Evidence map›Paper›PMID 36900012›Full record

ReviewDiagnostics (Basel, Switzerland)2023

Similarities in Pathogenetic Mechanisms Underlying the Bidirectional Relationship between Endometriosis and Pelvic Inflammatory Disease.

Hiroshi Kobayashi

Full text readReview
In one paragraph

Review in Diagnostics (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  6. Colo-Ovarian Fistula With a Background of Endometriosis: A Report of Three Cases.The journal of obstetrics and gynaecology research · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Hiroshi KobayashiDepartment of Gynecology and Reproductive Medicine, Ms.Clinic MayOne, Kashihara 634-0813, Japan.ORCID 0000-0002-8124-6269

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndometriosis is a common inflammatory disease characterized by the presence of endometrial cells outside of the uterine cavity. Endometriosis affects 10% of women of reproductive age and significantly reduces their quality of life as a result of chronic pelvic pain and infertility. Biologic mechanisms, including persistent inflammation, immune dysfunction, and epigenetic modifications, have been proposed as the pathogenesis of endometriosis. In addition, endometriosis can potentially be associated with an increased risk of pelvic inflammatory disease (PID). Changes in the vaginal microbiota associated with bacterial vaginosis (BV) result in PID or a severe form of abscess formation, tubo-ovarian abscess (TOA). This review aims to summarize the pathophysiology of endometriosis and PID and to discuss whether endometriosis may predispose to PID and vice versa.

methodsPapers published between 2000 and 2022 in the PubMed and Google Scholar databases were included.

resultsAvailable evidence supports that women with endometriosis are at increased risk of comorbid PID and vice versa, supporting that endometriosis and PID are likely to coexist. There is a bidirectional relationship between endometriosis and PID that shares a similar pathophysiology, which includes the distorted anatomy favorable to bacteria proliferation, hemorrhage from endometriotic lesions, alterations to the reproductive tract microbiome, and impaired immune response modulated by aberrant epigenetic processes. However, whether endometriosis predisposes to PID or vice versa has not been identified.

conclusionsThis review summarizes our current understanding of the pathogenesis of endometriosis and PID and discusses the similarities between them.

Indexed as

endometriosisimmune responsemicrobiotapelvic inflammatory diseasetubo-ovarian abscess

Identifiers

PMID36900012
PMCPMC10000848

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Registered trials

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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.