Cerebrospinal fluid pentraxin 3 early after subarachnoid hemorrhage is associated with vasospasm

Purpose To investigate plasma and cerebrospinal fluid (CSF) concentrations of pentraxin 3 (PTX3), a prototypic long pentraxin protein induced by proinflammatory signals, in subarachnoid hemorrhage (SAH), and its relation with SAH-associated vasospasm. Methods Serial plasma and CSF samples were colle...

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Published in:Intensive care medicine Vol. 37; no. 2; pp. 302 - 309
Main Authors: Zanier, Elisa R., Brandi, Giovanna, Peri, Giuseppe, Longhi, Luca, Zoerle, Tommaso, Tettamanti, Mauro, Garlanda, Cecilia, Sigurtà, Anna, Valaperta, Serenella, Mantovani, Alberto, De Simoni, Maria Grazia, Stocchetti, Nino
Format: Journal Article
Language:English
Published: Berlin/Heidelberg Springer-Verlag 01-02-2011
Springer
Springer Nature B.V
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Summary:Purpose To investigate plasma and cerebrospinal fluid (CSF) concentrations of pentraxin 3 (PTX3), a prototypic long pentraxin protein induced by proinflammatory signals, in subarachnoid hemorrhage (SAH), and its relation with SAH-associated vasospasm. Methods Serial plasma and CSF samples were collected from 38 consecutive SAH patients admitted to the Neurosurgical Intensive Care. PTX3 concentrations were analyzed in relation to clinical status and clinical vasospasm (defined as neuro-worsening and angiographic confirmation of vessel narrowing). Since neutrophils are an important source of preformed PTX3, myeloperoxidase (MPO) in CSF was measured to assess the correlation with CSF PTX3 and establish whether blood contamination was the determinant of PTX3 increase. Results PTX3 was elevated in all SAH patients both in plasma and CSF. Acute peak (first 48 h after SAH) CSF PTX3 was significantly higher in patients who later developed vasospasm [median 13.6 (range 2.3–51.9) ng/ml] compared to those who did not [3.2 (0.1–50.5) ng/ml, p  = 0.03]. The temporal pattern of CSF PTX3 in patients with vasospasm was triphasic with a peak during the first 48 h after SAH, a subsequent decrease in the following 48–96 h and a secondary significant increase with the occurrence of vasospasm. A loose correlation between CSF PTX3 and MPO was observed ( r 2  = 0.13), indicating that following SAH there is a brain production of PTX3. Conclusions Acute increased concentrations of PTX3 in CSF but not in plasma are related to the occurrence of vasospasm, indicating that measurement of CSF PTX3 associated with the clinical evaluation can improve early diagnosis of this complication.
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ISSN:0342-4642
1432-1238
DOI:10.1007/s00134-010-2075-2