Is Neonatal Uterine Bleeding Involved in Early-Onset Endometriosis?

Author:

Habiba Marwan1ORCID,Guo Sun-Wei2ORCID,Benagiano Giuseppe34ORCID

Affiliation:

1. Department of Health Sciences, University of Leicester and University Hospitals of Leicester, Leicester LE1 5WW, UK

2. Department of Biochemistry and Molecular Biology, Research Institute, Shanghai Obstetrics and Gynecology Hospital, Fudan University, Shanghai 200011, China

3. Faculty of Medicine and Surgery, “Sapienza” University of Rome, 00161 Rome, Italy

4. Geneva Foundation for Medical Education and Research, 1202 Geneva, Switzerland

Abstract

Background: There has been considerable progress in our understanding of endometriosis, but its pathophysiology remains uncertain. Uncovering the underlying mechanism of the rare instances of endometriosis reported in early postmenarcheal years and in girls before menarche can have wide implications. Methods: We conducted a literature review of all relevant articles on Medline. Results: In the review, we explore the pathogenetic theories of premenarcheal endometriosis, the role of retrograde menstruation in the adult and its potential role in early-onset disease, as well as the factors that argue against the existence of a link between early-onset endometriosis (EOE) and neonatal uterine bleeding (NUB). Conclusions: As with endometriosis in adult women, the pathogenesis of early-onset disease remains unclear. A link between NUB and EOE is plausible, but there are considerable challenges to collating supporting evidence. The state of our understanding of early uterine development and of the pathophysiology of NUB leaves many unknowns that need exploration. These include proof of the existence of viable endometrial cells or endometrial mesenchymal stem cells in NUB, their passage to the pelvic cavity, their possible response to steroids, and whether they can reside within the pelvic cavity and remain dormant till menarche.

Funder

National Natural Science Foundation of China

Shanghai Shenkang Centre for Hospital Development

Publisher

MDPI AG

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