The response of human endometriotic implants to the anti-progesterone steroid R 2323: a histologic and ultrastructural study.

The histology and ultrastructure of small endometriotic lesions were studied in 19 patients before and after hormonal therapy with the anti-progesterone steroid R 2323 (Gestrinone). Histologic results demonstrate that treatment of endometriosis with this steroid does not result in complete elimination of the endometriotic foci, although glandular proliferation and secretion are arrested in most implants. The ultrastructural results indicate that this inhibition of proliferation and secretion is related to an enhanced activity of the lysosomal system in the epithelial cells of some endometriotic foci. In other implants, or even in other cells of the same foci, epithelial cells with only a small amount of supranuclear cytoplasm but lacking lysosomes may be found. The morphologic data demonstrate that the cellular involutionary response to the antiprogesterone drug Gestrinone involves an activation of the lysosomal system, an abortive apocrine secretion of cell remnants and finally, in some implants, an extrusion of individual epithelial cells. Since this involutionary process of endometriotic cells mimics the pre-menstrual lysosomal degradation in the endometrium, it is suggested that the competitive binding of the antiprogesterone Gestrinone to the progesterone receptors of endometriotic epithelium may cause a cellular progesterone withdrawal effect.