Poor turnout

The ultrasound today did not go well. You may recall that when we saw 7 antral follicles at the baseline u/s, Dr. Y was careful to point out that

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

Well, at this point we’ve got two RSVPs – “Lefty,” the 14 mm lead follicle, and “Righty,” who is 11 mm. The other follicles are in there, but it seems they have other plans for Wednesday. So much for the virtues of estrogen- and androgen-priming…

Dr. Y said the chances of party crashers at this point is very very small. He said that he might be able to retrieve both big follicles…and that both might fertilize…and that both might grow into blasts.

He also said that there’s a good chance we could get nothing out in the end.

Our options, then, are to quit, convert to an IUI cycle (“so that at least you get something out of it”), or continue with IVF. It definitely seemed like Dr. Y thought the sensible thing would be to convert to an IUI. In that case, we would be refunded most of the $10K we paid last time, and could return the leftover meds for a restocking fee.

Ugh.

Since this was my first IVF appointment without C, I was trying to ask enough questions to be able to anticipate what C would want to know. Although I kept myself together, tears kept ‘leaking’ out of my eyes, and the poor nurse kept trying to pass me tissues.

I called C on my way out the door (he was on the way back from dropping friends at the airport) and we met a few minutes later at the beach. We sat on a bench and stared at the ocean and talked through the options. And we decided to move forward.

It’s probably stupid, but we thought we’d feel better knowing that we tried.

Will we feel ten thousand dollars better? I don’t know. But we both felt better knowing that we were moving ahead with the plan. We walked back to my car and I injected myself with my first dose of ganirelix. (No alcohol wipe or anything. Fuck it!) C also called Dr. Y and talked through our reasoning with him. He sounded good with it, once he was sufficiently convinced that we were informed and were comfortable with the cost.

So that’s where we are. The chances of success at this point are very slim. In the likely event that it doesn’t work out, we’ll probably pursue a second opinion and/or starting alternative therapy (acupuncture + supplements) to see if it helps with my responsiveness.

*****

I hope you’ll forgive me, but I’m feeling a bit deflated at the moment and not really in the mood to write a chemistry post about ganirelix. I may feel like it Monday, or maybe not.

Advertisements

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.

*****

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!

*****

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.

Image

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…)

Image

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!

*****

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

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!

My colorful protocol

Today, C and I went in for our IVF medications “teach class”. I’m not sure why they need to add the word ‘teach’ in there. Are there classes that don’t involve any teaching that they need to distinguish this one from? Are they distinguishing this class from a “learn class”? (Our legal counsel informs us that we can’t promise that you’ll learn anything, but by God, we’ll teach you!) Actually, maybe I can use this…I think I’m going to rename all my courses “teach classes” to spare myself any responsibility for my students actually learning anything…

Anywho, it turns out IVF is a hell of a lot more work than medicated IUI. (Once again, I can hear all the seasoned IFers in unison…No shit!) The list of medications that I have to take is long and expensive, and I can see why my insurance drew the line after IUI…

It also seems like my protocol is a little unusual, so I thought I’d share the details of it here:

First, my calendar for May:

Image

And my calendar for June:

calendar a

Here’s my limited understanding of what everything is for:

  • Zithromax – to ensure that C & I are infection-free prior to beginning the cycle
  • Estradiol – to help me recruit more eggs and to prevent any new cysts from forming (which would force me to delay the cycle)
  • Testosterone (gel & patch) – to try and recruit a few more eggs (In explaining this one Dr. Y was careful to say “in theory” several times, leading me to think that this claim has not been proven…)
  • Aspirin – to improve blood flow to my uterus
  • Menopur – to stimulate multiple follicles to grow
  • Clomid – to stimulate multiple follicles to grow
  • Dexamethasone – to help with implantation
  • Growth hormone – to help the eggs develop/mature fully (to achieve better egg quality)
  • Ganirelix – to prevent premature ovulation (We don’t want those eggs to drop; we want Dr. Y to suction them out with a needle instead…)
  • Follistim (FSH) – same general idea as (and one of the ingredients of) Menopur; I think this serves as a little boost to get the eggs ready to go for retrieval the next day
  • hCG – stimulates ovulation; I’m guessing this finishes getting the eggs ready to drop, but that we’ll time it so that I go in for retrieval before they actually drop
  • Doxycycline – antibiotic prophylactic to prevent infection from the retrieval
  • Prednisone – not sure what the purpose of this steroid is…maybe prevent inflammation?

Has anybody else used testosterone in their cycles? From the mysterious way that Dr. Y talked about it, I get the idea that it’s not part of the typical IVF protocol.

I think another unusual (weird?) thing is that I’m using pretty low doses of stims (especially considering the fact that I’ve got diminished ovarian reserve): 100 mg of Clomid and 150 IU of Menopur per day…that’s less than half the daily dose of Menopur that I used for IUI. Dr. Y says that they’ve found that success rates with the low stim protocol are comparable to those with high stim, but at much lower cost.

Lastly, you may have noticed that the calendar above doesn’t include an embryo transfer. Dr. Y insisted that an important feature of this protocol – and one that he recommends for old lady patients (and patients with old lady ovaries, like me) is that it does NOT involve a fresh embryo transfer following retrieval. Instead, the plan is to flash freeze (vitrify) my embryos and store them for a full cycle while my body purges itself of the colorful drug cocktail listed above. In particular, the Clomid is supposed to make for a somewhat hostile uterine environment. According to Dr. Y, for older women, postponing the transfer for a month actually gives higher pregnancy rates.

My read of the clinic stats seems to validate Dr. Y’s claim: In 2011, the % of FETs resulting in clinical pregnancy was 58.3% for 38-40 year-olds, compared to 56.3% for fresh transfers for the same age group – despite transferring more embryos on average for the fresh transfers (2.1 per transfer versus 1.8). For younger women, the fresh transfer is definitely better, so the only question is whether this 34-year-old with diminished ovarian reserve will behave more like the average infertile 38-40 year-old, or like the average infertile <37 year-old…

I guess we’ll see! Anyway, I trust Dr. Y and am perfectly happy to go with his professional judgment. (Of course, my trust for Dr. Y’s judgment didn’t prevent me from trying to mine the SART data to answer this question, but it turns out that my clinic didn’t treat enough <37 year-olds with DOR to give meaningful data…)

The punch line of this is that assuming my sonogram in two weeks looks good (crossing my fingers for lots of follicles and no more cyst!), I’ll be moving ahead with the egg retrieval in mid-June, and assuming we get any good embryos (fingers crossed yet again), I’ll take a uterus-cleansing drug holiday in July followed by a frozen embryo transfer in August!

Hypothetical of a hypothetical

So we’re moving along with Plan D – completing our IVF homework. Here’s what I’ve accomplished in the last week:

  1. Repeated my day 3 bloodwork. This revealed virtually the same bad numbers as before. Actually, to be fair, they were a smidge better…but probably not statistically significant; FSH went from 13.7 to 13.5, E2 went from 24.6 to 27.2; AMH went from 0.17 to 0.22. More importantly, they didn’t get worse in the past 4 months, which I’ll take as good news. (Funny story about the blood draw: after so many IF-related blood draws, I decided that I was now a needle badass and would therefore watch as the phlebotomist drew my blood…naturally, that was the first time ever that someone missed the vein and had to stick me a second time! I did NOT watch the second stick. So much for being a badass.)
  2. Took blood pregnancy test. No surprises here. This test was a liability necessity before they’d do #4.
  3. Start Zithromax with C. Apparently they want to make sure neither of us has any infections prior to IVF (not sure why this isn’t required for IUI…) I’ll write about the chemistry of Zithromax below…
  4. Saline sonogram & mock transfer. Dr. Y filled my uterus with saltwater and observed it by ultrasound to make sure there were no obstructions that might pose a problem for an embryo. (Kind of like the HSG, except with saltwater in place of the dye and ultrasound instead of x-rays.) He also practiced inserting a catheter to get the ‘lay of the land’ for the real transfer. The whole thing was very anticlimactic. The most uncomfortable part was that I had to do it with a full bladder. (I have a very small bladder and practically live in the bathroom…) I would have asked C to take a picture of this, but it didn’t really look like anything. My HSG photo was much cooler.
  5. Sign & initial 9-page informed consent document. The first 6 1/2 pages of the thing discussed various aspects of the medical interventions involved. Yes, I understand that there may be side-effects of drugs, complications of surgery, that I may have multiples, and that the whole procedure may fail miserably…The unsettling part was the other 2 1/2 pages, which consisted of depressing hypothetical scenarios and our decisions about what we would want to do with our hypothetical embryos. For example, what should happen to our hypothetical embryos…
  • if we fail to pay our embryo storage bill?
  • if one of us dies?
  • if both of us dies?
  • if we are legally separated or get a divorce?
  • after I exceed my “normal reproductive life”? (defined as age 50; phew!)

C was no help at all, and I struggled with how seriously to take the whole thing. On the one hand, I was making a decision about what would happen to our precious embryos – C’s and my potential children (and the only that I might ever have). On the other hand, we were planning for a doomsday hypothetical of a hypothetical. Given my antral follicle count, we’ll be lucky to get one or two ‘good’ embryos to transfer. What are the chances that we’ll have ‘extras’ to store and worry about in the event of further hypothetical catastrophes? In the end, I tried my best to take the questions seriously…If we stop paying our bill or don’t use the hypothetical embryos by the time I’m 50, we’ll donate them to research; if one of us dies or we get divorced, they’ll be made available to the partner who wants them (probably only pertains to me, since if I die or we get divorced, C can make cheaper babies with his new wife!), and if we both die, they can be donated to another couple. Gosh I hope this post is the last time I have to think about such bummer scenarios!

 Still on our ‘To Do before IVF’ list:

  1. Submit C’s semen culture (after we finish the Zithromax course) to confirm no infection.
  2. Attend a ‘teach class’ with the nurse to learn how to do our new injections.
  3. Call the finance lady at the IVF clinic to work out arrangements for payment.
  4. Start taking estrogen (estrace) and testosterone gel.
  5. Do a blood draw (including a progesterone test, and others?) to confirm that my hormones are ‘turned off’ before officially beginning our cycle.

And finally, here’s your IF chemistry lesson for the day:

Image

Azithromycin (aka Zithromax) is a macrolide antibiotic. That just means that it contains a large (15-member, in the case of azithromycin) lactone ring (shown in blue). Actually, a lactone is defined as a cyclic ester, so “lactone ring” is redundant…kind of like “ATM machine”. Anyway, azithromycin is a synthetic analog of the natural product 🙂 erythromycin, produced by the soil bacterium Saccharopolyspora erythraea. Like erythromycin and other macrolide antibiotics, azithromycin has a sugar part (technically, two sugar parts, shown in green) that dangle off of the lactone ring.

Plan D

I made a mistake in my post about progesterone… Despite the suppositories, AF showed up a few hours after my last post. So yesterday morning I snuck out during my students’ final to call the clinic right when they opened.

C and I had decided our plan was to do a baseline ultrasound on cycle day 2 or 3, and see how many antral follicles were visible – if it was 3 or fewer, we would do medicated IUI again; if there were more, we would try for IVF. But when the advice nurse called me back, she said that Dr. Y wanted me to come in on Tuesday – too late for medicated IUI.

When I explained our ‘plan’, she said that upon further reflection, Dr. Y really felt that IVF was our best option and we should just go ahead with that. At this unexpected disruption in the plan – and to my complete surprise – I burst into tears on the phone. (I should probably mention that I have never been a very emotional person. For our first year together, C teasingly referred to me as ‘The Robot’. But infertility is doing its damnedest to change that.) Anyway, the nurse ultimately relented and said they could squeeze me in at 4:30.

The ultrasound showed 6 follicles (lame by most standards, but tied for my best count). It also showed a small cyst (Dr. Y said that wasn’t surprising after coming off a medicated IUI cycle), which means we couldn’t do medicated IUI this cycle anyway. We all agreed to move ahead with IVF, assuming the cyst goes away before next month. (We need a month to do our IVF ‘homework’ anyway.)

Once again, it feels good to have a plan, and to feel like we are moving forward (to what, I don’t know, but I’ll settle for movement toward anything at this point). I would title this post ‘Plan B’, except IVF was certainly not our plan B. By my count, we are on Plan D. Here’s a summary of our plan/backup plan/backup to the backup plan, etc:

Plan A: Pull the goalie and get pregnant “the old fashioned way.”

Plan B: Timed intercourse, using charting (phase 1), charting + OPKs (phase 2), and charting + OPKs + Clearblue Easy Fertility Monitor (phase 3)

Plan C: Medicated IUI with Menopur

Plan D: IVF with my (scarce, presumably crap) eggs

Plan E: IVF with donor eggs

Plan F: Adoption

Plan G: Wait for Guy on a Buffalo to drop off a prairie orphan. (If you don’t know what I’m talking about, click below.)

Plan H: No idea. Suggestions?

Rookie mistake

I made a rookie mistake this week. Since I was feeling so optimistic about this cycle, I decided to test early – at 8 dpo (that’s 8 days past ovulation, for the non IFers). I saw the faintest second line, and woke C. to tell him that we were pregnant. I tried not to get TOO excited (after all, C. and I know all too well that a BFP is a far cry from a live baby…), but in my head, I had calculated the due date, lamented the end of my blog (okay, not much of a lament, but I thought about it nonetheless), and imagined how quickly all this ‘infertility stuff’ would be a distant memory. Not wanting to burst my bubble, C. gently asked “What’s the chance that it could still be due to the trigger shot?” to which I replied, “It’s been 10 days. There is no way that protein could still be detectable in my pee after 10 days!!!) I fantasized about our rainbow baby all the way to work, and then decided to Google it. And guess what?

hCG can totally remain at detectable levels…for up to 14 days following a trigger shot!

Ugh. I’m sure all the seasoned IFers out there are like “Duh!”

So what did I do? I tested again at 9dpo, 10dpo, and 11dpo. And the second line was like faint, fainter, gone. 😦

So today C. and I went to meet with Dr. Y. to plan our our next step. (One ‘perk’ from the accident: C. is available to go with me to all my appointments!) I found this meeting super depressing, which is to say, it was exactly like every other meeting at that office… “Yadda yadda yadda, diminished ovarian reserve, yadda yadda, born with all the eggs you’ll ever have, yadda, let’s do another day 3 blood test and antral follicle count, yadda yadda, we can try IVF but you’ll be lucky to get 5 eggs out, yadda yadda yadda…” You get the idea.

Rather than rehash the rest of the conversation, or the tear-filled ride home, I’d prefer to learn and then write about the biochemistry behind how home pregnancy tests work.

Here’s a nifty image I found online. I’ll attempt to caption it in my own words.

Image

(A) So the purple blobs are hCG, which is present in the urine of pregnant women (and of wannabe pregnant women who had a trigger shot 10 days ago…)

Capillary action carries hCG along the stick (or down in this particular figure; nevermind that HPT instructions definitely do not say to hold the test with pee end up like that…) Anyway, capillary action carries hCG toward where the action is.

(B) The reddish things that look kind of like lobsters holding a blue balloon are the anti-α-hCG antibodies which were pre-deposited on the stick (between the pee end and the viewing end). The antibodies have a pigment attached (in the case of the test I used – FRER – the pigment is pink, not blue). They will grab the hCG (specifically the alpha subunit of hCG – for more about the structure of hCG, see this post) and hold on tight…and be pink.

Now, capillary action will carry the bound-to-hCG anti-α-hCG antibodies, and the free anti-α-hCG antibodies (there are extras that don’t get any hCG) along the stick.

(C) At the ‘test line’, there is a line of anti-β-hCG antibodies (blue lobsters in the figure, although they are actually colorless) that are fixed to the stick. These antibodies also grab onto hCG (specifically, the beta-subunit) and hold tight…and don’t go anywhere. Everybody holds on tight, and the resulting group of anti-β-hCG—hCG—anti-α-hCG sandwiches appear as a pink line on the stick.

Meanwhile, the free anti-α-hCG antibodies (that is, the ones that didn’t get any hCG) continue to be carried by capillary action along the stick.

(D) Finally, the free anti-α-hCG antibodies reach the ‘control’ line, where there is a line of antibodies that specifically bind to the anti-α-hCG antibodies (no hCG needed). These antibodies are the green turtle-heads in the figure, and are themselves fixed to the stick. The resulting antibody—anti-α-hCG complex appears as the pink control line.

I go in for a blood pregnancy test (which works a bit differently; but I’m too lazy to figure out how right now…) on Saturday, but with a negative HPT at 11dpo, I’m decidedly not optimistic about it. I’m also not optimistic about moving forward with IVF, but I’m sure that will pass. In the mean time, I think I’ll console myself with a glass of wine tonight.

Turkey baster day!

Today, C. and I went in to the clinic to get this turkey basted (that is, for intrauterine insemination or IUI). Here’s what was involved:

  1. C. prepared his sample right before we left for the clinic, then kept it warm in his pocket during our drive. (It takes a half hour for it to ‘liquefy’ prior to washing.)
  2. We arrived at the clinic and waited. This part was long enough to stress us out a bit, since the specimen is supposed to be processed within an hour.
  3. Once in the back, we handed over the sample to the nurse and signed a form stating that it was indeed from C.
  4. We waited again, this time for the doctor (Dr. H.) to ‘wash’ the sperm. More about that in a minute…
  5. Dr. H. came in, and confirmed again that the sample was indeed from C. (After being asked again, we started to actually worry! What if our sample got mixed up with one of the people in the waiting room?…) She complemented C. on his excellent sample. (She counted 78 million sperm per milliliter upon arrival, and 30 million ‘good swimmers’ that made it through the washing procedure and to the final sample. This raised our confidence that they were actually C.’s! 😉 ) Then she explained what was going to happen.
  6. The next part started like a pap smear: me in stirrups, mildly uncomfortable; doctor inserted speculum then swabbed my cervix with a big Q-tip… Then out came the turkey baster! (Actually it looked more like a syringe with a little tube…)
  7. After the basting was done, Dr. H. tilted the bed back and left me there for ~30 minutes to let gravity help the little guys along.
  8. She reiterated the advice to BD tomorrow, just to be sure. And that was it!

The whole thing really wasn’t bad! No cramping at all. (Dr. H. told me I have a ‘quiet uterus’. I guess that makes sense; they’ve had two geriatric ovaries for neighbors this whole time…)

The sperm washing part was interesting to me, since it involves organic chemistry. 🙂 So, why wash sperm?

Aside from the high quality ‘Michael Phelps’ sperm cells, semen also contains slower-moving or dysfunctional sperm, prostaglandins, and bacteria (ew!) The cervix normally acts as a natural ‘qualifying round’ to keep out everybody except those super-swimmers. Since IUI bypasses the cervix, another gatekeeper is needed – hence the sperm ‘washing’.

Here’s the chemical structure of the two major prostaglandins in semen. Prostaglandins are made from fatty acids (hence the long chains on the right side), and always have a five-membered ring.

Image

Prostaglandins stimulate muscle contractions, which might be good when you’re trying to help sperm get into the uterus (or if you’re 42 weeks pregnant and trying to induce labor – not exactly something I’ve had to worry about…), but if inserted directly into the uterus, the prostaglandins can cause severe cramping, vomiting, fever, and diarrhea. Not so nice.

The next step for me is a progesterone blood test on Wednesday, followed by progesterone suppositories to support a pregnancy (in case there is one!)

Ever the pessimists, we also scheduled an IVF consultation with Dr. Y. so that we have a clear idea of our options if this doesn’t work. Hopefully we won’t need it!

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 (http://www.fertilityplus.com/faq/iui.html), 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!

Image

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!