Identification of genetic factors associated with susceptibility to angiotensin-converting enzyme inhibitors-induced cough

@article{Grilo2011IdentificationOG,
  title={Identification of genetic factors associated with susceptibility to angiotensin-converting enzyme inhibitors-induced cough},
  author={Antonio Grilo and Mar{\'i}a P S{\'a}ez-Rosas and Juan Santos-Morano and Elena S{\'a}nchez and Concha Moreno-Rey and Luis Miguel Real and Reposo Ram{\'i}rez-Lorca and Mar{\'i}a Eugenia S{\'a}ez},
  journal={Pharmacogenetics and Genomics},
  year={2011},
  volume={21},
  pages={10–17}
}
Background and objective Angiotensin-converting enzyme inhibitors (ACEi) are the first selected drugs for hypertensive patients because of its protective properties against heart and kidney diseases. Persistent cough is a common adverse reaction associated with ACEi, which can bind to the treatment cessation, but its etiology remains an unresolved issue. The most accepted mechanism is that the inhibition of ACEi increases kinins levels, resulting in the activation of proinflammatory mechanisms… 
Association between genetic polymorphisms and angiotensin-converting enzyme inhibitor-induced cough: a systematic review and meta-analysis.
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It is demonstrated that ACE I/D but not BDKRB2-58T/C polymorphism could be a predictor for the risk of ACE inhibitor-induced cough, especially in east Asians and the aged.
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TLDR
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TLDR
Results indicate that SNPs in KCNIP4 may modulate ACEi-induced cough risk, and identify associations on chromosome 4 in an intron of KCnIP4.
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TLDR
In this meta-analysis, a significant association between the ACE insertion/deletion polymorphism and ACEI cough was not found and one gene region (XPNPEP2) was associated with ACEI-induced angioedema in three studies.
Angiotensin-Converting Enzyme (ACE) Gene Insertion/Deletion Polymorphism and ACE Inhibitor-Related Cough: A Meta-Analysis
TLDR
Synthesis of the available evidence supports ACE I/D polymorphism as an age-dependent predictor for risk of ACEI-related cough.
SLCO1B1 Variants and Angiotensin Converting Enzyme Inhibitor (Enalapril) -Induced Cough: a Pharmacogenetic Study
TLDR
This study highlights, for the first time, SLCO1B1 variants are strongly associated with an increased risk of enalapril-induced cough, and will be useful to provide pharmacogenetic markers for enAlapril treatment.
Meta-analysis of genome-wide association studies on the intolerance of angiotensin-converting enzyme inhibitors
TLDR
Results indicate that genetic variation in the above-mentioned genes may increase the risk of ACE-inhibitor-induced adverse reactions.
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TLDR
Genotypes for common polymorphisms for ACE, chymase, and B2-bradykinin receptor do not explain the occurrence of ACE inhibitor-related cough, and there was no evidence for association between genotype at either gene examined and cough.
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TLDR
Susceptibility to develop cough is associated with a genetic variant of the bradykinin B2 receptor promoter; thus, it may be possible to identify those patients who will develop this adverse reaction to ACE inhibitors in advance.
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TLDR
A genetic variant of the bradykinin receptor is involved in the elicitation of ACE inhibitor-related cough and it may be possible to predict the side effects of ACE inhibitors in advance.
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TLDR
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TLDR
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TLDR
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