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A Syngeneic Murine Model of Endometriosis using Naturally Cycling Mice
Published on: November 24, 2020
Pathophysiology of cyclic hemorrhagic ascites and endometriosis
Anastasia Ussia1, George Betsas, Roberta Corona
1Department of Obstetrics and Gynecology, Villa Giose, Crotone, Italy.
Abstract:
Massive hemorrhagic ascites (4470 mL, range 1-10 L) in women with endometriosis is a rare condition occurring predominantly in black women. Of the 43 case reports published, 42 are compatible with the hypothesis that the hemorrhagic ascites is predominantly a consequence of excessive ovarian transudation similar to a Meigs syndrome. Indeed, bilateral ovariectomy cures the condition without recurrences, whereas after unilateral ovariectomy or cystectomy recurrence rate is more than 50%; during ovarian suppression by luteinizing hormone-releasing hormone agonist ascites disappears, but reappears after treatment. Superficial pelvic endometriosis also contributes to the ascites because after superficial endometriosis destruction the recurrence rate is only 4 in 14. Based on these data, it is suggested, to scrutinize the ovaries for tumors given the analogy with Meigs syndrome. In women desiring fertility, conservative treatment with destruction of endometriosis only can be attempted given the cure rate of some 20%. It is unknown what the effect of ovulation induction would be.
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At puberty, GnRH begins a pulsatile release pattern, which triggers the anterior pituitary gland to secrete follicle-stimulating hormone (FSH) and luteinizing hormone (LH). The frequency and amplitude of GnRH pulses vary across the menstrual cycle, with faster pulses favoring LH release and slower pulses favoring FSH release.
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