ANGIOTENSIN-II IMMUNOREACTIVITY IS ELEVATED IN ASCITES DURING SEVERE OVARIAN HYPERSTIMULATION SYNDROME - IMPLICATIONS FOR PATHOPHYSIOLOGY AND CLINICAL MANAGEMENT

Citation
A. Delbaere et al., ANGIOTENSIN-II IMMUNOREACTIVITY IS ELEVATED IN ASCITES DURING SEVERE OVARIAN HYPERSTIMULATION SYNDROME - IMPLICATIONS FOR PATHOPHYSIOLOGY AND CLINICAL MANAGEMENT, Fertility and sterility, 62(4), 1994, pp. 731-737
Citations number
24
Categorie Soggetti
Obsetric & Gynecology
Journal title
ISSN journal
00150282
Volume
62
Issue
4
Year of publication
1994
Pages
731 - 737
Database
ISI
SICI code
0015-0282(1994)62:4<731:AIIEIA>2.0.ZU;2-I
Abstract
Objective: To investigate the ovarian renin-angiotensin system (RAS) d uring severe ovarian hyperstimulation syndrome (OHSS). Design: Simulta neous sampling of blood and ascitic or peritoneal fluid (PF) during th erapeutic paracentesis or laparoscopy. Setting: University Hospital. P atients: Twelve patients were investigated: three patients presenting severe OHSS, three patients with a spontaneous first trimester pregnan cy, three normally cycling women during the early luteal phase, and th ree patients with ascites of nonovarian origin. Main Outcome Measure: Renin-like activity and angiotensin II (ANG II) immunoreactivity were measured simultaneously in the plasma and the ascites or PF. Results: Angiotensin II immunoreactivity was much higher in the ascites or PF t han in corresponding plasma during severe OHSS, first trimester pregna ncy, and in the early luteal phase, while it was lower in ascites of n onovarian origin. Renin-like activity and ANG II immunoreactivity were the highest in the ascites of severe OHSS and in the PF from part of the patients with a spontaneous first trimester pregnancy. Conclusions : The present findings argue for the ovarian origin of the elevated re nin-like activity and ANG II immunoreactivity in the ascites of severe OHSS and suggest a stimulatory role of hCG on the ovarian RAS whether during severe OHSS or first trimester spontaneous pregnancy. The vaso active peptide ANG II may contribute to the maintenance of the ascites in severe OHSS but is probably not responsible for the formation of t he ascites. The efficiency of paracentesis during severe OHSS could be explained at least partially by the removing of great amounts of ANG II from the peritoneal cavity.