Chronic Endometritis
Conditions
Brief summary
Women with PCE represent a treatment-resistant phenotype in whom the endometrial inflammatory and immune status remains abnormal despite antibiotic therapy. GnRH agonist pretreatment may be most beneficial in endometrial phenotypes marked by persistent or residual inflammatory impairment rather than in all frozen embryo transfer populations.We therefore conducted a single-center prospective cohort study to investigate whether GnRH-HRT, compared with non-GnRH-based preparations, improve clinical pregnancy and live birth in women with PCE undergoing FET,
Interventions
DRUGConventional estrogen-progesterone artificial cycle for endometrial preparation
No GnRH-a down-regulation. Oral estrogen is initiated directly on early menstrual cycle, followed by progesterone transformation to prepare endometrium for FET in patients with persistent chronic endometritis.
DRUGGnRH agonist plus estrogen-progesterone for endometrial preparation
Long-acting GnRH agonist is administered on day 2-3 of menstruation for pituitary down-regulation. After satisfactory hormonal suppression, sequential oral estrogen and progesterone are used to prepare endometrium before frozen embryo transfer in patients with persistent chronic endometritis.
Sponsors
Guoxia Yang
Study design
Observational model
COHORT
Time perspective
PROSPECTIVE
Eligibility
Sex/Gender
FEMALE
Age
20 Years to 40 Years
Inclusion criteria
* Aged 20-40 years; confirmed persistent chronic endometritis (PCE) via hysteroscopy plus CD138 immunohistochemistry, defined as positive endometrial pathology after two-course antibiotic treatment for CE. * Frozen-thawed embryo transfer (FET) with available transferable cleavage-stage or blastocyst embryos from IVF/ICSI cycles. * No acute pelvic infection at enrollment; ≥1 month elapsed after completion of last antibiotic therapy for endometritis. * Normal uterine cavity except for inflammatory changes of PCE; no severe uterine malformation or severe intrauterine adhesion requiring surgical intervention. * Voluntarily sign informed consent and complete full follow-up of pregnancy outcomes
Exclusion criteria
* History of pelvic tuberculosis, intrauterine adhesions, submucous uterine myoma or endometrial polyp before FET * Uncontrolled systemic endocrine disorders, autoimmune diseases (APS, SLE), severe hepatic/renal/cardiopulmonary dysfunction. * Known allergy to GnRH agonist for down-regulation regimen; prior long-acting GnRH-a intolerance. * Recent use of immunosuppressant, long-term glucocorticoid or drugs interfering endometrial development within 3 months before enrollment. * Lost to follow-up or plan to abandon embryo transfer after enrollment.
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Clinical pregnancy rate | 6-7 weeks | Clinical pregnancy was defined as the visualization of at least one gestational sac on transvaginal ultrasonography at 6-7 weeks of gestation |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| miscarriage rate | 24 weeks | Miscarriage rate was defined as the proportion of clinical pregnancies ending in spontaneous pregnancy loss before 24 gestational weeks. Early miscarriage was defined as pregnancy loss occurring before 12 weeks of gestation. |
| Live birth rate | 37 weeks | Live birth was defined as the delivery of at least one live-born infant at ≥24 weeks of gestation. |
Outcome results
None listed