Evidence in Support for the Progressive Nature of Ovarian Endometriomas
Ding Ding, Xi Wang, Yishan Chen, Giuseppe Benagiano, Xishi Liu and Sun-Wei Guo
J Clin Endocrinol Metab, July 2020, 105(7):2189–2202
Context: Whether endometriosis is a progressive disease is a highly contentious issue. While progression is reported to be unlikely in asymptomatic deep endometriosis, progression in symptomatic deep endometriosis has recently been reported, especially in menstruating women. However, pathophysiological reasons for these differences are unclear.
Objective: This study was designed to investigate whether ovarian endometrioma (OE) is progressive or not.
Setting, Design, Patients, Intervention and Main Outcome Measures: Thirty adolescent patients, aged 15 to 19 years, and 32 adult patients, aged 35 to 39 years, all laparoscopically and histologically diagnosed with OE, were recruited into this study after informed consent. Their demographic and clinical information were collected. Their OE tissue samples were collected and subjected to immunohistochemical analysis for E-cadherin, α-smooth muscle actin (α-SMA), desmin, and adrenergic receptor β2 (ADRB2), as well as quantification of lesional fibrosis by Masson trichrome staining.
Results: OE lesions from the adolescent and adult patients are markedly different, with
the latter exhibiting more extensive and thorough progression and more extensive fibrosis, suggesting that lesions in adults progressed to a more advanced stage. Adult lesions and higher staining level of α-SMA and ADRB2 are positively associated with the extent of lesional fibrosis, while the lesion size and the E-cadherin staining are negatively associated.
Conclusions: Our data provide a more definitive piece of evidence suggesting that OE is a progressive disease, since the adult lesions have had a longer time to progress. In addition, the pace of progression depends on lesional age as well as the severity of endometriosis-associated dysmenorrhea, if any. (J Clin Endocrinol Metab 105: 2189–2202, 2020)
Freeform/Key Words: adrenergic receptor β2, endometriosis, epithelial-mesenchymal transition, fibroblast-to-myofibroblast transdifferentiation, fibrogenesis, progression
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