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Volume 91, Issue 3, Pages 698-704 (March 2009)


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Defining the proliferative phase endometrial defect

Jason G. Bromer, M.D., Tamir S. Aldad, B.A., Hugh S. Taylor, M.D.Corresponding Author Informationemail address

Received 28 August 2007; received in revised form 18 December 2007; accepted 19 December 2007. published online 04 March 2008.

Objective

To evaluate proliferative phase endometrial development in a heterogeneous infertility population.

Design

Retrospective study.

Setting

University-based infertility practice.

Patient(s)

Two hundred forty-six treatment cycles.

Intervention(s)

Clomiphene citrate or FSH ovarian stimulation, followed by IUI or IVF.

Main Outcome Measure(s)

Endometrial thickness according to transvaginal ultrasonography; clinical pregnancy rate.

Result(s)

Endometrial growth began from a nadir of approximately 4.5 mm on cycle day 4 and increased linearly to a plateau of approximately 10 mm on cycle day 9. This same pattern was observed in all cycles, regardless of pregnancy, drug, or underlying diagnosis. Follicle-stimulating hormone–stimulated cycles showed a significantly increased endometrial thickness compared with clomiphene citrate cycles (10.1 vs. 8.3 mm). Maximum endometrial thickness achieved showed a correlation with age, body mass index, and maximum E2 level. Subjects who carried a primary diagnosis of polycystic ovary syndrome, endometriosis, or recurrent pregnancy loss all achieved a significantly lower peak endometrial thickness than control subjects. There was a trend toward increased endometrial thickness in cycles resulting in pregnancy compared with those not (10.1 vs. 9.6 mm, respectively).

Conclusion(s)

Endometrial development follows a predictable pattern, with a plateau in growth at cycle day 9. Diseases associated with infertility manifest a proliferative phase defect that can be recognized clinically.

Division of Reproductive Endocrinology and Infertility, Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale University School of Medicine, New Haven, Connecticut

Corresponding Author InformationReprint requests: Hugh S. Taylor, M.D., Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520 (FAX: 203-785-7819).

 J.G.L.B. has nothing to disclose. T.S.A. has nothing to disclose. H.S.T. has nothing to disclose.

PII: S0015-0282(07)04339-7

doi:10.1016/j.fertnstert.2007.12.066


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