Sleep Disorders Center, Department of Neurological Sciences, University of Bologna, Bologna, Italy.
Sleep. 2009 Nov;32(11):1491-7. doi: 10.1093/sleep/32.11.1491.
To contribute to the anthropometric and metabolic phenotyping of orexin-A-deficient narcoleptic patients, and to explore a possible risk of their developing a metabolic syndrome.
We performed a cross-sectional study comparing metabolic alterations in patients with narcolepsy with cataplexy (NC) and patients with idiopathic hypersomnia without long sleep time.
University hospital.
Fourteen patients with narcolepsy with cataplexy and 14 sex and age-matched patients with idiopathic hypersomnia without long sleep time.
N/A.
Metabolic parameters were evaluated by measuring body mass index (BMI), waist circumference (also with abdominal computed tomography), blood pressure, and daily calorie intake (3-day diary). Chronotypes were assessed through the morningness-eveningness questionnaire. Lumbar puncture for cerebrospinal fluid orexin-A determination and HLA typing were performed. Patients with narcolepsy with cataplexy (all HLA DQB1*0602 positive and with cerebrospinal fluid orexin-A levels < 110 pg/mL) had a higher BMI and BMI-independent metabolic alterations, namely waist circumference, high-density lipoprotein cholesterol, and glucose/insulin ratio (an insulin resistance index), with respect to patients with idiopathic hypersomnia without long sleep time (cerebrospinal fluid orexin-A levels > 300 pg/mL). Despite lower daily food intake, patients with narcolepsy with cataplexy displayed significant alterations in metabolic parameters resulting in a diagnosis of metabolic syndrome in more than half the cases.
BMI-independent metabolic alterations and the relative hypophagia of patients with narcolepsy with cataplexy, as compared with patients with idiopathic hypersomnia without long sleep time, suggest that orexin-A influences the etiology of this phenotype. Moreover, considering that these dysmetabolic alterations are present from a young age, a careful metabolic follow-up of patients diagnosed with narcolepsy with cataplexy is mandatory.
为了对食欲素-A 缺乏性发作性睡病患者进行人体测量学和代谢表型分析,并探讨其发生代谢综合征的风险。
我们进行了一项横断面研究,比较了伴有猝倒的发作性睡病(narcolepsy with cataplexy,NC)患者和无长睡眠时相的特发性嗜睡症(idiopathic hypersomnia without long sleep time,IHS)患者的代谢改变。
大学医院。
14 例伴有猝倒的发作性睡病患者和 14 例性别和年龄匹配的无长睡眠时相的特发性嗜睡症患者。
无。
通过测量体重指数(body mass index,BMI)、腰围(同时行腹部计算机断层扫描)、血压和每日热量摄入(3 天日记)来评估代谢参数。通过晨型-晚型问卷评估昼夜节律类型。进行腰椎穿刺以测定脑脊液食欲素-A,并进行 HLA 分型。伴有猝倒的发作性睡病患者(均 HLA DQB1*0602 阳性,脑脊液食欲素-A 水平<110 pg/mL)的 BMI 较高,且存在 BMI 不依赖的代谢改变,包括腰围、高密度脂蛋白胆固醇和血糖/胰岛素比值(胰岛素抵抗指数),与无长睡眠时相的特发性嗜睡症患者(脑脊液食欲素-A 水平>300 pg/mL)相比。尽管每日食物摄入量较低,但伴有猝倒的发作性睡病患者的代谢参数仍存在显著改变,导致超过一半的患者被诊断为代谢综合征。
与无长睡眠时相的特发性嗜睡症患者相比,伴有猝倒的发作性睡病患者存在 BMI 不依赖的代谢改变和相对的食欲减退,这表明食欲素-A 影响了该表型的发病机制。此外,鉴于这些代谢紊乱改变从年轻时就存在,对诊断为伴有猝倒的发作性睡病的患者进行仔细的代谢随访是必要的。