A rare case of extensive placenta accreta in twin pregnancy after GnRH agonist treatment of adenomyosis.

Shilpi Agrawala, Jeevitha Patil, Sukhkamal Campbell, Terri Lynn Woodard
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引用次数: 4

Abstract

Background: Adenomyosis remains an enigma for the reproductive endocrinologist. It is thought to contribute to sub-fertility, and its only curative treatment is hysterectomy. However, studies have documented increased live birth rates in women with adenomyosis who were treated with gonadotropin releasing hormone agonist (GnRHa).

Case: Here we present a case of a 52-year-old woman with adenomyosis who had three failed frozen embryo transfers (FETs) prior to initiating a 6-month trial of GnRHa. GnRHa therapy resulted in a decrease in uterine size from 11.5 × 7.9 × 7.0 cm to 7.8 × 6.2 × 5.9 cm and a decrease in the junctional zone (JZ) thickness from 19 to 9 mm. Subsequently, she underwent her fourth FET, which resulted in live birth of twins. The delivery was complicated by expansive accretas of both placentas requiring cesarean hysterectomy. The final pathology of the placentas demonstrated an extensive lack of decidualized endometrium that was even absent outside the basal plate.

Conclusions: GnRHa therapy in patients with adenomyosis may improve implantation rates after FET. Previous molecular studies indicate that genetic variance in the expression of the gonadotropin releasing hormone receptor (GnRHR) could explain the expansive lack of decidualized endometrium after GnRHa therapy. Further investigations are needed to determine if GnRHa therapy contributes to the pathologic process of placenta accreta.

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GnRH激动剂治疗子宫腺肌病后双胎妊娠出现广泛胎盘增生的罕见病例。
背景:子宫腺肌病对生殖内分泌学家来说仍然是一个谜。它被认为会导致生育能力低下,唯一的治疗方法是子宫切除术。然而,研究表明,使用促性腺激素释放激素激动剂(GnRHa)治疗的子宫腺肌病妇女的活产率增加。病例:在这里,我们提出了一个52岁的女性子宫腺肌症患者,在开始为期6个月的GnRHa试验之前,她进行了三次失败的冷冻胚胎移植(fet)。GnRHa治疗后,子宫大小由11.5 × 7.9 × 7.0 cm减小至7.8 × 6.2 × 5.9 cm,结膜厚度由19 mm减小至9 mm。随后,她进行了第四次FET手术,最终生下了一对双胞胎。分娩是复杂的扩张性增生的两个胎盘需要剖宫产子宫切除术。胎盘的最终病理显示广泛缺乏去个体化的子宫内膜,甚至在基底板外也没有。结论:GnRHa治疗可提高子宫腺肌症患者FET术后的着床率。先前的分子研究表明,促性腺激素释放激素受体(GnRHR)表达的遗传变异可以解释GnRHa治疗后子宫内膜普遍缺乏去个体化。需要进一步的研究来确定GnRHa治疗是否有助于胎盘增生的病理过程。
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