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脂联素型前列腺素 D 合酶水平在发作性睡病和特发性嗜睡症患者中升高。

Lipocalin-type prostaglandin D synthase levels increase in patients with narcolepsy and idiopathic hypersomnia.

机构信息

Department of Pulmonary Medicine, Peking University People's Hospital, Beijing, China.

Sleep and Psychosomatic Medicine Center, The Third People's Hospital of Hainan Province, Sanya, Hainan, China.

出版信息

Sleep. 2021 Apr 9;44(4). doi: 10.1093/sleep/zsaa234.

Abstract

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 (p < 0.001) were 22%-25% lower in control subjects than in patients with EDS complaints, including NT1, NT2, and IH. In contrast to significant differences in CSF Hcrt-1 levels, CSF L-PGDS levels and serum L-PGDS were comparable among NT1, NT2, and IH (p > 0.05), 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.

摘要

研究目的

日间过度嗜睡(EDS)是咨询的常见原因,也是发作性睡病和特发性嗜睡(IH)的定义性症状。相关机制尚不清楚。脂联素型前列腺素 D 合酶(LPGDS)是一种合理的诱导睡眠候选物。本研究旨在比较中枢性嗜睡患者(包括 1 型发作性睡病(NT1)、2 型发作性睡病(NT2)和 IH)与健康对照组(Con)的脑脊液(CSF)和血清 LPGDS 水平。

方法

通过 ELISA 法测量 122 例发作性睡病患者(106 例 NT1 和 16 例 NT2)、27 例 IH 和 51 例 Con 的血清 LPGDS、CSF LPGDS 和 CSF 食欲素-1(Hcrt-1)水平。

结果

与 EDS 主诉患者(包括 NT1、NT2 和 IH)相比,对照组 CSF(p = 0.02)和血清(p < 0.001)中的 LPGDS 水平低 22%-25%。与 CSF Hcrt-1 水平的显著差异相比,CSF L-PGDS 水平和血清 L-PGDS 在 NT1、NT2 和 IH 之间相当(p > 0.05),除了 IH 中的血清 LPGDS 略低于 NT1(p = 0.01)。在嗜睡症患者中,血清 LPGDS 与 MSLT 上的睡眠潜伏期呈适度负相关(r = -0.227,p = 0.007)。

结论

作为一种产生睡眠的酶,CSF/血清 LPGDS 可能成为中枢性 EDS 的新生物标志物,并暗示存在共同的发病关联,但会补充而不是替代食欲素标志物。

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