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