Abstract
Aneurysmal subarachnoid hemorrhage (SAH) is associated with high morbidity and mortality. In SAH patients, plasma osteopontin (OPN) has been shown to independently predict poor outcome. The aim of the study is to investigate, in a selected population with severe SAH, OPN time course in cerebrospinal fluid (CSF) and plasma during the first week after aneurism rupture, and OPN prognostic value. We included 44 patients with the following criteria: (1) age 18 and 80 years, (2) diagnosis of SAH from cerebral aneurysm rupture, (3) insertion of external ventricular drain. Plasma and CSF were sampled at day 1, 4, and 8. OPN levels, in CSF and plasma, displayed a weak correlation on day 1 and were higher, in CSF, in all time points. Only in poor prognosis patients, OPN levels in CSF significantly increased at day 4 and day 8. Plasma OPN at day 1 and 4 was predictor of poor outcome. In conclusion, plasma and CSF OPN displays a weak correlation, on day 1. The higher levels of OPN found in the CSF compared to plasma, suggest OPN production within the CNS after SAH. Furthermore, plasma OPN, at day 1 and 4, seems to be an independent predictor of poor outcome.
Highlights
Aneurysmal subarachnoid hemorrhage (SAH), is one of the most life-threatening diseases, with high mortality and disability rates [1]
Osteopontin (OPN) is a pleiotropic acidic glycoprotein that was first described as a bone-specific sialoprotein [5] and as a molecule expressed in activated T cells, called the “early T cell activated gene” (ETA-1) [6]
The aim of the present study is to investigate, in a selected population with severe SAH that needs an external ventricular cerebrospinal fluid (CSF) drainage, how the level of OPN changes in CSF during the first week after aneurism rupture, its relation with OPN plasma level and the possible prognostic value
Summary
Aneurysmal subarachnoid hemorrhage (SAH), is one of the most life-threatening diseases, with high mortality and disability rates [1]. Cells 2019, 8, 695 i.e., early brain injury (EBI) and vasospasm with delayed cerebral ischemia (DCI). EBI occurs within minutes after the rupture of an intracranial aneurysm and it seems to be related to the increase of intracranial pressure, decreased cerebral blood flow, and global cerebral ischemia [2]. SAH induced vasospasm is the delayed narrowing of intracranial arteries that takes place between the 4th and the. EBI and subsequent vasospasm initiate secondary injuries, such as blood–brain barrier disruption, neuroinflammation and oxidative pathways, release of biological active molecules, microembolism, spasm of the arteries and little vessels that might lead to injury expansion and brain damage [4].
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