腭咽组织脂质异位积累及瘦素的检测

The effect of ectopic accumulation of lipid in the pharyngeal tissue and leptin on the pathogenesis of OSAHS

目的探讨腭咽组织中脂质异位积累及瘦素(leptin)在阻塞性睡眠呼吸暂停低通气综合征(obstructivesleepapneahypopneasyndrome,OSAHS)发病机制中的作用。方法OSAHS患者和无鼾症患者19例,按体重指数配对研究:①HE、油红-O脂肪染色观察腭咽组织病理学特点;②SABC法观察瘦素及瘦素蛋白b型受体(Ob-Rb)在腭咽组织中的表达;③分别用生化法和放射免疫法检测血脂和血瘦素水平;④统计学分析运用t检验和相关分析。结果①OSAHS患者腭咽组织中脂质沉积,小唾液腺类型改变;②瘦素及Ob-Rb主要表达于腭咽组织黏膜层、小血管壁和小唾液腺腺泡边缘,两组间表达量差异无显著性意义(P>0.05);③OSAHS患者存在明显的脂代谢紊乱,且与呼吸暂停低通气指数(apneaandhypopneaindex,AHI)呈显著正相关。结论①腭咽组织中脂质异位积累可能是OSAHS患者咽部气道塌陷的重要原因;②腭咽黏膜上皮细胞、血管内皮细胞和小唾液腺细胞可能是产生瘦素的潜在部位,瘦素和Ob-Rb并存说明瘦素具有外周性作用,二者表达量无组间显著性差异,可能是导致脂质异位积累的重要原因;③脂代谢紊乱可能非OSAHS发病机制中的决定性因素;④内源性高瘦素血症可能是机体针对呼吸障碍及脂代谢紊乱的保护性反应,还可能与OSAHS患者持续的高交感活性有关。血浆瘦素水平可以反映OSAHS病情的严重程度。

OBJECTIVE To study the effect of ectopic accumulation of lipid and leptin on the pathogenesis and development of OSAHS. METHODS Thirty eight patients were enrolled into this study. They were divided into 2 groups： OSAHS group and non-snoring group. Each group had 19 cases and were coupled according to BMI. HE staining and oil red-O lipid staining was used to observe the pathologic characteristic of the pharyngeal tissue. The expression of leptin and Ob- Rb in the pharyngeal tissue was investigated by SABC staining technique. The level of lipid and leptin in plasma was examined by biochemical and radio-immunological methods respectively. RESULTS ① Fat infiltrated in the pharyngeal tissue of OSAHS patients, and the type of the minor salivary glands changed. ② In both groups, leptin and Ob-Rb were distributed in the mucous layer, the wall of small vessel and the edge of the minor salivary glands with no significant difference （P〉 0.05）. ③ All of the OSAHS patients suffered serious lipid metabolic disorders. CONCLUSION ① Fatty infiltration in the pharyngeal tissue may lead to collapse of the pharyngeal airway during sleep. ② The epithelial cells of mucosa, endothelial cells of small vessels and glandular cells of minor salivary glands can potentially produce leptin. Leptin existing with Ob-Rb shows the peripheral action of leptin. The positive expression of leptin and Ob-Rb had no significant difference between the two groups, which may explain the ectopic accumulation of ripid. ③ Disordered tipid metabolism may not be the determinant factor in the pathogenesis of OSAHS ④ Endogenous hyperleptinemia may be the protective response to respiratory disturbance and disordered lipid metabolism, and is also associated with the continuous hypersympathetic activity. The level of leptin in plasma has a positive correlation with the severity of OSAHS.