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Fertility-sparing partial hysterectomy for placental-site trophoblastic tumour.

机译:保留生育力的部分子宫切除术治疗胎盘部位滋养细胞肿瘤。

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摘要

A previously healthy 30-year-old woman presented in August 2002 with vaginal bleeding 11 weeks into her first pregnancy. Ultrasound suggested a molar pregnancy and her serum human chorionic gonadotrophin (hCG) concentration was >200 000 IU/L (normal range <4 IU/L). After evacuation, histology showed a complete hydatiform mole. She waa registered with the national Gestational Trophoblastic Disease service for serial monitoring of the hCG concentration over time. 2 months later her hCG concentration had plateaued suggesting malignant change and she was referred to Charing Cross Hospital (London, UK) for further management. On admission, her hCG concentration was 11339 IU/L, Doppler ultrasound of the pelvis showed a vascular focal lesion in the uterus consistent with trophoblastic tumour, and chest radiograph was normal. She started single-agent chemotherapy with intramuscular methotrexate (50 mg on days 1, 3, 5, and 7) alternating with oral folinic acid (15 mg on days 2, 4, 6, and 8) repeated for 2 weeks. The hCG concentration initially fell, but then plateaued at about 1000 IU/L (figure 1) indicating drug resistance. She was switched to combination chemotherapy with etoposide, methotrexate, and dactinomycin, alternating weekly with cyclophosphamide and vincristine. Her hCG concentration briefly normalised, but occasional increases to 8 IU/L during consolidation chemotherapy were noted. The significance of these increases was unclear and treatment was subsequently stopped. Between March and August, 2003, her serum hCG concentration remained raised between 7-24 IU/L (figure 1). Repeat staging investigations during this time, including CT of the body, MRI of the brain, and Doppler ultrasound and MRI of the pelvis, initially only showed increased vasculariry in a small area in the right uterine fundus. However, by July, 2003, repeat MRI and Doppler ultrasound of the pelvis both showed a 2.5 cm right fundal uterine mass associated with the abnormal vascularity. 18-fluorodeoxyglucose ([~(18)F]FDG)-PET was positive in this area with a standardised uptake value of 3.5 ([~(18)F] FDG-PET is valuable for identifying active tumour sites, including those related to gestational trophoblastic tumours). Given the indication of recurrent uterine gestational trophoblastic tumour by imaging and the small increase in hCG concentration, a placental-site trophoblastic tumour was considered possible. Therefore, hysterectomy was discussed with the patient as the treatment of choice for this subtype of trophoblastic disease. However, the patient wished to retain her fertility, so she was started on third-line chemotherapy with gemcitabine (1000 mg/m~2) on days 1 and 8 combined with carboplatin (AUC5) on day 1 repeated every 3 weeks. Her hCG concentration initially rose during the first cycle to 261 IU/L but then fell to 71 IU/L (figure 1). However, MRI of the pelvis in November, 2003, showed an increase in the size of the uterine mass to 3.5 cm (figure 2).
机译:一名先前健康的30岁妇女于2002年8月首次怀孕11周后出现阴道出血。超声提示为磨牙妊娠,其血清人绒毛膜促性腺激素(hCG)浓度> 200 000 IU / L(正常范围<4 IU / L)。撤离后,组织学显示完整的葡萄胎状葡萄胎。她曾在国家妊娠滋养细胞疾病服务机构注册,以便随时间连续监测hCG浓度。 2个月后,她的hCG浓度趋于稳定,表明发生了恶性变化,她被转诊到Charing Cross医院(英国伦敦)进行进一步治疗。入院时她的hCG浓度为11339 IU / L,骨盆多普勒超声检查显示子宫内有血管局灶性病变,与滋养细胞肿瘤一致,胸部X线片正常。她开始进行单剂化学疗法,重复2周,反复进行肌注甲氨蝶呤(第1、3、5和7天为50 mg)和口服亚叶酸(第2、4、6和8天为15 mg)。 hCG浓度最初下降,但随后稳定在约1000 IU / L(图1),表明耐药。她改用依托泊苷,甲氨蝶呤和放线菌素联合化疗,每周交替用环磷酰胺和长春新碱。她的hCG浓度短暂恢复正常,但在巩固化疗期间偶尔升高至8 IU / L。这些增加的意义尚不清楚,随后停止治疗。在2003年3月至8月之间,她的血清hCG浓度保持在7-24 IU / L之间升高(图1)。在这段时间内重复进行分期检查,包括身体CT,脑MRI,多普勒超声和骨盆MRI,最初仅显示右子宫底小区域的血管扩张。但是,到2003年7月,骨盆的重复MRI和多普勒超声检查均显示2.5 cm右子宫底肿物与异常血管相关。 18-氟脱氧葡萄糖([〜(18)F] FDG)-PET在该区域呈阳性,标准摄取值为3.5([〜(18)F] FDG-PET对于识别活动性肿瘤部位,包括与妊娠滋养细胞肿瘤)。通过影像学检查可以发现复发性子宫滋养细胞肿瘤,并且hCG浓度升高很小,因此认为胎盘部位滋养细胞肿瘤是可能的。因此,与患者讨论了子宫切除术,作为这种滋养细胞疾病亚型的治疗选择。但是,患者希望保留其生育能力,因此,她每隔3周开始在第1天和第8天接受吉西他滨(1000 mg / m〜2)联合卡铂(AUC5)的三线化疗。她的hCG浓度最初在第一个周期内上升到261 IU / L,但随后下降到71 IU / L(图1)。但是,2003年11月的骨盆MRI显示子宫肿块的大小增加到3.5 cm(图2)。

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