Aneurysmal subarachnoid hemorrhage induces the expression of Pentraxin3 in patients

Introduction

Aneurismal subarachnoid hemorrhage (SAH) is an extremely severe illness associated with a high mortality rate and permanent severe neurological dysfunction in two-thirds of all affected patients. One of the major complications of SAH is vasospasm-associated cerebral ischemia. Clinical and experimental data suggest that vasospasm is linked to the inflammatory response associated with SAH. The goal of this study was to investigate the expression of Pentraxin3 (PTX3), a prototypic long pentraxin protein induced by proinflammatory signals in the brain, in SAH patients to test the hypothesis that SAH is followed by an upregulation of PTX3, and establish a temporal relationship between the expression of PTX3 and the induction of vasospasm. We also attempted to establish that PTX3 is detectable in cerebrospinal fluid (CSF).

Methods

We studied eight severe SAH patients admitted to our neuroscience ICU with a median World Federation Neurosurgical Score of 4 and a Fisher score of 4. Arterial, jugular venous blood and CSF samples were routinely obtained every 12 hours for 7 days. PTX3 levels were measured by ELISA in plasma and CSF samples.

Results

Compared with plasma levels of PTX3 in normal volunteers (<2 ng/ml [1]), SAH induced a marked increase in plasma PTX3 expression. During the first 48 hours following SAH (acute phase), PTX3 arterial and jugular venous levels increased to 36.93 ± 24.32 ng/ml and 33.64 ± 28.76 ng/ml, respectively, and then subsequently decreased concomitantly with the reduction of the inflammation (48–96 hours: subacute phase). PTX3 is detectable in the CSF: mean CSF levels of PTX3 were 4.07 ± 3.64 ng/ml during the acute phase and 0.69 ± 0.44 ng/ml during the subacute phase (t test: P < 0.05 compared with the acute phase). In the presence of vasospasm (four patients), we detected a second peak of PTX3 (4.03 ± 2.85 ng/ml) in CSF samples (t test: P < 0.05 compared with the subacute phase) that was not detectable in plasma.

Conclusion

SAH is characterized by the production of PTX3 and the induction of vasospasm is associated with an upregulation of PTX3 in the CSF that is not detectable in plasma.