Medroxyprogesterone in the management of primary and recurrent or metastatic uterine adenocarcinoma
Medroxyprogesterone in the management of primary and recurrent or metastatic uterine adenocarcinoma
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甲羟孕酮治疗原发性和复发性或转移性子宫腺癌
DOI：
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发表时间：
1972
期刊：
影响因子：
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通讯作者：
J. Bonté
中科院分区：
文献类型：
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作者：
J. Bonté
开展了一项临床研究计划，其中包括 2 项试验：其中一项试验使用甲羟孕酮对复发性子宫腺癌进行对症治疗，另一项试验则将甲羟孕酮联合放疗和手术治疗原发性或复发性病变。在第一组中，70 名患有播散性或复发性子宫腺癌的患者每周接受 1000 毫克甲羟孕酮治疗。大多数复发位于骨盆处。 37 名患者仅使用甲羟孕酮就获得了持续 4 个月至 6 年的完全消退。 18名患者死亡；其余19名患者仍然活着并且健康状况良好。仅当临床放射学和组织学检查结果证实时，才会记录腺癌病灶完全消失。安宫黄体酮对子宫腺癌的作用机制似乎包括对癌组织的直接作用和局部作用，引起分化、成熟、上皮化生萎缩，最后肿瘤结构消失。甲羟孕酮治疗期间的重复穿刺活检证明，所有这些变化最终都会导致癌组织萎缩和消失。在第二项试验中，通过对 19 名阴道壁激素抵抗性腺癌患者进行补充放疗，结果得到改善。放射激素治疗的作用机制可能是双重的；首先，电离辐射的杀癌作用和孕激素的破坏性活性的总和导致腺癌通过分化和化生直至萎缩和纤维化，最终实现腺癌病灶的真正放射增敏。
A clinic research program was conducted that included 2 trials: in 1 medroxyprogesterone was used for symptomatic treatment of recurrent uterine adenocarcinoma while in the other medroxyprogesterone was combined with radiotherapy and surgery in the treatment of primary or recurrent lesions. In the 1st group 70 patients with disseminated or recurrent uterine adenocarcinoma were treated with 1000 mg medroxyprogesterone per week. Most recurrences were located in the pelv is. In 37 patients complete regression lasting from 4 months to 6 years was obtained with medroxyprogesterone alone. 18 patients died; the remaining 19 patients are still alive and in good health. Complete disapperance of an adenocarcinomatous focus was recorded only if confirmed by the clinical radiographic and histologic findings. The mechanism of action of medroxyprogesterone on uterine adenocarcinoma seems to consist of a direct effect and local effect on the cancer tissue provoking differentiation maturation epithelial metaplasia atrophy and finally disappearance of neoplastic structures. Repeated punch biopsies during treatment with medroxyprogesterone proved that all these changes tended finally to result in atrophy and disappearance of cancer tissue. In the 2nd trial results improved by supplementary radiotherapy given to 19 patients with a more hormone-resistant adenocar cinoma in the vaginal wall. The mechanism of the action of the radiohormonal treatment might be twofold; at 1st the summation of the cancericide action of ionizing radiations and the destructive activity of progestogens leading the adenocarcinoma through differentiation and metaplasia to atrophy and fibrosis finally a real radiosensitization of the adenocarcinomatous focus.