Secondary S100B Protein Increase Following Brain Arteriovenous Malformation Rupture is Associated with Cerebral Infarction.

Lorenzo Garzelli,Kevin Premat,Alice Jacquens,Frédéric Clarençon,Stéphanie Lenck,Vincent Degos,Jonathan Cortese,Bertrand Mathon,Idriss Haffaf,Nader Sourour,Eimad Shotar,Caroline Amouyal

doi:10.3390/molecules25215177

Abstract

Early S100B protein serum elevation is associated with poor prognosis in patients with ruptured brain arteriovenous malformations (BAVM). The purpose of this study is to determine whether a secondary elevation of S100B is associated with early complications or poor outcome in this population. This is a retrospective study of patients admitted for BAVM rupture. A secondary increase of S100B was defined as an absolute increase by 0.1 μg/L within 30 days of admission. Fisher’s and unpaired t tests followed by multivariate analysis were performed to identify markers associated with this increase. Two hundred and twenty-one ruptures met inclusion criteria. Secondary S100B protein serum elevation was found in 17.1% of ruptures and was associated with secondary infarction (p < 0.001), vasospasm-related infarction (p < 0.001), intensive care (p = 0.009), and hospital length of stay (p = 0.005), but not with early rebleeding (p = 0.07) or in-hospital mortality (p = 0.99). Secondary infarction was the only independent predictor of secondary increase of S100B (OR 9.9; 95% CI (3–35); p < 0.001). Secondary elevation of S100B protein serum levels is associated with secondary infarction in ruptured brain arteriovenous malformations.

Highlights

Brain arteriovenous malformation (BAVM) rupture results in significant morbi-mortality, but the prognosis is better than primary hematoma [1]
Present study aims to describe S100B evolution and determine whether a secondary elevation is associated with early complications or poorer outcomes following brain arteriovenous malformations (BAVM) rupture
In this large population with ruptured BAVM, secondary S100B protein serum elevation was associated with ischemic complications, vasospasm-related infarction and a prolonged stay both in the intensive care unit and hospital

Summary

Introduction

Brain arteriovenous malformation (BAVM) rupture results in significant morbi-mortality, but the prognosis is better than primary hematoma [1]. Elevated S100B serum levels within the first 48 h of patient admission are found to be an independent predictor of in-hospital mortality following BAVM rupture [2]. Secondary complications following BAVM rupture include hydrocephalus, rebleeding, and vasospasm [4,5,6]. No study to this date has monitored S100B in ruptured BAVM beyond 48 h. The present study aims to describe S100B evolution and determine whether a secondary elevation is associated with early complications or poorer outcomes following BAVM rupture

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