Lavie Lena, Lotan Rachel, Hochberg Irit, Herer Paula, Lavie Peretz, Levy Andrew P
Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Sleep. 2003 Aug 1;26(5):592-5. doi: 10.1093/sleep/26.5.592.
Obstructive sleep apnea syndrome is associated with a marked increase in the risk for cardiovascular disease. Increased oxidative stress and leukocyte adhesiveness have been implicated as fundamental pathophysiologic mechanisms underlying the increased susceptibility in these patients. Haptoglobin is an antioxidant and immunomodulatory protein encoded by 2 alleles with profoundly different biophysical and biochemical properties. We therefore sought to determine if the haptoglobin phenotype was a determinant of cardiovascular disease in patients with obstructive sleep apnea syndrome.
Haptoglobin phenotype was determined by gel electrophoresis in 465 patients with and 757 individuals without obstructive sleep apnea syndrome.
Eight-bed Technion Sleep Medicine Center in Haifa, serving the northern part of Israel.
Patients referred for sleep recordings because of suspected breathing disorders in sleep and healthy industry workers.
Patients with obstructive sleep apnea syndrome and cardiovascular disease had a significantly different distribution of the 3 haptoglobin phenotypes as compared to patients with obstructive sleep apnea syndrome but without cardiovascular disease. No difference in the haptoglobin phenotype frequency was found between controls with and without cardiovascular disease. Log linear analysis revealed a significant interaction effect of haptoglobin phenotype and the presence of sleep apnea on the presence of cardiovascular disease. Logistic regression analysis revealed that the risk of cardiovascular disease in sleep apnea patients younger than 55 years with haptoglobin 2-2 was 2.32-fold higher than in their counterparts with haptoglobin 2-1.
These results suggest that haptoglobin phenotype is an important risk factor in determining susceptibility to cardiovascular disease in obstructive sleep apnea syndrome, which may be mediated by the decreased antioxidant and antiinflammatory actions of the haptoglobin 2 allelic protein product.
阻塞性睡眠呼吸暂停综合征与心血管疾病风险显著增加相关。氧化应激增加和白细胞黏附性增加被认为是这些患者易感性增加的基本病理生理机制。触珠蛋白是一种由两个等位基因编码的具有截然不同生物物理和生化特性的抗氧化和免疫调节蛋白。因此，我们试图确定触珠蛋白表型是否是阻塞性睡眠呼吸暂停综合征患者心血管疾病的决定因素。
通过凝胶电泳确定465例阻塞性睡眠呼吸暂停综合征患者和757例无阻塞性睡眠呼吸暂停综合征个体的触珠蛋白表型。
位于海法的拥有八张床位的以色列理工学院睡眠医学中心，服务于以色列北部地区。
因怀疑睡眠呼吸障碍而被转诊进行睡眠记录的患者以及健康产业工人。
与无心血管疾病的阻塞性睡眠呼吸暂停综合征患者相比，患有阻塞性睡眠呼吸暂停综合征和心血管疾病的患者三种触珠蛋白表型的分布有显著差异。有心血管疾病和无心血管疾病的对照组之间触珠蛋白表型频率无差异。对数线性分析显示触珠蛋白表型与睡眠呼吸暂停的存在对心血管疾病的存在有显著的交互作用。逻辑回归分析显示，年龄小于55岁且触珠蛋白为2-2型的睡眠呼吸暂停患者患心血管疾病的风险比触珠蛋白为2-1型的患者高2.32倍。
这些结果表明，触珠蛋白表型是决定阻塞性睡眠呼吸暂停综合征患者心血管疾病易感性的重要危险因素，这可能是由触珠蛋白2等位基因蛋白产物抗氧化和抗炎作用降低介导的。
