状细胞疾病中的低血:生物标志物调节和对病理生理学的相关性
B N Yamaja Setty1, Marie J Stuart, Carlton Dampier
1Department of Pediatrics and the Marian Anderson Sickle Cell Center Core Laboratory, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Lancet (London, England)
|November 7, 2003
概括
在患有状细胞疾病的儿童中,夜间氧血球脱与细胞粘附和激活的增加有关. 这表明血管封闭性危机和潜在的中风风险因素的机制.
科学领域:
- 血液学 血液学 血液学
- 儿科 儿科 儿科
- 心血管科学 心血管科学
背景情况:
- 夜间氧血球脱可能导致中枢神经系统 (CNS) 并发症和状细胞疾病 (SCD) 的痛苦危机.
- 对于了解SCD病理生理学来说,研究氧血球脱的生物学关系和血液学风险因素至关重要.
研究的目的:
- 检查氧血球脱和SCD儿童的血液学风险因素之间的生物学关系.
- 描述SCD儿童睡眠期间细胞激活标记和氧和水平之间的关联.
主要方法:
- 使用可溶性血管细胞粘附分子1,P-selectin,L-selectin和白血B4进行评估细胞激活.
- 通过脉冲氧度测量,测量了红细胞内皮质粘附,常规血液学变量和氧和 (SaO2) 在清醒和睡觉的儿童中.
- 将儿童分为四组:对照组,HbSC (正常性),HbSS (正常性) 和HbSS (低血症,平均睡眠SaO2 <或=93%).
主要成果:
- 睡眠时的SaO2与细胞体积有显著的相关性 (r=0.7;p<0.0001).
- 睡眠时SaO2与细胞粘附标记,白细胞,血小板和内皮激活 (p<0.01) 之间观察到不良关系.
- 患有HbSS和睡眠低氧症的儿童在清醒时也表现出持续的低氧症,SaO2和细胞激活标记之间的相关性相似.
结论:
- 研究结果表明,通过粘附相关途径,氧血球脱与SCD中增加的血管封闭性危机之间存在潜在的机制.
- 低氧介导的途径,包括细胞介导体释放和贫血,可能导致中枢神经系统血管病变和中风风险.
- 在SCD的老年儿童中,在白天轻度,未经治疗的缺氧可能会增加血管封闭性发作的风险.
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