Are patients with chronic fatigue syndrome just ‘tired’ or also ‘sleepy’?

It is presently unclear whether chronic fatigue syndrome (CFS) patients exhibit daytime sleepiness in addition to fatigue. Both, fatigue, such as that seen in CFS patients, and excessive daytime sleepiness, such as in sleep apnea–hypopnea syndrome (SAHS), remain poorly understood. Both daytime conditions are generally related to unrefreshing sleep and show affective symptoms. This study’s objective was to contribute to the understanding of the relationship between fatigue and sleepiness in CFS patients not co‐morbid for primary sleep or psychiatric disorders. We compared 16 untreated CFS patients (mean age 32.8, all females) with 13 untreated SAHS (mean age 47.7, all females) patients and 12 healthy controls (mean age 32.2, all females). Objective sleepiness was measured using multiple sleep latency tests (MSLT). Subjective sleepiness and fatigue were assessed with the Epworth Sleepiness Scale and the Fatigue Severity Scale, respectively. Mean Sleep Latency (SL) on the MSLT was significantly shorter in SAHS patients than in CFS patients and CFS patients showed significantly shorter mean SL than matched controls but within normal range. Subjective sleepiness was greatest in SAHS patients and subjective fatigue was highest in CFS patients. Affective symptoms showed highest intensities in CFS patients. While higher than the control group on all measures, compared to SAHS, the CFS group had higher subjective fatigue and lower subjective and objective sleepiness. Despite possible overlap in symptoms and signs of both daytime conditions, our data indirectly support the clinical distinction between fatigue and sleepiness.     

二肽精氨酰-谷氨酰胺对脂多糖致肠道上皮细胞损伤的保护作用

目的探讨二肽精氨酰-谷氨酰胺(Arg-Gln)对脂多糖(LPS)致肠道上皮细胞Caco-2炎性反应、细胞活力及屏障功能损伤的影响及其可能的机制。方法用不含Gln的培养液加入不同水平的Arg-Gln培养Caco-2细胞24 h,同时加或不加Gln合成抑制剂———甲硫氨酸亚矾胺(MS)4.0 mmol.L-1。然后分别进行如下实验:(1)加入LPS 0.05 g.L-1,再培养24 h,分别测定促炎细胞因子IL-8水平(ELISA法)、细胞活力(MTS法)变化;比较相同水平(2.5 mmol.L-1)Arg-Gln和Gln、Arg的抗炎效果。(2)加入LPS0.4 g.L-1,再培养24 h,测定Caco-2细胞跨上皮电阻(TER)变化。(3)加入LPS 0.05 g.L-1再培养5 h,测定细胞核因子-κB(NF-κB)及其抑制因子I-κB表达的变化(免疫印迹法)。结果与不加LPS的细胞相比,加入LPS 0.05 g.L-1培养24 h可显著刺激Caco-2细胞产生IL-8,抑制细胞活力(Pa<0.05);加MS时,大剂量LPS(0.4 g.L-1)导致TER明显下降(P<0.05)。1.25～5.00 mmol.L-1 Arg-Gln可抑制LPS诱导的IL-8水平(P<0.05);同样剂量时(2.5 mmol.L-1),Gln对IL-8的抑制效果优于Arg-Gln和Arg。2.0～4.0 mmol.L-1Arg-Gln明显促进LPS抑制的Caco-2细胞活力的恢复(Pa<0.05);Arg-Gln可抑制LPS诱导的TER下降(P<0.05)。LPS(0.05 g.L-1)或Arg-Gln(2.0 mmol.L-1)对NF-κB和I-κB表达均无明显影响。结论 Arg-Gln可减轻LPS诱导的肠道上皮细胞屏障障碍及炎性反应,恢复细胞活力;Arg-Gln的保护机制可能与NF-κB途径无明显关系。