Abstract
Objective To explore the predictive value of milk fat globule epidermal growth factor 8 (MFG-E8) in the occurrence of delayed cerebral ischemia (DCI) after an aneurysmal subarachnoid hemorrhage (aSAH). Methods We recruited 32 patients with aSAH as the case group and 24 patients with unruptured aneurysms as the control group. Serum MFG-E8 levels were measured by western blot and enzyme-linked immunosorbent assay. We analyzed the relationship between MFG-E8 levels and the risk of DCI. Results The levels of serum MFG-E8 in the case group (mean = 11160.9 pg/mL) were significantly higher than those in the control group (mean = 3081.0 pg/mL, p < 0.001). MFG-E8 levels highly correlated with the World Federation of Neurosurgical Societies (WFNS) and modified Fisher scores (r = −0.691 and − 0.767, respectively, p < 0.001). In addition, MFG-E8 levels in patients with DCI (5882.7 ± 3162.4 pg/mL) were notably higher than those in patients without DCI (15818.2 ± 3771.6 pg/mL, p < 0.001). A receiver operating characteristic curve showed that the occurrence of DCI could effectively be predicted by MFG-E8 (area under the curve = 0.976, 95%CI = 0.850–1.000). Kaplan–Meier survival analysis showed a remarkable decrease in the incidence of DCI in case group individuals with high levels of MFG-E8 (≥11160.9 pg/mL, p < 0.001). Conclusion MFG-E8 may be a useful predictive marker for DCI after an aSAH and could be a promising surrogate end point.
Highlights
Aneurysmal subarachnoid hemorrhage is an acute and critical disease with high morbidity and mortality [1,2,3,4]
Except for milk fat globule epidermal growth factor 8 (MFG-E8) level, hypertension, World Federation of Neurosurgical Societies (WFNS) scores, and modified Fisher scores were all closely related to the occurrence of delayed cerebral ischemia (DCI) (Table 4)
We suggest that the levels of MFG-E8, WFNS scores, and modified Fisher scores can be used in the evaluation of DCI occurrence
Summary
Aneurysmal subarachnoid hemorrhage (aSAH) is an acute and critical disease with high morbidity and mortality [1,2,3,4]. After aSAH, a cerebral vasospasm can effectively decrease blood flow and result in delayed cerebral ischemia (DCI). DCI, known as symptomatic cerebral vasospasm, is a common complication usually occurring 3–14 days after aSAH and is considered to be the main cause of poor prognoses [6,7,8]. In the diagnosis and treatment of aneurysms, early detection and prevention of DCI could help improve the patient’s quality of life and relieve the clinical burden [9]. Previous studies have found some evidence for the participation of cerebral vasospasm, microthrombosis, and inflammation in the pathophysiological processes of DCI [10,11,12,13,14]
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