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

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.