Stims

Yesterday at 7:45 am I had my first IVF monitoring appointment. Since Kaiser doesn’t cover IVF, Dr. Y does all his IVF appointments in the early morning, across town from his main office. Lucky for me, this is only about 10 minutes from my house. (The Kaiser office is about 10 minutes from my work, so it’s been pretty convenient all-around.) I liked my new clinic. The waiting room looked much nicer than the Kaiser facility: lots of good magazines, friendly staff, and a beautiful aquarium. I sat and watched the fish eating their breakfast while C studied his iPhone.

And… my follies are growing, but slowly (which Dr. Y insisted isn’t necessarily a bad thing). The biggest one measured 8 mm. Estradiol level was 83. Dr. Y said to keep taking the same dose of Clomid & Menopur (and dexamethasone, although he didn’t mention that), and to come back on Saturday.

Oh, and we paid the first big bill: $10,115 “Global Fee” for IVF + ICSI. This amount covers all the monitoring appointments and labs, the egg retrieval, and the embryology part. The Global Fee does NOT cover meds, “Embryo Banking” (freezing and storing the embryos), or frozen embryo transfer, so a complete account of the full cost will have to wait.

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Given where I’m at in my cycle, it seems like my stims would be a good science topic for today, but first the usual:

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!

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So, stims…

My ovarian stimulation regimen is low-dose menopausal gonadotropins (Menopur, 150 IU), and clomiphene (Clomid, 100 mg). The goal is to get my ovaries to produce not one but several large, mature, healthy eggs. To understand how these drugs are supposed to accomplish this goal, it would probably help to provide some background. And I feel the need to point out, once again, that I am not an expert. (This blog is not called ‘the infertile endocrinologist’! But if you find a blog with that title, please let me know. I’d love to read it.) So anyway, here’s how I think it works:

Sex hormone signaling 101

Normally, when my body wants to produce estradiol (the most important of the estrogens), my brain sends a signal to my pituitary gland. The pituitary responds by sending a signal to my ovaries, which respond by doing a bunch of things, including making estradiol. The estradiol itself acts as a signal that travels around and tells various body parts to do things.

The carrier pigeons transmitting all these signals are hormones. So, more precisely, my brain produces a hormone called luteinizing hormone releasing hormone (LHRH, also known as gonadotropin-releasing hormone or GnRH), which travels to my pituitary and tells it to produce two more hormones: luteinizing hormone (LH) and follicle stimulating hormone (FSH). These hormones travel to my ovaries and stimulate them to do a bunch of things – like grow eggs and make estradiol…which itself helps to prep the uterine lining, and so on.

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Feedback

As the level of estradiol increases, it circulates through the bloodstream and some of it reaches my brain. Once there, the estradiol tells my brain to stop sending the signal to make more estradiol (in other words, to stop making LHRH). This is a natural “negative-feedback loop”.

Estrogen signaling under the influence

While I’m on my stims, the goal is to get lots of follicles to grow at once. This takes high levels of FSH in there, for an extended period of time. There are two main ways of doing this:

  1. Make more of my own FSH. This is what Clomid aims to accomplish. Clomid blocks estradiol from telling the brain to STOP making LHRH. In this case, two wrongs do make a right, and blocking a stop signal is effectively the same as telling the brain to GO! The brain makes LHRH, which stimulates the pituitary to make LH and FSH, which stimulates the ovaries to grow follicles. Nice.
  2. Add in FSH from the outside. This is what I’m doing when I inject Menopur into my belly each night. Technically, Menopur is a mixture of both FSH and LH, but I think FSH plays the bigger role in follicle development (at least, that’s what its name would lead me to believe…)

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The downside of Clomid is that it doesn’t just block estradiol from talking to my brain. It blocks estradiol from talking to anyone…including my ovaries and uterus (who it’s supposed to tell to start prepping the uterine lining for implantation and making lots of sperm-friendly eggwhite cervical mucus). Clomid steals the entire message from the estradiol carrier pigeon.

Enter my weird protocol. Since the Clomid will prevent my uterine lining from being ‘embie-proofed’ in time for transfer this month, we’ll flash freeze those little guys (hopefully lots of them!) and let them chill for a month. This should give me time to do some nesting and get everything nice and ready to welcome the little tykes!

Why such a low dose of Menopur?

It seems counterintuitive that I would be using a low dose of Menopur, since the conventional wisdom is that patients with diminished ovarian reserve are generally less responsive to stims, and should therefore need more stims… For reference, I used 300 – 375 IU (4 or 5 vials) per day for my IUI cycle…more than twice as much as I’m using for IVF. From what I can tell from my limited reading of the literature, it sounds like for DOR patients with few eggs that are available for stimulation, adding more stims doesn’t increase the number of eggs recruited…and might harm egg quality.

Why Clomid?

I haven’t been able to find a clear reason why Clomid is a good choice in my case. The best I can think is that maybe in poor responders using two strategies for increasing FSH levels will work better than just one? Obviously, the fact that we aren’t doing a fresh transfer is a large part of why Clomid becomes a viable option.

What I know for sure

Clomid plus low-dose Menopur is much cheaper than the high-stims alternative.

Aside from a small crop of pimples on my forehead (which I’m guessing is due to the dexamethasone), I haven’t noticed any side-effects so far. I’m grateful for this!

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That’s where we are for now! We’ll see how the follies are doing bright and early Saturday morning!

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Green light

Today we had our baseline sonogram for IVF#1. As you may recall, our goal for today was:

  • lots of antral follicles (‘lots’ is relative; the most I’d ever had was 6, the fewest was 3…; more follicles ≈ better IVF outcomes)
  • no ovarian cysts (I had a cyst visible on my last sonogram, and if it hadn’t resolved by now, we would have to delay IVF; small cyst + stims = really big cyst)

And [drumroll please…] I’m happy to announce that Dr. Y observed 7 follicles, and no cyst! We have been given the green light to proceed with our IVF protocol for this month.

My inner skeptic: To be fair, 7 is still a pretty terrible number for IVF and Dr. Y really really had to hunt to find the last one… Dr. Y also made a point of saying,

“There’s no guarantee that everyone on the guest list will show up to the party.”

Translation: Not all the follicles that we see today will be successfully harvested as mature eggs (and not all those eggs will successfully fertilize to embryos)…

My inner Pollyanna: It’s still the best AFC I’ve ever had and I’ll take it! My usually lazy right ovary doubled its production from last month (from 1 follicle to 2). Maybe it’s all the CoQ10 I’ve been taking. Maybe Dr. Y is being more liberal in his interpretation of what a ‘follicle’ is (Hell if I can see what he’s pointing to!) Maybe all your well-wishes/prayers/baby dust found their way through the ether to motivate my ovaries… Whatever it is, I’ll take it!

So now the plan is to continue my estrace and testosterone-priming for now, and start stims (injections and other goodies) at the end of next week. This also means that I no longer have an excuse to postpone forking over $1K for my non-Kaiser-covered drugs. You can expect upcoming posts on the chemistry of these new (to me) drugs, the biology behind my unconventional protocol (I’ve been doing some more research into this lately), and the finances of all this (I finally talked to the clinic financial administrator)…

 

But before I go, I’ve been thinking about this lovely post from Rain Before Rainbow. In it, redbluebird explains why she has chosen to keep her blog anonymous and not to share it with her IRL (in real life) friends and family.

By contrast, I’d say that this blog is semi-anonymous. I’ve avoided using any real names or photos of my face and have tried to be vague enough to minimize the temptation to find me out. But to be fair, anyone who knows me even a little bit who happens to come across this blog will easily figure out it’s me (my dogs and wedding photo are easy giveaways). Academics or chemistry-types who don’t already know me but who have even a slight detective bent could also find me using information on this blog. And if that weren’t enough, I’ve shared the blog with select friends and family members who want to follow along with our journey. (Judging by our IRL conversations, I’m pretty sure that only a small fraction of them actually read it.)

The downside of having some IRL acquaintances reading this blog is well articulated by redbluebird. For one thing, I can’t go into ‘angry infertile rant mode’, however much I might want to. (Not that I’d ever rant about anybody I’ve shared this blog with, but I’m afraid to rant about other people, lest someone I love even think that I might be ranting about them…) I also find myself watching my language (a bit) and being careful about TMI (a tiny bit).

But there are also clear advantages to sharing my blog with my IRL friends and family. The first is a major reason I started this blog – to avoid having to tell the same bad news, and explain the same sad lessons in reproductive biology over and over. In this regard, the blog has already served me quite well.

One unforeseen – and amazing – benefit is that a few especially empathetic IRL friends have used information from my blog to anticipate my moods and do exactly the right thing to make me feel awesome (or less awful, depending on the situation). Such was the case a few weeks ago, after a particularly demoralizing RE appointment. My friend A invited us over for dinner and had a bottle of good red wine waiting for me. 🙂

Or last night, when I arrived home from work to find a beautiful bouquet of flowers and a card from S & Q, wishing us Good Luck for our appointment this morning. I didn’t even know that they knew we had an appointment today!

ImageThank you S & Q for the amazing flowers! I hope at the end of all this we have some gorgeous hapa babies just like yours! And thank you to everyone (IRL and cyber friends alike) who are reading this and wishing us well. I firmly believe that it makes a difference!