Serum concentration of adhesion molecules in patients with delayed ischaemic neurological deficit after aneurysmal subarachnoid haemorrhage: the immunoglobulin and selectin superfamilies

Abstract

Objectives-Adhesion molecules are involved in the pathogenesis of cerebral ischaemia and may play a part in the pathophysiology of delayed ischaemic neurological deficit (DIND) after aneurysmal subarachnoid haemorrhage. It was hypothesised that after aneurysmal subarachnoid haemorrhage, adhesion molecules may play a part in the pathophysiology of DIND as reflected by significantly altered serum concentrations in patients with and without DIND. Methods-In a prospective study, mean serum concentrations of ICAM-1, VCAM-1, PECAM, and E, P, and L-selectin were compared between patients without (n=23) and with (n=13) DIND in patients with World Federation of Neurological Surgeons (WFNS) grades 1 or 2 subarachnoid haemorrhage. Serum was sampled from patients within 2 days of haemorrhage and on alternate days until discharge. Concentrations of adhesion molecules were measured by standard procedures using commercially available enzyme linked immunoabsorbent assays. Results-There were non-significant diVerences in serum concentrations of ICAM-1 (290.8 ng/ml v 238.4 ng/ml, p=0.0525), VCAM-1 (553.2 ng/ml v 425.8 ng/ml, p=0.053), and PECAM (22.0 ng/ml v 21.0 ng/ml, p=0.56) between patients without and with DIND respectively. The E-selectin concentration between the two patient groups (44.0 ng/ml v 37.4 ng/ml, p=0.33) was similar. The P-selectin concentration, however, was significantly higher in patients with DIND compared with those patients without DIND (149.5 ng/ml v 112.9 ng/ml, p=0.039). By contrast, serum L-selectin concentrations were significantly lower in patients with DIND (633.8 ng/ml v 897.9 ng/ml, p=0.013). Conclusions-Of all the adhesion molecules examined in this study, P and L-selectin are involved in the pathophysiology of DIND after aneurysmal subarachnoid haemorrhage. (J Neurol Neurosurg Psychiatry 2001;71:329-333)

Serum and cerebrospinal fluid concentrations of E-selectin in patients with aneurysmal subarachnoid hemorrhage

“…This may provide an opportunity for prophylactic anticipatory therapy. Our findings are consistent with those in which serum selectin molecules were detected in human stroke, but not with the study by Nissen et al (36).…”

“…There was no statistically significant correlation between E-selectin concentrations and the clinical profile of the patients, consistent with previous human SAH studies related to E-selectin (35,36). Nevertheless, we think that this may be due to the small number of patients studied here.…”

“…The role of CAMs, principally selectins, in SAH is less clear and few studies have investigated the changes in selectin molecules in aneurysmal SAH (35,36). Polin et al (35) showed marked elevation of soluble forms of Eselectin in the CSF of 17 patients with ruptured SAH compared with levels in the CSF of 16 controls, patients with unruptured aneurysms, and patients tested months after the occurrence of SAH.…”

“…In addition, 3 patients with angiographically demonstrated VS showed higher levels of E-selectin than the average for all other SAH patients. More recently, in a prospective study, Nissen et al (36) compared the serum concentrations of three selectin molecules in patients with and without delayed ischemic neurological deficit (DIND) after grade 1 or 2 SAH. The Eselectin levels were similar for the two groups.…”

Microthrombosis after Aneurysmal Subarachnoid Hemorrhage: An Additional Explanation for Delayed Cerebral Ischemia

“…Increased platelet activation and aggregation are suggested by increased levels of b-thromboglobulin, thromboxane B2, soluble platelet selectin (sP-selectin), and platelet-activating factor (Ohkuma et al, 1991;Hirashima et al, 1997a;Frijns et al, 2006 b;Nissen et al, 2001). Interestingly, increased procoagulant activity is already present within a few days after SAH, that is, in a time period before vasospasm develops.…”