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Thoracic endometriosis

INTRODUCTION

Endometriosis is defined as the presence of endometrial glands in stroma outside the confines of the uterine cavity and musculature. Growth and maintenance of endometriotic implants is dependent upon the presence of ovarian steroids, and therefore endometriosis occurs almost exclusively among women of reproductive age or among those on estrogen replacement therapy [1]. However, endometriosis has also been described in men receiving estrogen [2].

Endometriosis most commonly involves structures within the pelvis, particularly the ovaries, cul-de-sac, broad ligaments, and uterosacral ligaments. However, endometrial tissue can be found outside of the pelvis in the abdomen, thorax, brain, and skin [3].

The thoracic endometriosis syndrome (TES) will be reviewed here. Issues related to the general clinical features and treatment of endometriosis are discussed separately. (See "Pathogenesis, clinical features, and diagnosis of endometriosis" and "Overview of the treatment of endometriosis".)

PATHOGENESIS

Several hypotheses have been proposed to explain the pathogenesis of pelvic and thoracic endometriosis. The Sampson’s theory of retrograde menstruation through fallopian tube leading to auto-transplantation of endometrial tissue into the peritoneal cavity has been proposed as one mechanism [4]. However, a meta-analysis suggested that endometrial tissue differed significantly from eutopic endometrium in clonality, enzymatic activity, protein expression, and histologic properties [5]. Decreased apoptosis causing failure of the normal mechanisms that clear ectopic endometrial cells has also been suggested as a potential mechanism [6]. Altered immune responses leading to the failure to clear peritoneal endometrial tissue, has been reported [7]. Finally, development of ectopic endometrial tissue from a group of multipotential cells residing within the endometrial basal cell layer capable of transformation into endometrial cells has been proposed as mechanism [8,9].

The potential mechanism for migration of endometrial tissue from the pelvis to the thoracic cavity also remains uncertain. Possible routes include microembolization through the pelvic veins [1,10,11], and trans-diaphragmatic movement through diaphragmatic defects [12-14]. The hypothesis that microembolization might be a pathogenic mechanism has been questioned, as micro-embolization would be expected to affect both hemithoraces approximately equally, but TES has an overwhelming occurrence in the right hemithorax [15]. In addition, the relatively high prevalence of pelvic endometriosis in women of reproductive age suggests that a comparably high number of TES cases would occur, if micro-embolization were the mechanism [16]. Instead, the relatively low prevalence of TES makes micro-embolization a less likely explanation.

          

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Literature review current through: Jun 2014. | This topic last updated: Feb 25, 2014.
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