Abstract
BackgroundRitodrine, a tocolytic β2-agonist, has been used extensively in Europe and Asia despite its safety concerns. This study was designed to identify associations between β2-adrenergic receptor (ADRB2) polymorphisms and adverse drug events (ADEs) in patients with preterm labor treated with ritodrine.ResultsThis follow-up study was prospectively conducted at Ewha Womans University Mokdong Hospital in Korea. Five single nucleotide polymorphisms (SNPs) of the ADRB2 gene (rs1042713, rs1042714, rs1042717, rs1042718, and rs1042719) were analyzed in 186 pregnant women with preterm labor. Patients with the AA genotype of rs1042717 had significantly lower incidence of ADEs compared to those with the G allele (p = 0.009). In multivariate analysis, one of the predictors of ADEs was the maximum infusion rate of ritodrine (AOR 4.47, 95% CI 1.31–15.25). Rs1042719 was also a significant factor for ritodrine-induced ADEs. The CC genotype carriers had 78% decreased risk of ADEs compared to those with other genotypes.ConclusionsThis study demonstrates that ADEs induced by ritodrine are associated with ADRB2 gene polymorphisms, as well as the infusion rate of ritodrine in pregnant women with preterm labor.
Highlights
Ritodrine, a tocolytic β2-agonist, has been used extensively in Europe and Asia despite its safety concerns
A total of 216 women were hospitalized for threatened preterm labor and were treated with ritodrine
The central findings of this paper are that the β2Adrenergic receptor (ADRB2) gene polymorphism may decrease Adverse drug event (ADE) induced by ritodrine and the maximum infusion rate of ritodrine can increase the incidence of ADEs
Summary
A tocolytic β2-agonist, has been used extensively in Europe and Asia despite its safety concerns. Preterm birth, defined as birth that occurs before the completion of 37 weeks of pregnancy, is known as the primary cause of perinatal mortality and morbidity [1]. It is the second most frequent cause of infant mortality, ranking only behind birth defects [2]. Beta-2 agonists such as ritodrine inhibit myometrial contractions by stimulating adenylyl cyclase activity via ADRB2. In this way, cytosolic cyclic adenosine monophosphate (cAMP) is generated, which activates protein kinases and phosphorylates cytosolic and membrane proteins. There is reduced interaction between actin and myosin, which is the key factor of cell contraction [5]
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