进行了Delphi共识，以评估编码促性腺激素和促性腺激素受体的基因中的单核苷酸多态性（SNP）对辅助生殖技术（ART）治疗后的临床卵巢刺激结果的影响。
九位专家和两位科学协调员讨论和修改了声明，以及科学协调员提出的支持参考资料。声明通过在线调查分发给36名专家，他们对每项声明的同意或分歧进行了投票。如果同意或不同意声明的参与者比例>66％，则达成共识。
开发了11个声明，其中两个语句被合并。总的来说,八项声明达成共识，两项声明未达成共识。这里总结了达成共识的声明。（1）卵泡刺激素受体（FSHR）中的SNP，rs6166（c.2039A>G，p.Asn680Ser)(N=5个陈述):Ser/Ser载体具有比Asn/Asn载体更高的基础FSH水平。Ser/Ser携带者在卵巢刺激期间需要比Asn/Asn携带者更高的促性腺激素。Ser/Ser携带者在卵巢刺激过程中产生的卵母细胞比Asn/Asn或Asn/Ser携带者少。有混合证据支持这种变异与卵巢过度刺激综合征之间的关联。(2)FSHR的SNP,rs6165(c.919G>A,p.Thr307Ala）（N=1声明）：很少有研究表明Thr/Thr携带者比Thr/Ala或Ala/Ala携带者需要更短的促性腺激素刺激持续时间。(3)FSHR的SNP,rs1394205（-29G>A）（N=1声明）：特定种族的有限数据表明，A/A等位基因携带者在卵巢刺激期间可能需要更高的促性腺激素，并且比G/G携带者产生更少的卵母细胞。（4）FSHβ链（FSHB）的SNP，rs10835638(-211G>T)(N=1陈述):有矛盾的证据支持该变体与基础FSH水平或卵母细胞数量之间的关联。（5）黄体生成素β链（LHB）和LH/绒毛膜促性腺激素受体（LHCGR）基因的SNP（N=1声明）：这些可能会影响卵巢刺激结果，并可能代表ART药物基因组学研究的潜在未来目标。尽管数据仍然非常有限。
本德尔菲共识提供了来自不同国际专家组的临床观点。共识支持促性腺激素/促性腺激素受体基因中的一些变异与卵巢刺激结果之间的联系；然而，需要进一步的研究来澄清这些发现.
A Delphi
consensus was conducted to evaluate the influence of single nucleotide polymorphisms (SNPs) in genes encoding gonadotropin and gonadotropin receptors on clinical ovarian stimulation outcomes following assisted reproductive technology (ART) treatment.
Nine experts plus two Scientific Coordinators discussed and amended statements plus supporting references proposed by the Scientific Coordinators. The statements were distributed via an online survey to 36 experts, who voted on their level of agreement or disagreement with each statement.
Consensus was reached if the proportion of participants agreeing or disagreeing with a statement was >66%.
Eleven statements were developed, of which two statements were merged. Overall, eight statements achieved
consensus and two statements did not achieve
consensus. The statements reaching
consensus are summarized here. (1) SNP in the follicle stimulating hormone receptor (FSHR), rs6166 (c.2039A>G, p.Asn680Ser) (N=5 statements): Ser/Ser carriers have higher basal FSH levels than Asn/Asn carriers. Ser/Ser carriers require higher amounts of gonadotropin during ovarian stimulation than Asn/Asn carriers. Ser/Ser carriers produce fewer oocytes during ovarian stimulation than Asn/Asn or Asn/Ser carriers. There is mixed evidence supporting an association between this variant and ovarian hyperstimulation syndrome. (2) SNP of FSHR, rs6165 (c.919G>A, p.Thr307Ala) (N=1 statement): Few studies suggest Thr/Thr carriers require a shorter duration of gonadotropin stimulation than Thr/Ala or Ala/Ala carriers. (3) SNP of FSHR, rs1394205 (-29G>A) (N=1 statement): Limited data in specific ethnic groups suggest that A/A allele carriers may require higher amounts of gonadotropin during ovarian stimulation and produce fewer oocytes than G/G carriers. (4) SNP of FSH β-chain (FSHB), rs10835638 (-211G>T) (N=1 statement): There is contradictory evidence supporting an association between this variant and basal FSH levels or oocyte number. (5) SNPs of luteinizing hormone β-chain (LHB) and LH/choriogonadotropin receptor (LHCGR) genes (N=1 statement): these may influence ovarian stimulation outcomes and could represent potential future targets for pharmacogenomic research in ART, although data are still very limited.
This Delphi
consensus provides clinical perspectives from a diverse international group of experts. The consensus supports a link between some variants in gonadotropin/gonadotropin receptor genes and ovarian stimulation outcomes; however, further research is needed to clarify these findings.
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