Role of Atosiban in Recurrent Implantation Failure

Recurrent Implantation Failure

Recurrent implantation failure, IVF, Atosiban, Embryo Transfer

ET is the final stage of IVF which independently influences the treatment outcome. Successful embryo implantation is dependent on uterine receptivity. Atosiban is a novel class of drug which is effective in priming the uterus for implantation. It reduces uterine contractions and increases endomyometrial perfusion, both of which have potential benefits regarding improved IRs, CPR, and ongoing pregnancy rates. Atosiban has a good embryonic safety profile. It has no systemic toxicity, no mutagenic effects, and no carcinogenic effects

ET is a critical step of an IVF cycle that merits the utmost attention. Its success depends on the frequency of uterine contractions, the endometrial receptivity and the quality of embryos transferred. Uterine contractions are the most fundamental constituents of the uterine receptivity. Excessive contractions may decrease the implantation potential of embryos by expelling the embryos from the uterus. Studies have revealed a six-fold increase in uterine contractility in IVF cycles when measured before ET as compared to the condition before ovulation in natural cycles. Excessive manipulation of the cervix such as the use of tenaculum during difficult ET can also trigger uterine contractions, consequently leading to failure of embryo implantation. IVF success rates have been potentially improved by the use of drugs that inhibit pronounced uterine contractions at the time of ET. Treatment strategies such as the use of beta-agonists or nonsteroidal anti-inflammatory agents for tocolysis have not been beneficial in IVF-ET procedures. Atosiban is a combined oxytocin/vasopressin V1A antagonist. It functions mainly by blocking oxytocin and vasopressin V1a receptors to decrease the frequency and amplitude of uterine contractions, which enhances implantation and pregnancy rates. RIF remains unexplained in most cases, which results in considerable variation in how RIF is treated and managed. Atosiban competes with oxytocin at oxytocin receptors in endometrial cells and inhibits oxytocin-induced PGF2α release, thus inhibiting uterine contractions and increasing chances of embryo implantation and may add value in improving the outcome in RIF patients. Recently published studies showed that atosiban inhibits oxytocin-induced PGF2α and uterine contractility, consequently leading to improved IRs. Studies have shown a considerable reduction in the frequency of uterine contractions before and after the administration of atosiban in women undergoing ET.

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