Evidence map›Paper›PMID 28423456›Full record

ReviewActa obstetricia et gynecologica Scandinavica2017

Progesterone resistance in endometriosis: origins, consequences and interventions.

Bansari G Patel, Martin Rudnicki, Jie Yu, Yimin Shu, Robert N Taylor

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Acta obstetricia et gynecologica Scandinavica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed, 4 pooled it
27.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

161 citing papers in PubMed, 4 syntheses or guidelines pooled it, 309 citations in OpenAlex.

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  2. Endometriosis and aspirin: a systematic review.Frontiers in endocrinology · 2024
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101 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Bansari G PatelDepartment of Obstetrics and Gynecology, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Martin RudnickiDepartment of Obstetrics and Gynecology, Odense University Hospital, Odense, Denmark.ORCID http://orcid.org/0000-0002-5115-1445
Jie YuDepartment of Obstetrics and Gynecology, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Yimin ShuDepartment of Obstetrics and Gynecology, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Robert N TaylorDepartment of Obstetrics and Gynecology, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Wake Forest University · USOdense University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometriosis is a common cause of pelvic pain and affects up to 10% of women of reproductive age. Aberrant progesterone signaling in the endometrium plays a significant role in impaired decidualization and establishment of ectopic endometrial implants. Eutopic endometrial cells from women with endometriosis fail to downregulate genes needed for decidualization, such as those involved in cell cycle regulation, leading to unbridled proliferation. Several causes of progesterone resistance in the endometrium have been postulated, including congenital "preconditioning", whereby the in utero environment renders infants susceptible to neonatal uterine bleeding and endometriosis. Progesterone action is crucial to decreasing inflammation in the endometrium, and deviant progesterone signaling results in a proinflammatory phenotype. Conversely, chronic inflammation can induce a progesterone-resistant state. Repetitive retrograde endometrial shedding begets chronic peritoneal inflammation, which further exacerbates progesterone resistance. Genetic causes of progesterone resistance include progesterone receptor gene polymorphisms, altered microRNA expression, and epigenetic modifications to progesterone receptors and their targets. Environmental toxins such as dioxin play a possible role in the genesis of endometriosis by permitting an inflammatory milieu. A consequence of impaired progesterone action is that hormonal therapy is rendered ineffective for a subset of women with endometriosis. Synthetic progestins, such as dienogest, may overcome this phenomenon by increasing progesterone receptor expression and decreasing proinflammatory cytokines. Other modalities include high dose depot formulations of progestins, medicated intrauterine devices and the likely advent of oral GnRH antagonists. Unearthing root causes of progesterone inaction in endometriosis will aid in the development of novel therapeutics geared toward prevention and treatment.

Indexed as

EndometriosisEndometriumEnvironmental PollutionFemaleHumansProgesteroneReceptors, ProgesteroneProgesteroneReceptors, ProgesteroneEndometriosisendometriuminfertilitypelvic painprogesteroneprogesterone receptor

Identifiers

PMID28423456
OpenAlexW2605912824

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.