The ultrasound today seemed to go fine. Lefty is at 17 mm, with Righty lagging behind… still measuring 11 mm. (Dr. Y also measured a third at 8 mm, but didn’t say anything about it.) C and I think that Dr. Y was disappointed with Righty’s slow growth, but felt sorry for us and refrained from saying anything… He recommended continuing stims + Antagon for a couple more days to give them more time to grow. He’d like Lefty to be at 20 mm for retrieval.

The next ultrasound will be Wednesday, with tentative retrieval on Friday – possibly later. Back when we started the cycle, Dr. Y said that it will be good if we can get a couple extra stim days prior to retrieval, so I’m going to stick with that and say this is a good thing…


So, Antagon

I’m on day 3 of Antagon (aka ganirelix), which I inject into my belly every morning by way of a prefilled syringe with an annoyingly dull needle. (It doesn’t hurt that much, but it actually bounces off of my skin if I don’t shove it hard enough!) Aside from looking like a human pincushion, I haven’t observed any side-effects.

Despite my disappointing Saturday, I didn’t want to put off writing about Antagon for too much longer, since it is actually the drug that I find the most interesting, but first:

I am NOT an endocrinologist, or any kind of medical professional! This blog does NOT purport to offer medical advice, medical opinions, or recommendations. Please take this for what it is – the ramblings of an infertile woman trying to make sense of her complicated treatment protocol!


Before explaining what Antagon does, it’s probably worth reviewing how this whole sex hormone signaling cascade is supposed to go normally.


First, my brain sends a signal to my pituitary, which in turn sends a signal to my ovaries, which in turn make estrogen, grow eggs, and ovulate.

The ‘signal’ that my brain sends to my pituitary is carried by a peptide hormone called gonadotropin-releasing hormone (GnRH; also known as luteinizing hormone-releasing hormone or LHRH).

The ‘signal’ that my pituitary sends to my ovaries is carried by two proteins – our old friends FSH and LH. Normally, FSH stimulates one or two of the follicles to grow and develop into a single mature egg. LH (released in a surge) signals the ovaries to ‘drop’ the mature egg.

Of course, in the case of IVF, we don’t want to just have one mature egg, and we don’t want to have it get released before we are good and ready for it.

Here’s where Antagon comes in.


As its name suggests, Antagon (aka ganirelix) is a GnRH antagonist, which means that it looks a lot like GnRH, but it doesn’t act like GnRH. You can see this if you look at the chemical structures of the two (below). Antagon is about the same size and shape as GnRH; it has similar atoms and functional groups (I highlighted the differences in red for your convenience). As a result, it can fit into the same tight spaces that GnRH can fit into – like the inside of the receptor protein ‘switch’ that GnRH normally turns on to make the pituitary send its signal…


While Antagon looks like GnRH, it doesn’t act like GnRH. So when Antagon fits into the GnRH receptor protein, it doesn’t actually flip the switch ‘on’.

To pick another analogy, GnRH is the key that opens a lock on the pituitary gland. Antagon is like another key that fits into the same keyhole…but doesn’t open the lock. Having lots of Antagon around filling up keyholes makes it really hard for GnRH to actually turn any locks. (In biochemistry-speak, Antagon is a competitive inhibitor.) The effect is the same as if we had somehow removed all the GnRH from the system.

Without GnRH stimulating the pituitary gland, the pituitary gland doesn’t produce LH (or FSH, but we’re more concerned with LH at the moment), and we don’t get the surge, and ovulation is prevented (left panel, below).


What about Lupron?

Interestingly, using a GnRH antagonist isn’t the only (or even the most popular) option for preventing ovulation.

The other, more common, method involves using a GnRH agonist (such as Lupron, aka leuprolide). A GnRH agonist both looks and acts like GnRH.

Lupron has a chemical structure that is even closer to that of GnRH. In fact, they differ by only one amino acid (in blue on the previous chemical structure drawing). Lupron also flips the GnRH receptor protein ‘on’…and keeps it on for longer than GnRH does.

But I thought we were trying to prevent GnRH from sending its signal?

The initial response of the agonist is to increase the GnRH signal – the opposite of what we want. But we’re counting on what happens next. All this signaling is very carefully regulated, so after a few days of having its GnRH switch frozen in the ‘on’ position, the pituitary figures out that something is wrong. It absorbs the GnRH receptors (the keyholes) from the cell surface, and all further signaling in the pathway gets shut down (above right).

It’s like the sirens go off, red lights start flashing, and the pituitary says “TERMINAL ERROR DETECTED. COMMENCE SYSTEM SHUTDOWN.

With the signal shut down, the pituitary doesn’t continue to make LH, and ovulation can be prevented until we’re ready for it.

What does DOR have to do with it?

Despite sounding more complicated, the agonist protocol is the more commonly-used option, or ‘plain Vanilla IVF’ if you prefer, and works well for the majority of IVF patients. However, some recent studies seem to suggest that using an antagonist might be better for poor responders (like people with diminished ovarian reserve). I think this is still pretty controversial, though.

I think the theory is that for DOR patients, the traditional agonist long protocol suppresses signaling for too long and gets in the way of recruiting the already-poorly-responsive eggs. For the agonist protocol to work, the agonist has to begin to be administered relatively early – before there are any follicles ready to drop (otherwise the initial burst of LH & FSH might trigger ovulation before the desired ‘System Shutdown’), so things are shut down for a relatively long period. By contrast, the antagonist can be administered later in the cycle, for just a few days.


Whatever the reason, I’m gambling on the short, antagonist protocol. Odds are that I’m going to lose this poker hand, but dammit, I am not folding!


Trigger shot

I had my estradiol and follicles checked today. Two looked like they could drop any minute, so the nurse practitioner – D. – administered the hCG trigger shot while I was there. (Poor C. didn’t get to “stick me” after all!)

For all the data monkeys (like me) out there, here’s a summary of my test results:

Estradiol (E2):

  • baseline estradiol (taken during infertility workup 1/26) = 25 pg/mL
  • estradiol on 4/17 (after 4 days of injections) = 281 pg/mL
  • estradiol today (4/19, after 6 days of injections) = 572 pg/mL

According to this FAQ (, the target is 200-600 pg/mL per big follicle; since I only have two big follicles, I think this means I’m good.

Follicle size & count:

  • On Wednesday (4/17) I had three visible follicles, measuring 14.5 mm, 13 mm, and 11 mm.
  • Today (4/19) the same follicles measured 18.5 mm, 16.6 mm, and 11.5 mm. Below is a picture of my biggest follicle, viewed on ultrasound. (The follicle is the black oval just left of center with the dotted cross through it). 18.5 millimeters sounded huge to me, so I posed a penny (also 18.5 mm in diameter) in the photo for reference!


According to that same FAQ above, it looks like 16-18 mm is a good range for Menopur-stimulated follicles, which is consistent with what nurse D. said. She expects that the smaller one will probably not release, so we’re looking at two follicles this cycle.

Things are slightly less than ideal. For our best chances of pregnancy, our target would have been 3-4 big follicles (to increase the odds of at least one ‘good’ egg taking). But 2 is better than 1, and better than 5+ (in which case we would’ve had to cancel the cycle or risk a multiple pregnancy). In addition, it would have been better to inseminate 36 hours after the trigger shot, but since the clinic is closed on Sunday, 24 hours will have to do! Nurse D. pointed out that it’s better to inseminate early than late, since the sperm can “wait for the egg”, while the egg can’t do the same. (I’m sure there’s a sexist joke to be made there…) She also suggested BDing on Sunday to be sure…

So I’ll be back tomorrow for the insemination. Wish me luck!

Looking good!

So today I had a blood estradiol (E2) test, and ultrasound to see how I’m responding to the Menopur, and all looks good. 🙂

The annoying part is that they only do the estradiol test at the hospital lab across town, and only from 7-7:30 am. So I had to wake up at 5:30 this morning to get ready and drive east to the hospital, and then drive back west in rush-hour traffic to teach my 8:30 class. Fortunately, the infertility clinic is on this side of town, so making it to my 10:30 ultrasound appointment was no problem.

Anyway, the result is that I have two decent-sized follicles, and one smaller one. This is good news, since our target is 2-3 follicles for IUI. Based on the size of the follicles and on my estradiol (281 pg/mL), the nurse practitioner recommended upping my dose of Menopur from 300 IU to 375 IU per injection, and repeating the blood draw (5:30 am wakeup – Boo!) and ultrasound on Friday. Depending on those results, we may do the insemination as early as Saturday!