# Increased C-Reactive Protein Concentrations During Menstruation May Be Important for the Pathophysiology of Endometriosis and Possibly for Adhesion Formation—A Systematic Review

## TL;DR

This review suggests that increased C-reactive protein during menstruation may contribute to endometriosis and adhesion formation due to peritoneal inflammation.

## Contribution

The study systematically reviews evidence linking menstrual C-reactive protein increases to peritoneal inflammation and endometriosis.

## Key findings

- CRP concentrations increased by 80 ± 36% during menstruation and early follicular phase.
- The CRP increase is likely caused by retrograde menstruation and mesothelial cell retraction.
- Acute pelvic inflammation may enhance postoperative adhesion formation.

## Abstract

Objectives: The peritoneal cavity is a cavity outside the bloodstream, with a specific hormonal, immunological and microbiological micro-environment distinct from plasma. The mesothelial cells lining the peritoneal cavity react within seconds to minor trauma, such as blood, with retraction, acute inflammation and later inflammation. This mesothelial cell retraction exposes the basal membrane, facilitating the implantation of tumour cells. Acute inflammation enhances adhesion formation after surgery and causes pain. The aim of the review was to check the hypothesis that retrograde menstruation, occurring in most women, is sufficient to cause some peritoneal irritation. Design: A systematic review of menstrual C-reactive protein (CRP) concentrations, a non-specific marker of peritoneal inflammation (PROSPERO ID 536306). Results: All articles (n = 8) showed a variable increase in CRP concentrations during the menstrual and early follicular phase of 80 ± 36%. Conclusions: CRP concentrations are slightly increased during menstruation and the early follicular phase. This increase is likely due to retrograde menstruation, causing mesothelial cell retraction and acute pelvic inflammation. It seems logical that mesothelial cell retraction facilitates endometrial cell implantation and accounts for the anatomical distribution of endometriosis lesions. Acute pelvic inflammation may enhance postoperative adhesion formation.