Decreased expression of Syndecan- 1 (CD138) in the endometrium of adenomyosis patients suggests a potential pathogenetic role.

INTRODUCTION

Adenomyosis is a special subtype of endometriosis, affecting the myometrium, affecting about 20% of women in the reproductive age period. Clinical symptoms and intensity are diverse and can vary from heavy menstrual bleeding and dysmenorrhea to infertility and repeated pregnancy losses. Thus, patients often present with a long history of illness pending presumptive clinical or surgical diagnosis. A definitive diagnosis of adenomyosis is made upon histopathological examination verifying ectopic endometrial tissue (endometrial glands and/or stroma) within the myometrium, surrounded by hyperplastic and hypertrophic smooth muscles. However, nowadays ultrasonographic and/or MRI signs can precisely detect it as well. The precise etiology and pathogenesis remain unclear. One theory assumes that adenomyosis occurs through metaplastic transformation or migration of stem cell-like cells.

MATERIAL AND

METHODS

Our study examined the immunohistochemical expression of the transmembrane proteoglycan Syndecan-1 (CD 138), a multifunctional matrix receptor and signaling co-receptor, in the endometrium of 35 patients (n = 21 with adenomyosis and n = 14 as a control group) in the period 2016-2017.

RESULTS

As a pilot study, we concluded that Syndecan-1 is downregulated in adenomyosis patients compared to the control group, supporting its potential role in the development of adenomyosis. Our study did not find a correlation between the immune-expression of Syndecan-1 and the menstrual cycle phase.

CONCLUSIONS

For clinical significance in relation to our results, the investigated data showed that the downregulation of Syndecan-1 in adenomyotic patients in our study may suggest a role in promoting the invasiveness of endometriotic islands within the myometrium. However, further studies are still needed to understand the mechanistic contribution of Syndecan-1 to the pathogenesis of adenomyosis.