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Human Reproduction 2006 21(4):1102-1103; doi:10.1093/humrep/dei449
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© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Letter to the editor

Reply: Adenomyosis in endometriosis – prevalence and impact on fertility. Evidence from magnetic resonance imaging

Georg Kunz1,4, Dolores Beil2, Peter Huppert2, Marion Noe1,5, Stefan Kissler3 and Gerhard Leyendecker1,6

1 Departments of Obstetrics and Gynaecology and 2 Radiology I. Academic Teaching Hospital to the Universities of Frankfurt and Heidelberg/Mannheim, Klinikum Darmstadt, Grafenstr, 9, 64283 Darmstadt, Germany. 3 Department of Obstetric and Gynaecology, University of Frankfurt, Theodor-Stern-Kai 7, 60596 Frankfurt, Germany Present addresses: 4 Department of Obstetrics and Gynecology, St.-Johannes-Hospital, Johannesstr, 9, 44137 Dortmund, Germany; 5 Division of Gynaecological Endocrinology and Reproductive Medicine, Department of Obstetrics and Gyneacology, University of Vienna, Wehringer Gürtel 17-19, 1090 Vienna Austria

6 To whom correspondence should be addressed at: E-mail: gerhard.leyendecker{at}t-online.de

Sir,

We thank the authors for their interest in our work. The bulk of the MR imaging scans of our study was obtained during 1999 through 2001. That is why we used the same MRI method as described in our publication of 2000 (Kunz et al., 2000Go). With this method, high quality scans were obtained (Figures 1 and 4 of our paper) (Kunz et al., 2005Go) which allowed us to identify alterations of the junctional zone that were interpreted as signs of focal and diffuse adenomyosis, respectively, according to the data of Reinhold et al. (1999)Go. We were even more cautious in that a threshold value of more than 10 mm was chosen above which, with additional signs up to 12 mm, diffuse adenomyosis was assumed.

The authors report a lower prevalence of adenomyosis in endometriosis but confirm our finding of a significant impact of adenomyosis on subfertility and infertility in endometriosis. The discrepancy with respect to prevalence might be a matter of interpretation and the methods used. But it has also to be kept in mind that patient selection plays a key role in this respect.

According to our understanding of the disease process, minimal and mild endometriosis of the fertile woman, endometriosis in association with adenomyosis of the infertile woman and pre- and perimenopausal adenomyosis, respectively, constitute a pathophysiological continuum that could be summarized with the term ‘syndrome of dislocated basal endometrium’ and is characterized in its clinically most important form by pain, infertility and bleeding disorders. Circumstantial evidence suggests a causal relationship with uterine peristalsis and its dysfunctions. In women with normoperistalsis, minimal and mild endometriosis might develop without affecting fertility. Chronic uterine peristaltic activity throughout the reproductive period of life might result in pre- and perimenopausal adenomyosis. In our study, the prevalence of adenomyosis in the ‘total control group’ is largely due to the inclusion of women older than 35 years of age. This ‘functional ageing’ of the uterus might, in the general population, be further enforced by additional trauma such as pregnancy and delivery, as well as abortion curettage.

In infertile women, due to an abnormal stimulation of archimetral estrogen receptors that results in hyperperistalsis (Leyendecker et al., 2004Go), the process of the development of endometriosis and adenomyosis, respectively, is intensified and advanced. On a temporal scale, however, the development of the two disease varieties might not take place simultaneously but rather with a variable time interval with endometriosis usually coming first and followed by adenomyosis as the main determinant with respect to infertility. Thus, in this dynamic process of disease development no static value for the prevalence of adenomyosis in endometriosis can be expected. This value varies dependent on the study population chosen. In our study, all patients or couples including the ‘healthy’ and ‘total controls’ were suffering from infertility and were seeking treatment by assisted reproduction, increasing the probability that both the peritoneal and the uterine variant of the disease had developed in these women.

References

Kunz G, Beil D, Huppert P and Leyendecker G (2000) Structural abnormalities of the uterine wall in women with endometriosis and infertility visualized by vaginal sonography and magnetic resonance imaging. Hum Reprod 15,76–82.[Abstract/Free Full Text]

Kunz G, Beil D, Huppert P, Noe M, Kissler S and Leyendecker G (2005) Adenomyosis in endometriosis. Prevalence and impact on fertility. Evidence from resonance imaging. Hum Reprod 20,2309–2316.[Abstract/Free Full Text]

Leyendecker G, Kunz G, Herbertz M, Beil D, Huppert P, Mall G, Kissler S, Noe M and Wildt L (2004) Uterine peristaltic activity and the development of endometriosis. Ann N Y Acad Sci 1034,338–355.[CrossRef][Web of Science][Medline]

Reinhold C, Tafazoli F, Mehio A, Wang L, Atri M, Siegelman ES and Rohoman L (1999) Uterine adenomyosis: endovaginal US and MR imaging features with histopathologic correlation. Radiographics 19,S147–S160.


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