Pentraxin 3 as a marker of vasospasm following subarachnoid hemorrhage

Introduction

We studied the induction of Pentraxin 3 (PTX3), a prototypic long pentraxin protein induced by proinflammatory signals in subarachnoid hemorrhage (SAH) patients, to investigate a possible relation with SAH-associated ischemic brain damage.

Methods

PTX3 was measured in the plasma and cerebrospinal fluid (CSF) of 38 SAH patients admitted to the neuroscience ICU, who were divided into three groups: occurrence of vasospasm, defined as neuro-worsening (loss of at least one point of the Glasgow Coma Scale motor component and/or appearance of a new focal deficit) and angiographic confirmation of vasospasm; presence of an early hypodense lesion, defined as the appearance of a new hypodense lesion at CT scan following endovascular or surgical treatment, or around the initial intracerebral hematoma; and absence of a hypodense lesion. Arterial and CSF samples were obtained every 12 hours starting on the day of SAH and up 2 weeks post SAH.

Results

PTX3 was induced in the plasma and CSF of SAH patients. CSF peak concentrations were significantly higher in patients with vasospasm (21.5 ± 5.1 ng/ml) compared with those with no CT hypodense lesion (5.8 ± 4.5 ng/ml, P < 0.05). Patients with an early hypodense lesion showed a peak concentration that was intermediate between the other two groups (12.4 ± 5.2 ng/ml). No difference was observed in plasma levels among the three groups. The temporal pattern of CSF PTX3 in patients with vasospasm was triphasic: there was an initial increase of PTX3 during the first 48 hours following SAH (acute phase, up to 17.2 ± 5.2 ng/ml), followed by a subsequent decrease in the next 48–96 hours (subacute phase, up to 1.2 ± 0.3 ng/ml, P < 0.01 compared with the acute phase). With the appearance of vasospasm, a secondary peak of PTX3 was detected (up to 7.1 ± 1.4 ng/ml, P < 0.01 compared with the subacute phase). No changes were detectable in plasma.

Conclusion

PTX3 is induced in the CSF and in plasma following SAH; however, the CSF but not plasma levels are directly related to the degree of brain injury. In addition the data show that PTX3 measured in the CSF might be a reliable marker of vasospasm following SAH, and suggest that measurements of PTX3-CSF levels associated with clinical evaluation could improve early diagnosis of vasospasm in these patients.