Protopapas A, Grimbizis G, Athanasiou S, Loutradis D
1st Department of Obstetrics & Gynecology of the Medical School of the National and Kapodistrian University of Athens, Greece.
1st Department of Obstetrics & Gynecology of the Medical School of the Aristotle University of Thessaloniki, Greece.
Facts Views Vis Obgyn. 2020 Aug 5;12(2):91-104.
For many decades adenomyosis has been a histological diagnosis in hysterectomy specimens. Traditionally, it has been considered a disease of late reproductive and premenopausal years causing uterine enlargement, dysmenorrhoea and menorrhagia. Recent advances in pelvic and uterine imaging techniques including transvaginal sonography and magnetic resonance imaging were responsible for a shift towards a non-invasive diagnosis and made a significant contribution to a better understanding of its pathogenesis, epidemiology, histological spectrum, and clinical symptomatology. With these non-invasive tools it has been shown that adenomyosis is probably a condition affecting much younger populations and is frequently asymptomatic at an early stage of its development. Regarding symptomatic disease, the distribution and extent of adenomyotic lesions do not correlate consistently with the various symptoms that are considered typical of adenomyosis. More importantly, accurate diagnosis of adenomyosis suffers from a lack of consensus among experts on imaging and even histological diagnostic criteria. Several pathogenetic theories have attempted to shed light on the establishment, evolution and distribution of adenomyotic lesions within the uterine wall, including the tissue injury and repair (TIAR) mechanism, metaplasia, and the more recent genetic-epigenetic theory. So far, none of these can adequately and independently explain the appearance of all types of adenomyosis. This review paper attempts a correlation between the proposed pathogenetic theories and the clinical and histological spectrum of adenomyosis, in an effort to give a plausible explanation of the evolution of this condition from an asymptomatic state to a disease, through synthesis of the existing data.
几十年来，子宫腺肌病一直是子宫切除标本的组织学诊断。传统上，它被认为是一种发生在生殖后期和绝经前的疾病，可导致子宫增大、痛经和月经过多。盆腔和子宫成像技术的最新进展，包括经阴道超声检查和磁共振成像，促使了向非侵入性诊断的转变，并为更好地理解其发病机制、流行病学、组织学谱和临床症状学做出了重大贡献。借助这些非侵入性工具已表明，子宫腺肌病可能是一种影响更年轻人群的疾病，并且在其发展的早期阶段通常无症状。对于有症状的疾病，子宫腺肌病病变的分布和范围与被认为是子宫腺肌病典型症状的各种症状并不始终相关。更重要的是，子宫腺肌病的准确诊断在影像学甚至组织学诊断标准方面缺乏专家共识。几种发病机制理论试图阐明子宫壁内子宫腺肌病病变的形成、演变和分布，包括组织损伤与修复（TIAR）机制、化生以及最新的遗传 - 表观遗传学理论。到目前为止，这些理论中没有一个能够充分且独立地解释所有类型子宫腺肌病的出现。这篇综述文章试图将提出的发病机制理论与子宫腺肌病的临床和组织学谱进行关联，通过综合现有数据，努力对这种疾病从无症状状态发展为疾病的演变给出合理的解释。
