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未治疗的深部子宫内膜异位症的自然演变和激素抑制的影响:系统文献回顾和荟萃分析。

The natural evolution of untreated deep endometriosis and the effect of hormonal suppression: A systematic literature review and meta-analysis.

机构信息

Department of Clinical Sciences and Community Health, Academic Center for Research on Adenomyosis and Endometriosis, Università degli Studi, Milan, Italy.

Gynecology Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.

出版信息

Acta Obstet Gynecol Scand. 2024 Sep;103(9):1722-1735. doi: 10.1111/aogs.14887. Epub 2024 Jun 13.

DOI:10.1111/aogs.14887
PMID:38867640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11324912/
Abstract

INTRODUCTION

Peritoneal infiltrating and fibrotic endometriosis, also known as deep endometriosis, is the most severe manifestation of the disease that can cause severe complications including bowel and ureteral stenosis. The natural history of these lesions and the possible effect of hormonal treatments on their progression are undefined. Therefore, we conducted a systematic review and meta-analysis to investigate whether and how frequently deep endometriosis progresses over time without or with ovarian suppression. This could inform management decisions in asymptomatic and mildly symptomatic patients.

MATERIAL AND METHODS

For this pre-registered systematic review (CRD42023463518), the PubMed and Embase databases were screened, and studies published between 2000 and 2023 that serially evaluated the size of deep endometriotic lesions without or with hormonal treatment were selected. Data on the progression, stability, or regression of deep endometriotic lesions were recorded as absolute frequencies or mean volume variations. Estimates of the overall percentage of progression and corresponding 95% confidence intervals were calculated using a random-effect model. When studies reported lesion progression as pre- and post-treatment volume means, the delta of the two-volume means was calculated and analyzed using the inverse variance method.

RESULTS

A total of 29 studies were identified, of which 19 studies with 285 untreated and 730 treated patients were ultimately selected for meta-analysis. The overall estimate of the percentage of lesion progression in untreated individuals was 21.4% (95% CI, 6.8-40.8%; I = 90.5%), whereas it was 12.4% during various hormonal treatments (95% CI, 9.0-16.1%; I = 0%). Based on the overall meta-analysis estimates, the odds ratio of progression in treated vs untreated patients was 0.52 (95% CI, 0.41-0.66). During hormonal suppression, the mean volume of deep endometriotic lesions decreased significantly by 0.87 cm (95% CI, 0.19-1.56 cm; I = 0%), representing -28.5% of the baseline volume.

CONCLUSIONS

Untreated deep endometriotic lesions progressed in about one in five patients. Medical therapy reduced but did not eliminate this risk. Given the organ function failure potentially caused by these lesions, the decision whether to use hormonal treatments in asymptomatic or mildly symptomatic women should always be shared, carefully weighing the potential benefits and harms of the two alternatives after extensive counseling.

摘要

介绍

腹膜浸润性和纤维性子宫内膜异位症,也称为深部子宫内膜异位症,是疾病最严重的表现形式,可导致严重并发症,包括肠和输尿管狭窄。这些病变的自然史以及激素治疗对其进展的可能影响尚不清楚。因此,我们进行了系统回顾和荟萃分析,以调查在没有或使用卵巢抑制的情况下,深部子宫内膜异位症是否以及多久会随着时间的推移而进展。这可以为无症状和轻度症状患者的管理决策提供信息。

材料和方法

对于这项预先注册的系统评价(CRD42023463518),我们筛选了 PubMed 和 Embase 数据库,并选择了在 2000 年至 2023 年期间连续评估深部子宫内膜异位症病变大小的研究,这些研究既没有接受激素治疗也接受了激素治疗。记录了深部子宫内膜异位症病变进展、稳定或消退的绝对频率或平均体积变化。使用随机效应模型计算总体进展百分比及其相应的 95%置信区间。当研究将病变进展报告为治疗前后的体积平均值时,使用逆方差法计算并分析了两个体积平均值的差值。

结果

共确定了 29 项研究,其中 19 项研究(285 名未治疗患者和 730 名接受治疗患者)最终被纳入荟萃分析。未治疗个体中病变进展的总体估计百分比为 21.4%(95%CI,6.8-40.8%;I=90.5%),而在各种激素治疗期间为 12.4%(95%CI,9.0-16.1%;I=0%)。基于总体荟萃分析估计,治疗组与未治疗组相比,病变进展的优势比为 0.52(95%CI,0.41-0.66)。在激素抑制期间,深部子宫内膜异位症病变的平均体积显著减少 0.87cm(95%CI,0.19-1.56cm;I=0%),代表基线体积的-28.5%。

结论

未经治疗的深部子宫内膜异位症病变在约五分之一的患者中进展。医学治疗降低了但没有消除这种风险。鉴于这些病变可能导致器官功能衰竭,对于无症状或轻度症状的女性,是否使用激素治疗的决定应该始终是共享的,在广泛咨询后,仔细权衡两种替代方案的潜在益处和危害。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f6b/11324912/cf62790ca91f/AOGS-103-1722-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f6b/11324912/660fd3018b52/AOGS-103-1722-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f6b/11324912/d151a4b1d6fa/AOGS-103-1722-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f6b/11324912/490b3751e551/AOGS-103-1722-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f6b/11324912/cf62790ca91f/AOGS-103-1722-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f6b/11324912/660fd3018b52/AOGS-103-1722-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f6b/11324912/d151a4b1d6fa/AOGS-103-1722-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f6b/11324912/490b3751e551/AOGS-103-1722-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f6b/11324912/cf62790ca91f/AOGS-103-1722-g005.jpg

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