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首页> 外文期刊>Clinical and experimental allergy : >Pharmacogenetics of angiotensin-converting enzyme inhibitor-induced angioedema
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Pharmacogenetics of angiotensin-converting enzyme inhibitor-induced angioedema

机译：血管紧张素转换酶抑制剂诱导的血管后的药物遗传学

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Angioedema is a rare adverse effect of the commonly used angiotensin-converting enzyme inhibitors (ACEi) and is reported to occur with a prevalence of 0.1%-0.7%. Although most ACEi-induced angioedema (ACEi-A) cases are mild, severe cases requiring intensive care and even resulting in death have been reported in the literature. The mechanisms underlying ACEi-A are not yet fully understood, but bradykinin and/or substance P accumulation resulting from inhibition of ACE is believed to play a crucial role. ACEi-A occurs at variable frequencies across different racial groups, suggesting a genetic association with the development of ACEi-A. To date, one genome-wide association study and several candidate gene studies have been published on the association of genetic variation with ACEi-A. Genetic associations reported have been attributed to several distinct mechanisms: (a) genes coding for alternative enzymes responsible for the degradation of bradykinin and/or substance P in the diminution of ACE activity (b) ACE gene function, (c) bradykinin receptor genes, (d) genes implicated in immune and inflammation regulation and (e) genes in the fibrinolytic and coagulation pathway. Despite several plausible genetic associations, there are currently no genetic variants with sufficient effect to be clinically useful. The low incidence of ACEi-A suggests that a combination of genomic approaches with the capability to detect potentially important variants might be required to shed light on the mechanism of this adverse reaction. Additionally, many non-genetic risk factors associated with ACEi-A suggest the potential contribution of epigenetic dysregulation.
机译：血管血清是罕见使用的血管紧张素转换酶抑制剂（ACEI）的罕见不良影响，据报道，患病率为0.1％-0.7％。虽然大多数Acei诱导的血管后期（ACEI-A）病例是轻微的，但在文献中报告了需要重症监护甚至导致死亡的严重病例。尚未完全理解aci-a的机制，但由于抑制Ace而导致的Bradykinin和/或P物质累积据信起到至关重要的作用。 Acei-A发生在不同种族群体的可变频率下，建议与ACEI-A的发展产生遗传结合。迄今为止，已经发表了一种基因组 - 范围的协会研究和几种候选基因研究已经发表了Acei-A的遗传变异结合。报告的遗传关联已归因于几种不同的机制：（a）对负责Bradykinin和/或物质P的降解的替代酶的基因，在减少ACE活性（b）ACE基因函数中，（c）Bradykinin受体基因， （d）在纤维蛋白溶解和凝血途径中涉及免疫和炎症调节和（e）基因的基因。尽管有几个合理的遗传学协会，目前没有遗传变异，临床上有用充足的效果。 Acei-A的低发生率表明，基因组方法的组合具有检测潜在的重要变体的能力可能需要在这种不良反应的机制上脱光。此外，与Acei-A相关的许多非遗传危险因素表明表观遗传失调的潜在贡献。

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