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general condition. Diagnosis of tubal pregnancy by vaginal ultrasound
examination at this stage is not always possible. The presence of large ovaries
¬lling the pelvis makes ultrasound scanning of other structures dif¬cult. Fluid
in the pouch of Douglas is a sign of the presence of ascites. Shiau et al. (2004)
described a case of severe OHSS coexisting with a bilateral ectopic pregnancy.
A rare case of primary abdominal pregnancy that was detected after rapid
resolution of OHSS has been reported by Nakamura et al. (2001). While we
have rarely encountered OHSS associated with tubal, bilateral ectopic, ovarian,
heterotopic or abdominal pregnancies, we caution that all IVF pregnancies
should be screened carefully for these rare combinations (Rizk et al., 1990d, e,
1991b).


Gastrointestinal Surgery
Mesenteric resection after massive arterial infarction has been reported
(Aurousseau et al., 1995). Perforated duodenal ulcer attributed to
Helicobacter pylori in connection with the intense stress linked to critical
OHSS has also been reported (Uhler et al., 2001). Perforated appendicitis and
peritonitis has also been documented (Fujimoto et al., 2002).


Vascular Surgery
Vascular surgery is rarely required to treat thromboses that are complicated by
recurrent emboli or resistant to medical intervention. Posterolateral thor-
acotomy and subclavian arteriotomy and thromboarterectomy by the Fogarthy
technique have been reported (Aurousseau et al., 1995; Choktanasiri and
Rojanasakul, 1995; Germond et al., 1996). Inferior vena cava interruption to
prevent massive thromboembolism has been used by Mozes et al. (1965).


Pregnancy Termination
Pregnancy termination has been paradoxically performed in extreme cases and
has improved the clinical picture of neurological, hematological and vascular
complications (Dumont et al., 1980; Neau et al., 1989; Aurousseau et al., 1995;
Choktanasiri and Rozanasakul, 1995; Ryo et al., 1999; Southgate et al., 1999;
Yoshii et al., 1999; Shan Tang et al., 2000).
218 TREATMENT OF OVARIAN HYPERSTIMULATION SYNDROME




NOVEL MEDICAL TREATMENT FOR OHSS

A wide array of novel ideas for the treatment of OHSS are currently being
investigated (Rizk and Nawar, 2004; Rizk and Aboulghar, 2005; Rizk et al., 1997).


Blocking VEGFR-2
VEGF plays a central role in the pathogenesis of OHSS. Therefore, the role of
VEGF function inhibitors as potential drugs for the treatment of the syndrome
has been explored. The initial studies in this area came from the ¬eld of
oncogenesis, where it has been demonstrated that the inhibition of VEGF signal
transduction can inhibit tumor progression (Kim et al., 1993). These studies
were followed by other investigations that indicated that inhibition of VEGF
signaling inhibits many types of tumors (Neufeld et al., 1999).
Gomez et al., (2002) developed an in-vivo murine model to induce OHSS
and considered the two main characteristics of ovarian enlargement and
increased vascular permeability leading to ascites. They investigated the
hormonal conditions leading to OHSS, the involvement of VEGF in the
development of the syndrome, the tissue sources of VEGF and speci¬c VEGF
isoforms involving OHSS. They tested a new strategy for the prevention and
treatment of OHSS by blocking VEGFR-2 to inhibit vascular permeability.
SU5416 is a novel synthetic compound that was developed to inhibit KDR
signaling in different cancers by avoiding the initial VEGFR-2 phosphorylation.
SU5416 treatment does not affect surface expression or the af¬nity of the
receptor for VEGF. In fact, the durability of the SU5416 activity is attributed
to its long-lasting ability to inhibit VEGF-dependent phosphorylation of
¬‚k-1/KDR and subsequent downstream signaling. SU5416 is not an irreversible
inhibitor of ¬‚k-1/KDR tyrosine kinase (Mendel et al., 2000). The authors
observed that, although the ¬‚k-1/KDR is upregulated in the gonadotropin-
treated animals, the massive doses of SU5416 administered prevented the
possibility of any effect due to upregulation (Fong et al., 1999).
The authors observed that the administration of SU5416 during ovarian
stimulation with PMSG but not after the hCG injection was unable to block
increasing permeability (Figure VIII.5). This ¬nding agrees with the observa-
tion that OHSS appears during the luteal phase after hCG administration.
It also suggests that the temporary inhibition of VEGFR-2 previous to hCG
injection is not a valid strategy to avoid the onset of OHSS. Its injection after
hCG effectively reversed the increased vascular permeability (Figure VIII.5),
and their observations not only support the role of VEGF in OHSS but also
provide new insights and strategies to prevent and treat the syndrome based on
pathophysiologic mechanisms.


Anti-VEGF antibody
A novel potential approach is the anti-VEGF antibody available as a recom-
binant human monoclonal antibody from Genentech in San Francisco, CA,
219
NOVEL MEDICAL TREATMENT FOR OHSS




Fig. VIII.5: Vascular permeability is signi¬cantly inhibited after SU5416 administration
after hCG injection
Reproduced with permission from Gomez, Simon, Remohi et al. (2002). Endocrinology
143:4339À48


under the brand name Avastin (Meldrum, 2002; Jain, 2002; McDonough,
2003).


Cabergoline for Treatment of OHSS
Dopamine (D2) has been thought to be able to block VEGFR-2 phosphoryla-
tion which is the ¬rst step in VEGFR-2 downstream signaling. Gomez-Gallego
et al. (2005) investigated whether the dopamine (D2) agonist cabergoline could
block vascular permeability in OHSS and if these inhibitory effects were related
to decreased VEGFR-2 phosphorylation. They have utilized the same protocol
for ovarian stimulation used to study OHSS in rats (see Chapter III, the
role of progesterone in OHSS): hCG was given on day 26, and prolactin pellets
5 mg were implanted in OHSS rats to avoid functional luteolysis by the
administration of cabergoline 3 mg and 6 mg, 24 h later on day 27. Vascular
permeability was measured and quanti¬ed as the extravasation of a previously
injected dye and expressed as mg extravased dye per 100 g body weight. The
presence of functional luteolysis was evaluated by the assessment of pro-
gesterone by ELISA and prolactin by radioimmunoassay. To study VEGFR-2
phosphorylation, VEGFR-2 was previously immunoprecipitated from whole
ovarian extracts and then Western blot testing was performed using a phospho-
tyrosine antibody to detect phosphorylated VEGFR-2. The receptor phosphor-
ylation was expressed as phosphorylated VEGFR-2/VEGFR-2(total). Vascular
permeability in the cabergoline-treated rats was signi¬cantly lower compared
with the cabergoline-untreated rats. In fact, the vascular permeability factors
corresponded to the decrease in VEGFR-2 phosphorylation in the cabergoline
treated rats compared with the untreated rats (63% and 83% in the 3 mg
and 6 mg cabergoline groups). There were no luteolytic effects observed.
Gomez-Gallego et al. (2005) concluded that cabergoline is able to inhibit
220 TREATMENT OF OVARIAN HYPERSTIMULATION SYNDROME




vascular permeability in OHSS. These inhibitory effects are related to VEGFR-2
downstream signaling blockade and not to luteolytic effects. Gomez-Gallego
et al. (2005) suggested that cabergoline is a non-toxic as well as a speci¬c
approach to effectively treat OHSS.


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