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Human Reproduction, Vol. 18, No. 5, 1130, May 2003
© 2003 European Society of Human Reproduction and Embryology

Evidence that endometriosis results from the dislocation of basal endometrium?

Thomas M. D’Hooghe1 and Sophie Debrock

Leuven University Fertility Center, Department Obstetrics and Gynecology, University Hospital Gasthuisberg, Leuven, Belgium

1 To whom correspondence should be addressed. e-mail: Thomas.dhooghe{at}uz.kuleuven.ac.be

Dear Sir,

I read with great interest the article by Leyendecker et al. (2002Go) addressing the hypothesis that endometriosis results from the dislocation of basal endometrium. The study represents an in-depth analysis of estrogen receptor (ER) and progesterone (PR) expression in eutopic and ectopic endometrium from women with and without adenomyosis and endometriosis. However, we disagree with the interpretation of the results.

The authors mention in the Results section that there was no difference between the immunoreactive score (IRS) of ER and PR expression in the endometrium from women with and without endometriosis, and that the cyclical patterns of the IRS of ER and PR expression in endometriotic and adenomyotic lesions completely mimicked those of the deep basalis. In contrast, the prevalence of basal endometrium was found to be higher in menstrual blood from women with endometriosis when compared with those without endometriosis. Overall, the authors conclude that these data suggest that endometriosis results form the dislocation of basal endometrium.

Several issues need to be resolved: (i) It appears contradictory that, between women with and without endometriosis, there were no differences in ER and PR expression in eutopic endometrium in either basal or functionalis layer during any phases of the cycle, but huge differences in ER and PR expression were observed between endometrial tissue fragments of menstrual blood from women with endometriosis and those without endometriosis. How can this be explained? (ii) The analysis of basal endometrium in menstrual blood was very limited and the differences between women with and without endometriosis seem extremely high. Firstly, the presence of basal endometrium was detected using unspecified morphological criteria. How is it possible to discern basal from non-basal endometrium in menstrual blood based on morphology only? Secondly, only one section was analysed for ER, PR, PR B and P450A expression. Why did the authors not use the same semi-quantitative IRS score as used for the immunohistochemical analysis of eutopic and ectopic endometrium? Why did they not apply serial sectioning and did they not perform a more complete analysis? How did they select the four sequential sections that were analysed? How many sections were available per menstrual blood analysis? Did the investigators who performed the immunohistochemical analysis know whether the tissue came from patients with or without endometriosis? (iii) All data presented in this paper, except the menstrual fluid data, can be equally explained by the hypothesis that, during retrograde menstruation, viable endometrial cells from the functionalis layer implant on the pelvic peritoneum with subsequent metaplasia to characteristics typical for basal eutopic endometrium (such as cyclical pattern for ER and PR expression). The menstrual fluid data seem not solid enough to draw the highly speculative conclusion that endometriosis is caused by the dislocation of basal endometrium.

References

Leyendecker, G., Herbertz, M., Kunz, G. and Mall, G. (2002) Endometriosis results from the dislocation of basal endometrium. Hum. Reprod., 17, 2725–2736.[Abstract/Free Full Text]


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This Article
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