The presence of steroid binding sites in (or on) human spermatozoa was first suggested in the late 1970s, by studies showing that some steroids were able to influence sperm function. Subsequently, several effects exerted on spermatozoa by biological fluids, such as follicular fluid, were found to be probably linked to the action of steroids, and among them progesterone. Since the effects of progesterone on spermatozoa were rapid, dose-dependent and not affected by progesterone conjugation with high molecular weight proteins unable to cross the plasma membrane, the existence of a novel class of non-genomic progesterone receptors was strongly suspected. This hypothesis was further supported by the observation that some of the effects of progesterone on human spermatozoa were not abolished by inhibitors of the classical progesterone nuclear receptors, nor mimicked by progesterone genomic receptor agonists. Recently, surface progesterone binding sites were directly identified on the membranes of human spermatozoa, and their mechanism of action partially characterized.
The recurrence of pelvic endometriosis some time after the initial treatment is a common finding in clinical practice. When symptoms of endometriosis reappear several months after treatment, it is difficult to distinguish between recurrence and persistence of the disease. In this review, the current hypotheses about the biological basis of endometriosis recurrence/persistence are discussed. The results of several clinical trials estimating the recurrence rate of endometriosis after medical, surgical, and combined treatments are presented. In addition, a critical analysis of the tools available for the diagnosis of recurrent endometriosis is made, and some therapeutic options to treat recurrent endometriosis are discussed with recommendations for their use.
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