An Appraisal of the Tissue Injury and Repair (TIAR) Theory on the Pathogenesis of Endometriosis and Adenomyosis

子宫腺肌病 子宫内膜异位症 批判性评价 医学 认识论 心理学 病理 替代医学 哲学
作者
Marwan Habiba,Giuseppe Benagiano,Sun-Wei Guo
出处
期刊:Biomolecules [MDPI AG]
卷期号:13 (6): 975-975
标识
DOI:10.3390/biom13060975
摘要

As understanding their pathogenesis remains elusive, both endometriosis and adenomyosis are often referred to as "enigmatic diseases". The uncertainty and heightened interest are reflected in the range of expressed views and opinions. There is a sense of urgency because of the entailed patient suffering. The plethora of opinions calls for a critical analysis of proposed theories, both old and new. A series of papers published since 2009 proposed that both endometriosis and adenomyosis originate from the same aberrations occurring within the uterus. This came to be recognized as the tissue injury and repair theory, and the newly coined term "archimetrosis" posits that the two diseases share the same origin. While the theory opens an interesting channel for exploration, its claim as a unifying theory necessitates a critical appraisal. We, thus, undertook this review of the theory and analyzed its underpinnings based on a comprehensive review of the literature. Our appraisal indicates that the theory is open to a range of criticisms. Chief among these is the need for confirmatory evidence of features of abnormal uterine contractility and the lack of data addressing the question of causality. In addition, the theory has, as yet, no supporting epidemiological evidence, which is a major weakness. The theory suffers as it is not open to the test of falsifiability, and it lacks the ability to make useful predictions. It has not addressed the questions, such as why only a small percentage of women develop adenomyosis or endometriosis, given the ubiquity of uterine peristalsis. On the other hand, the triggers and prevention of hyper- or dys-peristalsis become critical to a theory of causation. We conclude that additional supportive evidence is required for the theory to be accepted.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
Dxm发布了新的文献求助10
刚刚
Qing完成签到,获得积分20
1秒前
tuanheqi应助wenqin采纳,获得20
1秒前
4秒前
眼药水发布了新的文献求助10
4秒前
得的完成签到 ,获得积分10
5秒前
5秒前
大模型应助zsping采纳,获得10
7秒前
yyyyangyixin完成签到,获得积分10
7秒前
DiJia完成签到 ,获得积分10
8秒前
简单文博发布了新的文献求助10
9秒前
研友_VZG7GZ应助无聊的寒烟采纳,获得10
9秒前
丘比特应助啵啵采纳,获得10
10秒前
AA发布了新的文献求助10
10秒前
Wilson发布了新的文献求助10
11秒前
13秒前
13秒前
英俊的铭应助DUANYALI采纳,获得10
13秒前
万从灵应助30采纳,获得10
14秒前
15秒前
科研通AI2S应助自然的含蕾采纳,获得10
15秒前
15秒前
8R60d8应助科研通管家采纳,获得10
16秒前
17秒前
CodeCraft应助科研通管家采纳,获得10
17秒前
吟賞烟霞发布了新的文献求助10
17秒前
17秒前
彭于晏应助科研通管家采纳,获得10
17秒前
8R60d8应助科研通管家采纳,获得10
17秒前
CodeCraft应助科研通管家采纳,获得10
17秒前
小二郎应助科研通管家采纳,获得10
17秒前
无花果应助科研通管家采纳,获得10
17秒前
17秒前
xiu-er完成签到,获得积分10
17秒前
19秒前
turbohero发布了新的文献求助30
21秒前
21秒前
一丢丢完成签到,获得积分10
21秒前
小点点发布了新的文献求助10
22秒前
23秒前
高分求助中
Licensing Deals in Pharmaceuticals 2019-2024 3000
Effect of reactor temperature on FCC yield 2000
Very-high-order BVD Schemes Using β-variable THINC Method 1020
PraxisRatgeber: Mantiden: Faszinierende Lauerjäger 800
Mission to Mao: Us Intelligence and the Chinese Communists in World War II 600
The Conscience of the Party: Hu Yaobang, China’s Communist Reformer 600
Geochemistry, 2nd Edition 地球化学经典教科书第二版,不要epub版本 431
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3301902
求助须知:如何正确求助?哪些是违规求助? 2936465
关于积分的说明 8477718
捐赠科研通 2610210
什么是DOI,文献DOI怎么找? 1425047
科研通“疑难数据库(出版商)”最低求助积分说明 662252
邀请新用户注册赠送积分活动 646421