无脑梗死组。大面
积脑梗死组患者术前 CCCK-18 浓度显著高于小面积脑梗死组和无脑梗死组（均 P＜0.001）。术前血清
CCCK-18 水平与继发性脑梗死的占位体积呈线性相关（P＜0.001）。受试者工作曲线分析提示术前血清
CCCK-18水平对术后继发性大面积脑梗死的曲线下面积为0.814（P＜0.001），以241 U/L为预测界值的准确
度达到83.50%。多因素logistic回归分析表明，CCCK-18＞241 U/L是单纯硬膜外血肿并脑疝患者术后继发
大面积脑梗死的独立危险因素（P＜0.001）。术后随访6个月，术前血清CCCK-18＞241 U/L患者的格拉斯哥
预后量表（GOS）评分明显低于CCCK-18＜241 U/L的患者（P＜0.001）。结论：术前血清CCCK-18增高与单
纯硬膜外血肿致脑疝患者术后继发性大面积脑梗死密切相关，可作为辅助决策此类患者去骨瓣减压手术模
式并预估长期神经功能预后的生物标志物。 |
| 英文摘要: |
| To analyze the correlation between serum caspase-cleaved cytokeratin 18 (CCCK-18)
elevation and the occurrence and development of cerebral infarction secondary to traumatic epidural hematoma
and concurrent cerebral herniation, and to clarify its early predictive ability and clinical decision-making value
for secondary cerebral infarction. Methods: Preoperative serum CCCK-18 levels in 206 enrolled patients with
cerebral herniation from isolated epidural hematoma were analyzed retrospectively for its potential correlation
with the occupying volume of postoperative secondary cerebral infarction. Results: Post-operative secondary
cerebral infarction was determined in 49 patients (23.78%). Among them, 32 cases (15.78%) had an occupying
volume larger than 20 mL and were assigned to the massive cerebral infarction group; 17 cases (8.25%) had an
occupying volume smaller than 20 mL and were assigned to the moderate cerebral infarction group, and the
remaining 157 cases (76.21% ) were assigned to the non-cerebral infarction group. The concentration of
CCCK-18 in the massive cerebral infarction group was significantly higher than that in the moderate cerebral
infarction group and that in the non-cerebral infarction group (each P<0.001). The preoperative serum CCCK-18
level was linearly correlated with the occupying volume of secondary cerebral infarction (P<0.001). Receiver
Operating Characteristic (ROC) showed that the area under the curve (AUC) of preoperative serum CCCK-18
was 0.814 (P<0.001), and the accuracy of assigning 241 U/L as the predictive threshold value was 83.50% .
Multivariate logistic regression analysis showed that a >241 U/L preoperative serum CCCK-18 was an
independent risk factor for postoperative massive cerebral infarction secondary to traumatic epidural hematoma
and concurrent cerebral herniation. At the end of the 6-month follow-up, the GOS (Glasgow Outcome Scale)
score of patients with serum CCCK-18 higher than 241 U/L was significantly lower than that of patients with
levels lower than 241 U/L (P<0.001). Conclusion: Preoperative increased serum CCCK-18 is closely related to
secondary massive cerebral infarction in patients with cerebral herniation from isolated epidural hematoma. It
can serve as a useful biomarker for assisting decision-making of decompressive craniectomy surgery and
predicting long-term neurological function. |
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