Department of Anesthesiology and Reanimation, Türkiye Yüksek İhtisas Hospital, Sıhhıye, 06100 Ankara, Turkey.
Mol Biol Rep. 2011 Jun;38(5):3383-9. doi: 10.1007/s11033-010-0446-y. Epub 2010 Nov 23.
The existence of interindividual drug response variability has been known for a long time. Individual susceptibility which might cause toxicity or inadequate treatment is important in drug therapy. Genetic polymorphisms in genes responsible for drug response are expected to be useful in keeping track of differences among individuals. Dexmedetomidine is a sedative drug, whose use in intensive care unit patients was confirmed by USA-Food Drug Administration (FDA) by the end of 1999. It was proven that dexmedetomidine shows its clinic effect via the α(2)-AR. However, to the best of our knowledge, to date, there is no investigation in clinic indicating the relation between dexmedetomidine and α(2A)-AR gene polymorphism. The aim of our study was to investigate the association between the effect of α(2A)-Adrenergic Receptor (ADRA2A) C-1291G gene polymorphism in the promoter region of the candidate gene and clinical effects (sedative and haemodynamics effects) of dexmedetomidine. One hundred and ten patients undergoing coronary artery surgery were prospectively studied. Anesthetic technique was standardized with fentanyl, midazolam and rocuronium bromide. Patients were monitorized with Bispectral Index (BIS) monitor in addition to the routine invasive haemodynamic monitorization in the operation room. The Ramsay Sedation Scale was also used in order to determine the sedation level just arriving to Intensive Care Unit (ICU). The genotyping of ADRA2A C1291G was done by Restriction Fragment Length Polymorphism-Polymerase Chain Reaction (RFLP-PCR). We found the frequencies of C1291C, C1291G and G1291G genotypes, as 43.6, 45.5 and 10.9%, respectively. Patients who carry variant genotype had higher BIS and Ramsay Sedation Scores, indicating a longer period for falling asleep. The results of our study are promising, considering the association between ADRA2A polymorphism and response to dexmedetomidine. However, further investigations on other ADRA2A locus or haplotypes might be useful to clarify the relation between this gene and dexmedetomidine activity.
个体间药物反应变异性的存在由来已久。药物治疗中,个体易感性可能导致毒性或治疗不足,这一点很重要。负责药物反应的基因中的遗传多态性有望有助于跟踪个体间的差异。右美托咪定是一种镇静药物,1999 年底,美国食品和药物管理局(FDA)确认其可用于重症监护病房患者。现已证实,右美托咪定通过α(2)-AR 发挥其临床作用。然而,据我们所知,迄今为止,临床上还没有研究表明右美托咪定与α(2A)-肾上腺素能受体(ADRA2A)基因多态性之间存在关系。我们的研究目的是探讨候选基因启动子区域的α(2A)-肾上腺素能受体(ADRA2A)C-1291G 基因多态性与右美托咪定临床效应(镇静和血液动力学效应)之间的关系。前瞻性研究了 110 例接受冠状动脉手术的患者。采用芬太尼、咪达唑仑和罗库溴铵标准化麻醉技术。除了在手术室进行常规有创血液动力学监测外,还使用双频谱指数(BIS)监测仪监测患者。还使用 Ramsay 镇静评分来确定到达重症监护病房(ICU)时的镇静水平。ADRA2A C1291G 的基因分型通过限制性片段长度多态性-聚合酶链反应(RFLP-PCR)进行。我们发现 C1291C、C1291G 和 G1291G 基因型的频率分别为 43.6%、45.5%和 10.9%。携带变异基因型的患者 BIS 和 Ramsay 镇静评分较高,表明入睡时间较长。考虑到 ADRA2A 多态性与右美托咪定反应之间的关系,我们的研究结果是有希望的。然而,对其他 ADRA2A 基因座或单倍型的进一步研究可能有助于阐明该基因与右美托咪定活性之间的关系。