脂代谢紊乱与阻塞性睡眠呼吸暂停低通气综合征的发病关系

目的　探讨脂代谢紊乱、咽部脂肪浸润在阻塞性睡眠呼吸暂停低通气综合征(OSAHS)发病机制中的作用。方法　选择OSAHS肥胖患者19例、非肥胖患者15例和正常对照组9例,比较3组脂代谢临床指标和悬雍垂大小,应用生化方法检测悬雍垂中脂肪量,光镜和电镜观察悬雍垂病理学改变。结果　肥胖组和非肥胖组OSAHS患者的TC、TC/HDL、悬雍垂重量和体积、悬雍垂中脂肪量与对照组差异有显著性意义,在肥胖与非肥胖组中,这些指标与呼吸暂停低通气指数(AHI)正相关(P<0 05)。肥胖组和非肥胖组的OSAHS患者悬雍垂存在着相似的病理组织学改变:光镜下悬雍垂中有明显的脂肪细胞浸润,肌纤维排列紊乱,呈多形性改变,包括局灶性肥大、萎缩和退变;电镜下两组肌纤维局灶性Z线模糊、扭曲和消失,部分呈点状或片状肌纤维断裂,肌节溶解消失,肌原纤维间有局灶性脂滴浸润。结论　肥胖和非肥胖OSAHS患者存在不同程度脂代谢紊乱,咽部过多的脂肪浸润可能通过改变气道大小、形状和咽壁顺应性,促成(加重)气道阻塞,从而成为OSAS发病的重要因素之一。

Clinical study on the effect of lipid metabolic disturbance to the pathogenesis of obstructive sleep apnea-hypopnea syndrome

Objectives To approach the effect of the disturbance of lipid metabolism, fatty infiltration in oropharyngeal tissues on the patient with obstructive sleep apnea hypopnea syndrome (OSAHS). Methods 19 obese patients of OSAHS, 15 nonobese patients of OSAHS and 9 healthy people (as control) were selected. Among the three groups, The related clinical index and size and the weight of uvula were measured. The fatty weight of uvula was analyzed by biochemical methods. The uvular tissue sections were evaluated by light microscope (LM) and transmission electron microscope (TEM). Results 1 Both the obese and nonobese groups, the TC, TC/HDL, size and weight and the adipose tissue in uvula were obviously different compared with control group( P <0 05). These parameters in obese and nonobese groups had a positive correlation with AHI. 2. Similar pathologic changes revealed by LM and TEM existed in obese group and nonobese group of OSAHS. The section of uvula in LM showed that there was excessive fatty infiltration. And muscle fibers were partially atrophied and/or hypertrophied. The fibrous tissue and muscle fibers arranged in a disordered way. The uvula myofibril in TEM showed focal or spotted rough and deformity of Z line, sarcomere loss and vacuolation. Lipid droplet infiltration was also detected in adjoin of myofibril. Conclusions The results suggested that lipid metabolic disturbance might exist in the patient with OSAHS. And abundant oropharyngeal fatty infiltration might be an important factor in pathogenesis of OSAHS that possibly contributed to change the size and shape of pharyngeal airway and compliance of pharyngeal wall