rikirees wrote:amh6967:
One of my causes for OHSS was the E2 level. At retrieval my E2 was at nearly 3600. In my last cycle (non OHSS- different Dr.) My highest E2 was 2400 and he got 34 eggs (25 fetilized). Unfortunately, once they know you are possible a OHSS they watch the numbers a lot closer. Sometimes it is just too late! I froze all 25 and just had 3 blasts trasnsfered on Friday. Now I play the waiting game.
E2 does not cause OHSS, but is an indicator of risk. The best indicator of risk is the follicle count.
In a natural cycle, one egg ovulates from one follicle, and one corpus luteum forms.
Following ovarian stimulation, many follicles mature. In those with significant risk of severe OHSS, many large follicles appear. These follicles also produce E2, hence the correlation with E2 level.
Then comes the usual hCG trigger. hCG causes the follicles to release a hormone called "vascular endothelial growth factor", or VEGF. VEGF seems to be the direct cause of OHSS.
One way to end OHSS is to trigger with something besides hCG. The most obvious alternative is a GnRH agonist (like Lupron, Buserelin, or Synarel). Unfortunately, most clinics use an agonist for pituitary suppression, and for pretty obvious reasons, you can't use it for both suppression and the trigger. So the only way you can use the agonist for trigger is if the patient is antagonist-regulated.
If triggered with the agonist instead of hCG, severe OHSS is almost impossible. Not only does it not cause the corpra lutea to release VEGF, it actually kills the corpra lutea, creating a condition called complete luteolysis. No corpra lutea, no VEGF, no OHSS. This theoretically makes severe OHSS impossible, and the published results agree with that theory. Nobody has published a case of severe OHSS after trigger with any GnRH agonist.
There's a lot more to this, but this is just an internet post.