# Impact of chronic endometritis on assisted reproductive technology outcomes: a propensity score inverse probability weighting cohort study

**Authors:** Wenjie Huang, Liqiong Duan, Liuyan Wei, Ni Tang, Jia Wei, Xuechang Chou, Yaping Ma, Lili Wei, Ming Zhang, Fangmei Lu, Li Fan, Kai Wang, Huawei Wang

PMC · DOI: 10.3389/fcell.2026.1749173 · Frontiers in Cell and Developmental Biology · 2026-01-28

## TL;DR

This study found that chronic endometritis, as defined by CD138+ plasma cells, does not significantly affect pregnancy or live birth rates in IVF treatments, and antibiotics do not improve outcomes.

## Contribution

The study provides new evidence that CE diagnosis and treatment do not significantly impact ART outcomes in a large cohort.

## Key findings

- Untreated CE patients had similar live birth and clinical pregnancy rates to non-CE patients in both IVF-ET and FET.
- Antibiotic treatment for CE did not improve outcomes compared to no treatment in either transfer type.
- CE was associated with a lower observed miscarriage risk after IVF-ET.

## Abstract

Chronic endometritis (CE), characterized by CD138+ plasma cell infiltration, has been proposed to impair reproductive outcomes in assisted reproductive technology (ART). However, current evidence remains inconsistent, and diagnostic criteria vary widely. This study aimed to evaluate whether CE diagnosis and antibiotic treatment influence clinical pregnancy, live birth, and miscarriage outcomes following in vitro fertilization with fresh embryo transfer (IVF-ET) and frozen embryo transfer (FET).

We retrospectively analyzed 3,041 embryo transfer cycles (1,507 IVF-ET; 1,534 FET) from 1,401 infertile women treated at the Reproductive Medicine Center of Liuzhou Hospital, Guangzhou Women and Children’s Medical Center (2008–2023). Chronic endometritis (CE) was primarily defined as the presence of ≥1 CD138+ plasma cell per 10 high-power fields (HPFs, ×400). Standard therapy was doxycycline 100 mg twice daily for 14 days. Outcomes were analyzed per transfer cycle using Poisson regression with robust standard errors and propensity score weighting.

Untreated CE patients had comparable live birth and clinical pregnancy rates to non-CE patients in both IVF-ET (live birth 37.7% vs. 36.7%) and FET (39.0% vs. 37.9%), and were also associated with a lower observed miscarriage risk after IVF-ET (adjusted RR 0.67, 95% CI 0.46–0.97). Among CE patients, antibiotic treatment did not improve outcomes compared with no treatment (IVF-ET live birth 36.8% vs. 37.7%; FET 41.5% vs. 38.7%; all p > 0.05). Similarly, post-treatment “cured” and “persistent” CE groups showed no significant differences in live birth or miscarriage rates in either transfer type. Exploratory analyses revealed context-dependent trends, but most interactions were nonsignificant.

In this large single-center cohort, CE defined by CD138+ plasma cell infiltration was not associated with reduced clinical pregnancy or live birth rates, and no statistically significant benefit of antibiotic treatment was observed. The observed reduction in miscarriage risk among CE patients suggests complex immunological dynamics. Routine CE screening in all ART candidates may be unnecessary, and targeted evaluation for high-risk subgroups warrants further investigation.

## Linked entities

- **Proteins:** SDC1 (syndecan 1)
- **Chemicals:** doxycycline (PubChem CID 54671203)
- **Diseases:** chronic endometritis (MONDO:0024279)

## Full-text entities

- **Genes:** BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581] {aka BCL2L4}, IL11 (interleukin 11) [NCBI Gene 3589] {aka AGIF, IL-11}, SDC1 (syndecan 1) [NCBI Gene 6382] {aka CD138, SDC, SYND1, syndecan}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, GNRH1 (gonadotropin releasing hormone 1) [NCBI Gene 2796] {aka GNRH, GRH, LHRH, LNRH}, BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596] {aka Bcl-2, PPP1R50}, AMH (anti-Mullerian hormone) [NCBI Gene 268] {aka MIF, MIS}, IGFBP1 (insulin like growth factor binding protein 1) [NCBI Gene 3484] {aka AFBP, IBP1, IGF-BP25, PP12, hIGFBP-1}
- **Diseases:** IVF (MESH:C537182), RIF (MESH:D051437), inflammation (MESH:D007249), ectopic pregnancy (MESH:D011271), Endometriosis (MESH:D004715), CE (MESH:D004716), male factor infertility (MESH:D007248), adenomyosis (MESH:D062788), uterine anomalies (MESH:C562565), microbial infection (MESH:D015163), autoimmune disease (MESH:D001327), UI (MESH:D007246), RPL (MESH:D000026), AUB (MESH:D014592), adhesions (MESH:D000267), RSA (OMIM:614389), immune dysregulation (OMIM:614878), endometrial abnormalities (MESH:D014591), polyps (MESH:D011127), Miscarriage (MESH:D000022), allergic (MESH:D004342)
- **Chemicals:** E2 (MESH:D004958), clomiphene (MESH:D002996), metronidazole (MESH:D008795), doxycycline (MESH:D004318), progesterone (MESH:D011374), levofloxacin (MESH:D064704), CE (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

36 references — full list in the complete paper: https://tomesphere.com/paper/PMC12910471/full.md

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Source: https://tomesphere.com/paper/PMC12910471