Lipocalin-type prostaglandin D synthase levels increase in patients with narcolepsy and idiopathic hypersomnia.
Lipocalin-type prostaglandin D synthase levels increase in patients with narcolepsy and idiopathic hypersomnia.
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DOI：
10.1093/sleep/zsaa234
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发表时间：
2020-11
期刊：
影响因子：
5.6
通讯作者：
Peipei Wang;Qinghua Li;Xiao-song Dong;H. An;Jing Li;Long Zhao;Han Yan;K. Aritake;Zhili Huang;K. Strohl;Y. Urade;Jun Zhang;F. Han
中科院分区：
文献类型：
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作者：
Peipei Wang;Qinghua Li;Xiao-song Dong;H. An;Jing Li;Long Zhao;Han Yan;K. Aritake;Zhili Huang;K. Strohl;Y. Urade;Jun Zhang;F. Han
研究提示：白天过度嗜睡（EDS）是一种常见的咨询原因，也是发作性睡病和特发性嗜睡（IH）的一种定义性症状。相关机制尚不清楚。脂质运载蛋白型前列腺素D合成酶（LPGDS）是一种可能的睡眠诱导候选者。本研究旨在比较中枢源性睡眠过度患者组（包括发作性睡病1型（NT 1）、2型（NT 2）和IH）与健康对照组（Con）的脑脊液（CSF）和血清LPGDS水平。方法采用酶联免疫吸附法（ELISA）检测122例发作性睡病患者（NT 1 106例，NT 2 16例）、27例IH患者和51例Con患者血清LPGDS、CSF LPGDS和CSF下丘脑泌素1（Hcrt 1）水平。结果CSF（p=0.02）和血清（p 0.05）中的LPGDS水平，除了IH中的血清LPGDS略低于NT 1（p=0.01）。在睡眠过度的受试者中，血清L-PGDS与MMP 3睡眠潜伏期呈中度负相关（r=-0.227，p=0.007）。结论：CSF/血清LPGDS作为一种促睡眠素产生酶，可作为中枢源性EDS的一种新的生物标志物，并暗示共同的发病相关性，但将补充而不是取代食欲素标志物。
STUDY OBJECTIVES Excessive daytime sleepiness (EDS) is a frequent cause for consultation and a defining symptom of narcolepsy and idiopathic hypersomnia (IH). The associated mechanisms remain unclear. Lipocalin-type prostaglandin D synthase (LPGDS) is a plausible sleep-inducing candidate. This study is to compare cerebral spinal fluid (CSF) and serum LPGDS levels in patients group with hypersomnia of central origin, including those with narcolepsy type 1 (NT1) and type 2 (NT2) and IH, to those in healthy controls (Con). METHODS Serum LPGDS, CSF LPGDS and CSF hypocretin-1(Hcrt-1) levels were measured by ELISA in 122 narcolepsy patients (106 NT1, and 16 NT2), 27 IH, and 51Con. RESULTS LPGDS levels in CSF (p=0.02) and serum (p0.05), except for slightly lower serum LPGDS in IH than in NT1(p=0.01). Serum L-PGDS correlated modestly and negatively to sleep latency on MSLT(r=-0.227, p=0.007) in hypersomnia subjects. CONCLUSIONS As a somnogen-producing enzyme, CSF/serum LPGDS may serve as a new biomarker for EDS of central origin and imply a common pathogenetic association, but would complement rather than replaces orexin markers.