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Mechanisms

Lower values of VEGF in endometrial secretion are a possible cause of subfertility in non-atopic asthmatic patients

, MD, , PhD, , DMSc, , MD & , DMSc
Pages 336-342 | Received 08 Jul 2014, Accepted 14 Sep 2014, Published online: 08 Oct 2014
 

Abstract

Objective: Using endometrial secretion analysis, we assessed whether altered inflammatory cytokine levels can be detected in the uterine environment in asthma patients, thereby providing a possible cause of reduced fertility in asthmatics. Methods: Forty-four unexplained infertile women (aged 28–44) underwent asthma and allergy testing, questionnaires, endometrial secretion and blood samples in the mid-secretory phase of the menstrual cycle (day 19–23) during assisted reproduction. Differences in cytokines and growth factors were analyzed. Results: Mean log-VEGF in uteri was lower in asthma patients compared with controls (2.29 versus 2.70, p = 0.028). This was mainly due to lower values of VEGF among women with non-atopic asthma compared with women with atopic asthma (1.86 versus 2.72, p = 0.009) and with healthy controls (1.86 versus 2.70, p = 0.01). Asthma treatment status had no effect on VEGF levels in uteri. Serum high sensitivity CRP was negatively correlated with VEGF in endometrial secretions. No other significant correlations were observed between peripheral blood values and markers found in utero. Conclusion: Asthma is associated with lower values of VEGF in uterine endometrial secretions, which might affect the receptiveness of the endometrium and thereby increase time to pregnancy. The effect appears to be associated with non-atopic asthma with general increased systemic inflammation.

Acknowledgements

A special thanks goes to Jan Blaabjerg and the staff at Copenhagen fertility center for their dedication, support and help in collecting samples and patients for the project.

Furthermore thanks to Prof. Dr Bart Fauser and Niels Eijkelkamp for their cooperation and assistance in the analysis of samples in their Laboratory of Neuroimmunology and Developmental Origins of Disease (NIDOD) in Utrecht, Netherlands.

Declaration of interest

E.J.G., S.F.T, S.L., N.S.M and V.B do not have a financial relationship with any commercial entity that has an interest in the subject of this manuscript.

This work has been supported by grants from FAPS (Union of Practicing Specialists) (Grant number: 29241/11), Lundbeck Pharmaceutical (Grant number: R100-A9502) and the Medical Association Denmark.

Supplementary material available online

Supplementary Table S1.

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