Latifa Hospital, Dubai 9115, United Arab Emirates.
Department of OBGYN, Faculty of Medicine, University Strasbourg, 6081 Strasbourg, France.
Int J Environ Res Public Health. 2022 May 31;19(11):6725. doi: 10.3390/ijerph19116725.
For 100 years, pelvic endometriosis has been considered to originate from the implantation of endometrial cells following retrograde menstruation or metaplasia. Since some observations, such as the clonal aspect, the biochemical variability of lesions and endometriosis in women without endometrium, the genetic-epigenetic (G-E) theory describes that endometriosis only begins after a series of cumulative G-E cellular changes. This explains that the endometriotic may originate from any pluripotent cell apart from the endometrium, that 'endometrium-like cells' can harbour important G-E differences, and that the risk is higher in predisposed women with more inherited incidents. A consequence is a high risk after puberty which decreases progressively thereafter. Considering a 10-year delay between initiation and performing a laparoscopy, this was observed in the United Arab Emirates, Belgium, France and USA. The subsequent growth varies with the G-E changes and the environment but is self-limiting probably because of the immunologic reaction and fibrosis. That each lesion has a different set of G-E incidents explains the variability of pain and the response to hormonal treatment. New lesions may develop, but recurrences after surgical excision are rare. The fibrosis around endometriosis belongs to the body and does not need to be removed. This suggests conservative excision or minimal bowel without safety margins and superficial treatment of ovarian endometriosis. This G-E concept also suggests prevention by decreasing oxidative stress from retrograde menstruation or the peritoneal microbiome. This suggests the prevention of vaginal infections and changes in the gastrointestinal microbiota through food intake and exercise. In conclusion, a higher risk of initiating endometriosis during adolescence was observed in UAE, France, Belgium and USA. This new understanding and the limited growth opens perspectives for earlier diagnosis and better treatment.
100 年来，人们一直认为盆腔子宫内膜异位症起源于逆行月经或化生后子宫内膜细胞的植入。由于一些观察结果，如克隆性、病变的生化变异性和没有子宫内膜的女性中的子宫内膜异位症，遗传-表观遗传（G-E）理论描述子宫内膜异位症仅在一系列累积的 G-E 细胞变化后才开始。这表明，除了子宫内膜以外，任何多能细胞都可能起源于子宫内膜异位症，“子宫内膜样细胞”可能具有重要的 G-E 差异，并且具有更多遗传事件的易患女性的风险更高。其结果是青春期后风险较高，此后逐渐降低。考虑到发病和进行腹腔镜检查之间有 10 年的延迟，这在阿联酋、比利时、法国和美国都有观察到。随后的生长变化与 G-E 变化和环境有关，但具有自限性，可能是由于免疫反应和纤维化。每个病变都有不同的 G-E 事件集，这解释了疼痛的可变性和对激素治疗的反应。可能会出现新的病变，但手术切除后的复发很少见。子宫内膜异位症周围的纤维化属于身体，不需要切除。这表明保守性切除或最小化肠段而无需安全边缘和浅层卵巢子宫内膜异位症治疗。这种 G-E 概念还表明通过减少逆行月经或腹膜微生物组的氧化应激来预防。这表明通过摄入食物和运动来预防阴道感染和胃肠道微生物组的变化。总之，在阿联酋、法国、比利时和美国，青春期子宫内膜异位症的发病风险较高。这种新的认识和有限的生长为早期诊断和更好的治疗开辟了前景。
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