Acute and transient increase of lipocalin-type prostaglandin D synthase (β-trace) level in cerebrospinal fluid of patients with aneurysmal subarachnoid hemorrhage

被引:31
作者
Mase, M [1 ]
Yamada, K
Iwata, A
Matsumoto, T
Seiki, K
Oda, H
Urade, Y
机构
[1] Nagoya City Univ, Sch Med, Dept Neurosurg, Nagoya, Aichi 4678602, Japan
[2] Maruha Corp, Cent Res Inst, Dept Biol Chem, Tsukuba, Ibaraki 3004295, Japan
[3] Osaka Biosci Inst, Dept Mol Behav Biol, Osaka 5650874, Japan
[4] Osaka Biosci Inst, CREST, Japan Sci & Technol Corp, Osaka 5650874, Japan
关键词
prostaglandin D synthase; subarachnoid hemorrhage; cerebrospinal fluid; beta-trace protein; cerebral aneurysm;
D O I
10.1016/S0304-3940(99)00494-2
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We measured the concentration of lipocalin-type prostaglandin D synthase (PGDS) in cerebrospinal fluid (CSF) and serum in patients 1, 3, 5, 7, 9, 11, 14 and 17 days after subarachnoid hemorrhage (SAH) due to ruptured cerebral aneurysms. The PGDS level in lumbar CSF increased about two-fold at day 3 (20.85 +/- 2.71 mu g/ml, mean +/- SE) and at day 5 (25.24 +/- 3.76), as compared with the level at day 1 (11.25 +/- 1.07). The CSF level gradually decreased and returned to the day 1 level at day 17. The serum PGDS level was much lower than the CSF level (0.39 +/- 0.06 at day 1) and almost unchanged until day 17. The neuron-specific enolase level in CSF, as an index of brain damage, was maximum at day 1 (29.83 +/- 7.32 ng/ml) and decreased at day 3 and at day 5 (18.28 +/- 2.65 and 11.95 +/- 1.82, respectively). These results suggest that the transient and delayed increase in the PGDS level in CSF is due to its induction of PGDS in the arachnoid membrane after SAH. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:188 / 190
页数:3
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