Evidence map›Paper›PMID 28729745›Full record

ArticleGeburtshilfe und Frauenheilkunde2017

Insufficient Angiogenesis: Cause of Abnormally Thin Endometrium in Subfertile Patients?

Joachim Alfer, Lars Happel, Ralf Dittrich, Matthias W Beckmann, Arndt Hartmann, Andreas Gaumann, Volker U Buck, Irmgard Classen-Linke

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Geburtshilfe und Frauenheilkunde, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
1.7field-weighted citation impact, top 17% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 74 citations in OpenAlex.

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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

8 authors at 4 institutions in 1 country.

Joachim AlferInstitute of Pathology, Kaufbeuren-Ravensburg, Ravensburg, Germany.
Lars HappelInstitute of Reproductive Medicine, IVF-Saar, Saarbrücken, Germany.
Ralf DittrichDepartment of Obstetrics and Gynecology, Erlangen University Hospital Friedrich-Alexander Universität, Erlangen-Nürnberg, Germany.
Matthias W BeckmannDepartment of Obstetrics and Gynecology, Erlangen University Hospital Friedrich-Alexander Universität, Erlangen-Nürnberg, Germany.
Arndt HartmannDepartment of Pathology, Erlangen University Hospital Friedrich-Alexander Universität, Erlangen-Nürnberg, Germany.
Andreas GaumannInstitute of Pathology, Kaufbeuren-Ravensburg, Ravensburg, Germany.
Volker U BuckInstitute of Molecular and Cellular Anatomy, Medical Faculty, RWTH Aachen University, Aachen, Germany.
Irmgard Classen-LinkeInstitute of Molecular and Cellular Anatomy, Medical Faculty, RWTH Aachen University, Aachen, Germany.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEMVZ Labor Ravensburg · DERWTH Aachen University · DEHochschule für Musik Saar · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThis study investigated subfertile patients with abnormally thin endometrium after infertility treatment. As they had adequate serum concentrations of hormones, an endometrial factor for subfertility was suspected.

methodsTo elucidate the cause of subfertility, endometrial biopsies were taken in each patient in the late proliferative and mid-secretory phases of one menstrual cycle. Endometrial biopsies from women with normal menstrual cycles and confirmed fertility who were undergoing hysterectomy for benign uterine disease were used as positive controls. The tissue samples were investigated for steroid hormone receptor expression and for the proliferation marker Ki-67. Immunohistochemistry was performed with antibodies against the marker molecules for endometrial receptivity - β

resultsThe steroid hormone receptors for estrogen (E2) and progesterone (P) were expressed normally (at the first biopsy) and were down-regulated (at the second biopsy) within the cycle. Strikingly, all of the marker molecules investigated showed negative or weak and inadequate expression in the mid-secretory phase. Numbers of LGLs remained as low as in the proliferative phase. In contrast, fertile patients were found to express these marker molecules distinctly in the mid-secretory phase.

conclusionsIt may be hypothesized that a severe deficiency of these angiogenesis-related marker molecules leads to defective development of the endometrium, which remains thin. Deficient angiogenetic development may thus provide an explanation for the endometrial factor that causes infertility. Further investigations will need to focus on identifying the regulating factors that act between steroid receptor activation and the expression of these marker molecules.

Indexed as

angiogenesisIVFLIFthin endometriumVEGFβ 3 integrin

Identifiers

PMID28729745
PMCPMC5514021
OpenAlexW2737085072

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.