11 weeks, NIPT, and Outlander spoilers

Sorry it’s been awhile since I’ve checked in. Last week was finals week, and the weeks leading up to it were a bit hectic, as usual.

A week ago, we hit the 10 week mark, which meant I could do a phone consult with the genetic counselor and have my blood drawn for the Non-Invasive Pregnancy Test (NIPT, which I’ve written about on this blog before, here).

I scheduled my appointment for the earliest slot they would let me, on Monday afternoon, and drove to the hospital for my blood draw the same day. As we have in each pregnancy, we checked the box to learn the gender of the baby at the same time. Then, we anxiously awaited the results. (The genetic counselor had said it would be “about a week”, but since I knew I had made it in time for Monday’s FedEx pickup, I was hopeful for a result on Thursday or Friday.) More so than with our previous pregnancies, I worried that this baby might have a chromosomal abnormality, both because of my age (my baseline risk now – at age 38 – is 1 in 50), and because after losing Jane, we no longer feel immune to even improbable adversity…

Thankfully, I had a full week of to distract me from thinking too much about it, with a speaking gig at a chemistry symposium at a nearby university Tuesday, and tickets to Hamilton (!) in San Francisco on Wednesday night. C had accrued enough points on his Ritz Carlton business card for an overnight stay, so we spent Wednesday night in style in the city before returning to reality. While away, I checked my email every 10 minutes for the message from Kaiser, which I finally got on Friday morning in the airport bathroom…

The subject line was “Good News!”, which came as no small relief. I waited until I was sitting with C to open the email and learn the gender of our little peanut.

If you had asked us before Friday what our preference was, we would have told you we preferred a girl – not as a replacement for Jane, but maybe as another chance at the imagined future we felt that we had lost with her: mother-daughter mani-pedis and father-daughter dances, a trip to England to visit Jane Austen’s house, C walking her down the aisle… On the practical side, a baby girl would also be able to make use of all the never-worn, adorable pink outfits and dresses still hanging in Jane’s closet.

The letter showed that we have a chromosomally-normal boy! And we are honestly so excited. We love the idea of a brother for C. Samuel (I actually had wished that Jane was a boy before I knew!), and I feel very comfortable cementing my identity as a “boy mom”, which seems easier in many ways. And while we aren’t totally ruling out the possibility of a third child, I have to admit that there is something romantic about the idea that Jane was our girl, and that we won’t have another.

***

In other news, in between late nights grading, I’ve been making my way through the Outlander series on Starz. It’s my guilty pleasure on nights when C isn’t home or goes to bed early. I really like the main characters (especially Sam Heoghan’s Jamie Fraser, sigh!) and the sets and costumes. The story isn’t as compelling or the dialog as clever as, say, Game of Thrones, but I enjoy it enough to have purchased the first two seasons on Amazon. That said, if you are easily disturbed by violence, you’d probably want to take a hard pass. Continuing with the GoT comparison, Outlander is not nearly as skull-crushingly gory as GoT…but I found several violent scenes to be at least as emotionally disturbing as anything I’ve seen on GoT.

heughan

I just had to add a photo of Heoghan (source and more photos)

At this point, I should give a SPOILER ALERT. If you think you might want to watch Outlander, or you are watching and haven’t yet made it into Season 2, Episode 7, then for heaven’s sake, don’t read further!

***

So, for those of you still here, the reason I bring up Outlander is that a) I just watched S2 E7 Friday night, and b) stillbirth figured prominently in the episode. It’s actually not the first time I’ve seen a stillbirth on TV since losing Jane. The first was in the series premier of This is Us. (I don’t even feel bad about spoiling that one, since it’s like halfway through the SERIES PREMIER and is not even the big surprise of the episode!)

I felt both portrayals were well done, and yet, neither initially felt like our experience.

In This is Us, the expecting couple goes in to deliver their babies (like us), who are triplets (not like us), and then have complications during delivery that result in the loss of one of the babies. We never see the baby that was stillborn, nor do we see the mother’s initial reaction to the news until a later episode. What we do see is a touching conversation between the obstetrician who delivered the babies and the young father. We see the father’s initial confusion and denial, and learn that the obstetrician had a stillborn child that motivated him into choosing to pursue obstetrics. The moment felt very real; the message, about making lemonade out of “the sourest lemon life can give you”, while undoubtedly hokey, feels honest and welcome, especially coming from someone who has been there.

In Outlander, the expecting mother is subjected to an intense situation that spurs early labor (not like us), then she is semi-unconscious, confused during delivery (not like us), and only learns that her child is stillborn after the delivery is over (not like us). The whole sequence took place in the first few minutes of the episode, and left me feeling very little. I felt guilty for eating chips and salsa through what I felt should have been a very emotional scene for me, but I didn’t feel much empathy for the character (who I really like and am generally very invested in). Another variable that undoubtedly affected my experience was the inclusion of a flash-forward at the start of the episode, that shows the same character with her future child. So we know from the beginning that she will eventually go on to have another child.

Then, as she is retelling the story to her husband (who wasn’t present for the birth), we see in a flashback that she in fact did get to see and hold her baby…

And there it was – the ‘real’ moment that got me. I cried as she lovingly and carefully examined her baby daughter’s hands and feet, remarking on the color and texture of her hair. I cried as she cradled her, and sang to her. And I cried especially hard when, after holding her daughter for hours, she reluctantly handed her over to be prepared for burial. It was heartbreaking, and beautiful, and exactly how I remember feeling.

Is there a sudden spate of authentic stillbirth story lines in television these days, or were they always there and I just wasn’t paying attention? Either way, I’m grateful to see elements of our experience portrayed for a wide audience. In both cases, the friends and loved ones of the grieving parents responded so well – never minimizing the loss (even in This is Us, when the couple had two healthy babies to take home); in the case of Outlander, they gave the baby a name, commented on how beautiful she was, and asked to hold her – like our loved ones did for Jane. ❤

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Well, fuck!

That’s what I said when I read my most recent email from Dr. Y’s nurse:

“YOU DAY 3 LAB WORK CAME BACK AND THE RESULTS SHOW AND ELEVATED FSH AND THE AMH IS LESS THATN 0.03. IT WOULD BE BEST IF YOU CAME IN AND HAD AN APPOINTMENT WITH DR Y. I WILL NOT HAVE ANY APPOINTMENTS UNTIL AFTER YOU RETURN FROM EUROPE. PLEASE CALL ME AT xxx-xxx–xxxx SO THAT WE CAN SCHEDULE AN APPOINTMENT”

Yes, she writes her emails all in caps like that, as if I needed any more reason to feel alarmed.

My AMH is less than 0.03. I didn’t know the test measured amounts that low.

In what feels like another lifetime, I once wrote a long post about what AMH (and FSH and estradiol) mean for fertility.

Here’s a summary of my results the four times I’ve taken these tests. Prior to yesterday, 0.17 ng/mL was the lowest AMH of anyone I know in real life (including my Resolve support group).

  1/26/13 5/4/13 4/24/15 10/8/16
estradiol (E2) 24.6 pg/mL 27.2 pg/mL 23 pg/mL 20 pg/mL
follicle stimulating hormone (FSH) 13.7 mIU/mL 13.5 mIU/mL 9.7 mIU/mL 17.7 mIU/mL
anti-Mullerian hormone (AMH) 0.17 ng/mL 0.22 ng/mL 0.31 ng/mL <0.03 ng/mL

 

I’m feeling pretty hopeless at the moment.

At least I get to go to Rome on Sunday.

When to try again

And now we arrive at the last of our unpleasant decisions following Jane’s passing:

Decision 10: When to try again.

By way of background for those of you who are new to my blog: three years ago, after an early miscarriage followed by 6 months of unsuccessful trying on our own, I was diagnosed with diminished ovarian reserve. I’m a non-responder to stims, having produced only a single egg during medicated IUI, and IVF cycles. Miraculously, we conceived our first rainbow baby C. Samuel spontaneously in between IVF cycles. After C. Samuel was born, we decided to try for #2 via natural cycle IUI. On the sixth month of this, we conceived Jane Margaret.

Some conclusions from our adventures in infertility:

  • I have precious few good eggs left. (One of my doctors predicted that I would go through menopause before age 40…I’ll be 38 next month.)
  • I consistently ovulate one (and only one) egg per month, with or without stims.
  • When we’ve been lucky enough to have one of C’s supersperm catch a good egg, the babies that result are beautiful and perfect (though I can’t say the same for the resulting placentas).  😦

Contrast that with the following advice re: trying again after stillbirth:

  • The American Pregnancy Association recommends waiting several months up to a year to try again after a stillbirth.
  • Dr. R recommended waiting 3-6 months before trying again.
  • Dr. R mentioned a study suggesting that shorter time between pregnancies may be correlated with shorter umbilical cords (part of Jane’s perfect storm), though she acknowledged that the study wasn’t especially compelling.

Having discussed all of these considerations and more, C and I quickly agreed on a decision:

We want to try again as soon as possible! 

We both find the egg scarcity argument more compelling than the emotional self-care concerns. What if I ovulate my last good egg on one of the months that we’re “waiting to try”?!

As it happens, my own body forced a bit of a compromise, since it took 11 weeks for my period to come back after Jane’s passing. My bitchy Aunt Flo showed up on Friday, and on Saturday I got my blood drawn to repeat my CD3 (in this case CD2) bloodwork. Unlike last time, my FSH went in the wrong direction (up to 17.7 mIU/mL). :/

.

At least C. Samuel is optimistic. He busted this song out during a recent visit to Ong Ba’s (Grandma & Grandpa’s) house. Neither C nor I had ever heard it before.

 

The Rainbow Song lyrics:

Red orange yellow green blue purple,

red orange yellow green blue purple,

red orange yellow green blue purple,

makes the rainbow bright bright bright!

.

[Deep breath] Here we go again.

Can we possibly have enough luck left over for another miracle?

Tests

After learning of Jane’s passing, I was subjected to a large number of blood and urine tests, and my placenta was sent to be examined by a pathologist. Most of the samples were collected in the hospital (while I was still in labor with Jane, or shortly after). A few more blood tests were added roughly a month later, after I shared some information about my family history (re: blood clots) with Dr. R.

I’m not a physician and haven’t spent a lot of time looking into these tests and what they mean. But on this 2 month anniversary of Jane’s birth and death, I’m parking them here for posterity, and also as an easy way to share them with my physician friends (or anyone else who cares to take a look). I’ll wait to summarize the key takeaways as they pertain to Jane’s death and to any future pregnancies in a future post about our follow-up appointment with Dr. R.

Without further ado, here are all my test results. Results outside the normal range are highlighted in orange. (UPDATE: It looks like the tabulated data doesn’t display on smartphones; I recommend viewing on a computer if you want to see my numbers and/or the standard ranges for each of these tests…)

 

Complete Blood Count

This is a routine test “used to evaluate…overall health and detect a wide range of disorders, including anemia, infection and leukemia” Source

23-Jul 19-Aug Standard Range
HCT 40.6 40.9 37.0-47.0 %
HGB 14.3 13.8 12.0-16.0 g/dL
MCH 32.5 31.6 27.0-35.0 pg/cell
MCHC 35.1 33.7 32.0-37.0 g/dL
MCV 92.4 93.7 81.0-99.0 fL
Platelets, Automated Count 167 188 130-400 x1000/mcL
RBC, Auto 4.39 4.36 4.20-5.40 Mill/mcL
RDW, Blood 13.2 12.4 11.5-14.5 %
WBC’s Auto 14.8 6 4.0-11.0  x1000/mcL

 

Clotting-related tests

One of the risk factors for fetal demise is maternal blood clotting, either due to an inherited thrombophilia, or an autoimmune disease that can lead to a “hypercoagulable state” like Lupus or antiphospholipid syndrome. From what I can gather, the following tests are all related to my tendency to form blood clots.

  • Activated partial thromboplastin time “(aPTT or APTT) is a medical test [used for] detecting abnormalities in blood clotting” Source
  • Fibrinogen is a “glycoprotein in vertebrates that helps in the formation of blood clots…[It is typically] elevated in pregnancy…Low levels of fibrinogen can indicate a systemic activation of the clotting system.” Source
  • Lupus, antiphospholipid syndrome, the prothrombin G20210A gene mutation, and factor V Leiden thrombophilia are all conditions that might predispose me to clotting problems.
  • Cardiolipin antibodies and beta-2 glycoprotein antibodies are commonly tested along with the Lupus anticoagulant screen. According to my Kaiser lab results, “Clinical associations [for cardiolipin antibodies test] include SLE (25-50%), Arterial or Venous Thrombosis, Recurrent Fetal Loss, Thrombocytopenia, Valvular Heart Disease.”
  • Homocysteine is an amino acid. “Abnormally high levels of homocysteine in the serum, above 15 µmol/L, are a medical condition called hyperhomocysteinemia. This has been claimed to be a significant risk factor for the development of a wide range of diseases, including thrombosis” Source
  • Protein C “plays an important role in regulating anticoagulation, inflammation, cell death, and maintaining the permeability of blood vessel walls in humans and other animals.” Source
  • Protein S has a “role in the anti coagulation pathway, where it functions as a cofactor to Protein C in the inactivation of Factors Va and VIIIa.” Source
  • Antithrombin III is a “small protein molecule that inactivates several enzymes of the coagulation system” Source
23-July 19-Aug Standard Range Notes
activated partial thromboplastin time (APTT) 26 25-37 sec
fibrinogen 554 218-441 mg/dL
thrombophilia, 20210G-A, F2 mutation analysis negative negative
APTT 35 23-38 sec All part of the Lupus anticoagulant screen
dilute Russell viper venom induced 36 29-43 sec
Lupus anticoagulant negative negative
cardiolipin IGG, EIA 2.5 <=14.9 GPL units
cardiolipin IGM, EIA 7.4 <=12.4 MPL units
beta 2 glycoprotein 1 IGG 1 <=20 SGU
beta 2 glycoprotein 1 IGM 4 <=20 SMU
beta 2 glycoprotein 1 IGA 3 <=20 SAU
thrombophilia, 20210G-A, F2 mutation analysis negative negative
factor V Leiden thrombophilia negative negative
homocysteine, subst conc, SERP 6 5-15 mcmol/L
activated protein C resistance ratio 1.9 >= 1.9 Factor V Leiden expected to cause APC resistance ratio below 1.9
protein-C activity (actual/normal) 116 95-172 % Factor VIII levels greater than 250% may lead to under-estimation of protein C level
protein-S – functional, plasma, QN 106 50-118 % Factor VIII levels greater than 250% may lower protein S measurements.
antithrombin III activity 109 80-120 %

 

Liver-related tests

I’m guessing liver function is of interest for detecting intrahepatic cholestasis of pregnancy, preeclampsia, HELLP syndrome, or acute fatty liver of pregnancy? Or maybe hepatitis?

  • Alanine transaminase (ALT) and aspartate transaminase (AST) are liver enzymes. “Serum AST level, serum ALT (alanine transaminase) level, and their ratio (AST/ALT ratio) are commonly measured clinically as biomarkers for liver health.” Source
  • Bile acids (including cholic acid, deoxycholic acid, and chenodeoxycholic acid) are “steroid acids found predominantly in the bile of mammals and other vertebrates…synthesized in the liver…[and] aid in the diagnosis of a number of conditions, including … intrahepatic cholestasis of pregnancy.” Source
  23-July Standard Range
ALT 8 <=54 U/L
AST 29 <=30 U/L
cholic acid: 3.7 <= 1.8 umol/L
deoxycholic acid: 1.5 <= 2.4 umol/L
chenodeoxycholic acid: <0.5 <= 3.1 umol/L
total bile acids: 5.2 <= 6.8 umol/L

 

Kidney-related tests

Poorly controlled diabetes is another maternal cause of fetal demise. The following tests evaluated my kidney function and blood glucose levels.

  • Creatinine is “an easily measured byproduct of muscle metabolism that is excreted unchanged by the kidneys”, so creatinine levels in blood rise if kidneys aren’t doing a good job of removing it. Glomerular Filtration Rate (GFR) is the “volume of fluid filtered from the renal (kidney) glomerular capillaries into the Bowman’s capsule per unit time.” Both are measures of renal function.
  • Blood glucose is the level of sugar in my blood. An abnormally high value might be indicative of diabetes.
  • Hemoglobin A1C (HGBA1C) screening measures hemoglobin (the oxygen-carrying protein in blood) that has been modified with a glucose molecule. In the presence of continually high blood glucose levels, HGBA1C builds up slowly over time, so its value gives you an idea of how well blood glucose has been controlled over the past three-months.
  23-July Standard Range Notes
Creatinine 0.46 <=1.10 mg/dL
Glomerular Filtration Rate >89 >89 mL/min/BSA
Glucose, Random 91 70-140 mg/dL
HGBA1C% 4.9 4.8-5.6% >6.5% is diagnostic of diabetes. 5.7-6.4% indicates increased risk for future diabetes

 

Tests for infections

  • Syphilis is a sexually-transmitted bacterial infection. Untreated in the mother, it can pass to a fetus and cause a variety of horrible outcomes including stillbirth. Source
  • Parvovirus B19 (aka fifth disease) is a mild viral disease that may, in rare cases, cause anemia and/or miscarriage. (Interestingly, I found the same said of Coxsackie virus, for example here, which I did get while pregnant with Jane… I’ll have to ask Dr. R about it…)
  • Cytomegalovirus is a virus in the herpes family that typically causes no or mild symptoms. It’s not clear to me whether a causal relationship has been established, but at least a few articles seem to point to a correlation with stillbirth (for example, see this source).
  • Toxoplasmosis is a parasitic infection caused by Toxoplasma gondii, commonly transmitted by eating undercooked foods (like rare steak), or coming in contact with cat poop (for example, when changing the litter box, or gardening). Toxoplasmosis usually causes mild or no symptoms in non-immunocompromised adults, but when it passes from a pregnant mom to a fetus, it can cause a variety of terrible outcomes, including stillbirth. Source

The latter three tests include tests for two different types of antibodies: IgG and IgM. The IgG antibodies are the long-term antibodies that are present if I have ever been infected with the pathogen; these antibodies confer immunity to future infections by the same pathogen. The IgM antibodies are part of the short-term response to an active or recent infection. Their presence in my blood at the time of Jane’s death would indicate an infection that happened during my pregnancy (i.e. one that could have impacted Jane). For more, see this.

As you can see below, it appears I have been infected by parvovirus B19 and cytomegalovirus at some point, but not a recent infection that might explain what happened to Jane. This is somewhat good news, since it means I am now immune to getting these infections in a future pregnancy. Unfortunately, I have not been infected by Toxoplasmosis… which means I’ll be stuck eating my steaks well done in any future pregnancy…

  23-July Standard Range Notes
Treponema pallidum AB, EIA (Syphilis screen) nonreactive nonreactive
Parvovirus B19 Ab IgG: 4.9 <0.9 IgG persists for years and provides life-long immunity
Parvovirus B19 Ab IgM: 0.2 <0.9 probably no current or recent infection
Cytomegalovirus IGG, SER, QN 5.4 <= 0.8 AI IgG antibody to CMV detected which may indicate exposure to CMV infection
Cytomegalovirus IGM, EIA < 8.0 <=29.9 AU/mL A positive test may indicate a current or recent infection.
Toxoplasma gondii IGG, SER, QN < 3 <9 IU/mL
Toxoplasma gondii IGM 0.06 <= 0.549 RFV No serologic evidence of infection with Toxoplasma gondii

 

Immune-related/antibody tests

  • Rhesus disease (in which the mother’s immune system attacks her baby’s red blood cells) is also on this list of possible causes for stillbirth.
  • The Coombs test for autoimmune hemolytic anemia is looking at whether my immune system is attacking my own red blood cells (I think).
ABO and RH blood type A Pos
Crossmatch Result Compatible
Indirect Coombs test: Blood Group Antibody Screen neg

 

Other blood tests:

Fetomaternal hemorrhage screen, aka  Kleihauer–Betke test, is “a blood test used to measure the amount of foetal hemoglobin transferred from a foetus to its mother’s bloodstream.” “Causes of increased foetal-maternal haemorrhage are seen as a result of trauma, placental abruption or may be spontaneous with no cause found…Foetal-maternal haemorrhage is one cause of intrauterine death (IUD).” (emphasis mine) Source

23-July Notes
Adult RBC, Blood 2000 Conducted by counting 2000 red blood cells in my blood
Fetal RBC, Blood 0 None of those cells were determined to be from Jane
Fetal/Adult RBC Ratio, Blood 0
Fetal-Maternal Hemorrhage Volume 0 mL

 

Thyroid stimulating hormone (TSH) is a protein hormone measured to test for hypothyroidism (or hyperthyroidism, but I can’t find anything in a quick Google search about that relating to pregnancy outcomes…) From what I can tell, thyroid disorders may be correlated with fetal demise and/or low birth weight. Source

  23-July Standard Range
TSH 1.8 0.35-4.00 mcIU/mL

 

Drug tests

Smoking and illicit drug use are associated with an increased risk of stillbirth. Source

I should point out that Dr. R gave me two doses of IV morphine while I was waiting for my blood test (and approval for my epidural). So it didn’t come as a surprise to anyone when I came back positive for opiates generally, or morphine specifically. The tests included two sets of screening tests (in which they homed in on morphine), followed by a confirmatory test using gas chromatography-mass spectrometry (GCMS).

Drug screen (AMP, METH, BAR, BZD, COC, OPI, PCP, THC, TCA), Urine, Using test w visual read

23-July Standard Range
THC, Urine negative negative
Phenylcyclidine, Urine screen negative negative
Cocaine, UR, QL, Screening test negative negative
Methamphetamine, UR, QL, Screening test negative negative
Opiates, Urine, QL Preliminary positive. Pending confirmation. negative
Amphetamine, UR, QL, Screening test negative negative
Benzodiazepines, Urine Screen negative negative
Tricyclic antidepresseants, Urine screen negative negative
Barbiturates, UR, QL, Screening test negative negative

 

Opioid Screen, Pain MGMT (BUP, FEN, 6MAM, MTD, OPI, OXYCOD, HDC, TRA), Urine, Automated Analyzer w EIA

  23-July Standard Range
Buprenorphine, UR, QL negative negative
Fentanyl, UR, QL negative negative
Hydrocodone, UR, QL neg neg
Heroin metabolite (6-MAM), UR, QL negative negative
Methadone, Urine screen negative negative
Opiates, Urine, QL POSITIVE negative
Oxycodone, UR, QL, Screening test negative negative
Tramadol, UR, QL, Screening test negative negative
pH, Urine 5.4 5.0-8.0
Specific gravity, Urine 1.01 1.002-1.030
Creatinine, Urine 35.5 >=20.0 mg/dL
Specimen validity, Urine normal

 

Opiates, Urine, Confirmatory GC/MS

Opiates, UR, Confirm morphine detected

 

Surgical pathology

I found the placental pathology report to be the most interesting item in the pages from my medical record that Dr. R shared with me…

FINAL PATHOGENIC DIAGNOSIS

Placental, vaginal delivery

  • Term placenta (40 weeks 6 days), size extremely small (~450 g expected, 225 g actual)
  • Thrombi of mainstem fetal vessels, organizing and old
  • Normal villous features (no increased immaturity, villitis or infarction)
  • Rare hemosiderin deposits within chorion, likely clinically insignificant
  • No evidence of decidual vasculopathy for chorioamnionitis
  • Short trivascular umbilical cord (>50 cm expected, 30 cm actual)

COMMENT

Although the placental weight can vary with maternal constitutional size, 225 grams is truly small and may, or may not have resulted in utero placental insufficiency. The more common causes of vascular thrombi are infection, cord compression and coagulopathy. In view of the short umbilical cord (if 30 cm is the true length), it is possible that there was compromised [sic] due the cord with the onset of labor.

[The report goes on to describe the appearance of the placenta, etc.]

Halfway there

It’s funny, when you can’t get pregnant, it feels like all you do is wait – for test results, your period to come, the next treatment cycle, or the dreaded two week wait. Time crawls by, marked by morbid milestones like big birthdays (Hello, Advanced Maternal Age), would-be due dates, number of years spent trying to have a baby, and so on…

But ever since I’ve made it past the nail-biter of a first trimester, time has flown by. Suddenly I’m halfway through the pregnancy wondering where the last two months went!

After the third email from a bloggy friend checking whether everything is alright, I have no choice but to admit that it has been far too long since I’ve written. For that I am sorry. (As always, I have been reading – celebrating, mourning, and above-all praying – right along with each of you, bloggy friends!)

Rest assured, all is well with me and Baby.

The day after my last post, I went in for the nuchal translucency ultrasound (part II of the so-called California Prenatal Screen). Seeing our baby in high-def should have been extremely cool, except that:

1)      I hit unexpected traffic on the way there, which caused me to panic that I would lose the appointment. (If you’re late at all to the full-bladder appointments, you have to reschedule…and get your bladder uncomfortably full again.)

2)      Despite following instructions to the letter, my bladder wasn’t full when I got there (maybe the traffic stress slowed things down?), and the technician made me feel rotten about it.

By this point, I was so stressed out that when the baby appeared on the screen, I found myself asking whether the technician could tell us if it was alive. She gave me a weird look as the baby on the screen proceeded to wave its arms and swallow gulpfuls of amniotic fluid…

3)      Then, I outsmarted myself…or not. After writing my previous post, I was convinced that I knew what I should be looking for – namely a nuchal translucency that was around 2 millimeters (or less) in width. So far so good, except that the measurements the technician was making were in centimeters. Embarrassingly, when this so-called-scientist saw the numbers creeping up to 0.18, 0.19, 0.21 cm, I was convinced that this was the equivalent of 18-21 millimeters! (For those of you who aren’t up on your metric system, 0.20 cm is equal to 2.0 mm.) Worse, my husband – the pediatric dentist who works on millimeter scale every day (or did, prior to the accident) – didn’t catch my error.

It wasn’t until we were outside the hospital that we realized something had to be off with our calculation.

Think about it, how could a baby the size of a peach (~3 inches from crown to rump) have the skin on the back of his neck be 21 millimeters (nearly an inch) thick?!

About an hour and a half later, I got the call from Kaiser telling me that everything was totally normal. Based on the combination of the 1st trimester blood test and the ultrasound, they adjusted my probability of having a baby with Down syndrome (from my original age-based estimate of 1 in 296) to an adjusted estimate of 1 in 5,000; and the probability of a baby with Edwards syndrome (originally 1 in 1152) to 1 in 95,000.

Several days later, on Friday afternoon, I got the call with the results from the NIPT blood test. (This was the brand new, more-accurate, qPCR-based blood test that I described here.) The test revealed that we were having a chromosomally-normal boy!

Great news…which I again managed to mess up in translation. But first, some unsolicited advice:

Do not tell your husband the gender of your baby-to-be in a text message.

I should explain. After waiting impatiently for the results of the NIPT scan, I finally got the call on Friday afternoon – while in a one-on-one meeting with my boss. Unwilling to wait until Monday for the news, I apologized to my boss and quickly left to take the call. Then, after learning such amazing news, I wanted to tell C immediately. (Somehow me knowing for more than a few minutes longer than him seemed horribly unfair.) But, I also felt an urgent need to return to my boss to apologize and continue our meeting…

So I sent C a text message.

He will never let me live it down.

Anyway, that was all our test news. I’m sorry to leave you with a cliffhanger for the last 7 weeks!

Other highlights of the last two months:

  • I ‘popped’ during Thanksgiving dinner. Once I switched to maternity pants, there was no going back…
  • I felt the first fluttering of movement on Christmas morning. It felt kind of like an upset, rumbly stomach, except without any feelings of queasiness. Feelings increased over the last weeks, so that now it actually feels like something is lightly tapping on me from the inside. After so much uncertainty, it is the most reassuring, wonderful feeling to know that he is alive and kicking in there! His most active time is from ~5-7am each day. The last few mornings I swear he has been doing cartwheels in there…
  • The Board of Trustees approved my promotion to Associate Professor (starting in Summer 2014)!
  • Saturday we hit 20-weeks. Say what?!
  • C felt movement for the first time on Sunday morning (during one of Baby’s gymnastics sessions).
  • We celebrated our 2nd wedding anniversary on Tuesday. Thanks in large part to our struggles with infertility and C’s life-threatening traffic accident (10 months later, it’s still causing him considerable pain), we’ve never been closer. I’m so glad I get to spend the rest of my life with this man!
  • Yesterday was our 20-week high-resolution ultrasound. The ultrasound technician wasn’t allowed to make any evaluative comments, but she narrated as she went, so we were able to count: two arms, complete with hands and five fingers on each; two legs with two adorable feet and ten toes; one stomach; one, four-chambered heart; two kidneys; one placenta; one umbilical cord (with blood flowing to the placenta); one head with a two-hemisphere brain (measuring 20w6d); and – oh yeah – a penis. (No surprise there, given our NIPT result, but it was nice to see it nonetheless!)

That’s about it. Now that my belly is swelling and I can feel ‘Baby Lou’ doing gymnastics in there, I’m actually letting myself believe that this is going to happen (although that doesn’t prevent me from middle-of-the-night panic attacks that something is wrong, like yesterday at 4am…) I’ve even relaxed enough to allow myself the occasional half-glass of wine, coffee, or Diet Coke. (Before you sic the Pregnancy Police on me, read this, or, if you prefer, this.)

And now, I’ll leave you with a picture of the beautiful flowers C got me for our anniversary. I’m enjoying the soft scent of lilies as I type this. 🙂

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Advanced Maternal Age

One week ago I turned 35. In pregnancy terms, this makes me officially old.

Visit with the genetic counselor

On Thursday, to celebrate, I got to meet with a genetic counselor through Kaiser (a meeting recommended for AMA women like me). Here’s what I learned:

At 35, my risk for chromosomal abnormalities is much higher than it was at 25. (Okay, so I already knew that!) The counselor was kind enough to point out that – despite the medical community’s black-and-white labeling method – there is nothing magic about the age 35. My risk increased slightly every year, so that now my risk of conceiving a baby with:

  • Down Syndrome (aka Trisomy 21) is 1 in 296
  • Edwards Syndrome (aka Trisomy 18) is 1 in 1152
  • Any chromosomal disorder is 1 in 134

(When you think about the fact that a few months ago, I was looking at odds of successful IVF with my eggs as about 1 in 4, 133 in 134 odds of having a chromosomally-normal baby really don’t look all that bad…)

I also learned a bit about the different disorders. Down syndrome (a disorder arising from three copies of chromosome 21, hence the name trisomy 21) is the most common, but is actually somewhere in the middle of the spectrum in terms of severity and prognosis.

Trisomies 13 (Patau syndrome) and 18 (Edwards syndrome) are more serious. The vast majority of babies with these disorders don’t survive a year. Those that do have severe disabilities.

Then there are the ‘milder’ sex chromosome disorders, like Klinefelter syndrome (in which baby boy gets an extra X chromosome, to get XXY) and Turner syndrome (in which baby girl gets an extra X, to get XXX). These may lead to slight reductions in cognitive function, health problems (e.g. diabetes in the case of Turner syndrome), abnormal physical characteristics (e.g. webbed neck in the case of Turner syndrome, small testicles and man boobs in the case of Klinefelter syndrome) and infertility. (I have to admit to finding it perversely amusing to think about infertility as the most minor of possible birth defects.)

(In case you’re wondering, XYY is also a possibility, but one that apparently doesn’t lead to any noticeable difference in cognitive or other abilities…)

 

Prenatal Screening Tests

To find out my likelihood of having a baby with one of these disorders, I was offered a variety of screening options.

I. California Prenatal Screening Program (PNS)

The first was the California Prenatal Screening Program. The charge for this test is $160 (fully covered by my insurance), and I found it interesting that that the money from all the women who get screened gets thrown into a communal pot. Uninsured women who get a positive screening test are eligible to use funds from the pot to pay for follow-up tests (like amniocentesis), and further prenatal care. Kind of cool.

Anyway, the California Prenatal Screening includes up to three different elements:

A.  A first-trimester blood test that measures levels of two molecules:

  1. human chorionic gonadotropin (hCG) – the protein hormone that’s used to confirm pregnancy in both home pregnancy tests and blood pregnancy tests, and
  2. pregnancy-associated plasma protein A (PAPP-A) an enzyme that chops up other proteins

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First trimester hCG levels tend to be a bit higher in Down syndrome pregnancies than in normal pregnancies, while PAPP-A levels tend to be a bit lower in Down syndrome pregnancies than in normal ones. Here are some figures I found on the interwebs showing the rough trends. In one-dimension:

ImageSource

In two-dimensions (hCG is on the x-axis; PAPP-A is on the y-axis):

ImageSource

Notice that there is a large overlap between Down syndrome and normal pregnancies in each plot. The genetic counselor also assured me that the levels change significantly over the course of the pregnancy, so a correct pregnancy date is crucial for an accurate result. Ultimately, this one blood test alone is insufficient to reliably predict Down syndrome risk, which is why the CA screening folks won’t give a result until they have at least one other piece of data, such as the following:

B.  A high-resolution ultrasound called nuchal translucency (NT) ultrasound is used to measure the thickness of a fluid-filled ‘translucent’ layer in the baby’s neck. More fluid in the neck is correlated with higher risk of congenital heart defects, which in turn is correlated with Down syndrome.

Here’s a figure showing normal (right) and Down syndrome (left) NT scans:

ImageSource

As with the blood test, this is all based on correlations, and just gives probabilities. (We infertiles just love probabilities…) Anyway, it is far from diagnostic.

These first two tests are sometimes referred to as the first trimester screen.

C.  The final data point that can be used as part of the California screen is a blood test in the second trimester. This test is sometimes called the quadruple test or quad screen, as it measures the levels of four molecules:

  1. human chorionic gonadotropin (hCG, see above)
  2. α-fetoprotein (AFP) – the most abundant plasma protein in human fetuses; its function in humans is unknown; AFP levels are elevated in pregnancies of babies with certain birth defects, including Down syndrome and neural tube defects like spina bifida.
  3. unconjugated estriol (UE3) – a  steroid hormone produced in pregnancy; low levels of UE3 may indicate chromosomal abnormalities
  4. inhibin A – a protein that inhibits follicle-stimulating hormone (FSH) production; inhibin levels are especially high in cases of Down syndrome, and especially low in cases of Edwards syndrome

 

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Like with the first trimester screen, the specific levels of these molecules can either more closely resemble a ‘normal’ or a ‘Down syndrome’ (or other chromosomal abnormality) pregnancy.

Even with all three data points, the best the CA screen can do is give probabilities of an abnormality. A probability of 0.5% (1 in 200) or greater is considered a positive test. In other words, the vast majority of women who get a ‘positive’ screening result will go on to have normal babies.

 

II. Non-Invasive Prenatal Test (NIPT)

The genetic counselor informed me that I’m also eligible for a very new blood test called the Non-Invasive Prenatal Test (or NIPT). This test is so new that Kaiser just began routinely offering it to women over 35 in June (which may explain why my OB failed to mention it in our first prenatal visit…even after C and I had made it clear that we wanted every non-invasive test available…)

This test is also a blood test, but instead of measuring the levels of proteins and small molecules in my blood, the NIPT looks at fragments of DNA in my blood. This post is getting rather long, but I’ll try to give the basic gist.

Apparently if you looked at all the DNA in my blood right now, about 10% of it would actually be pieces of DNA from my baby’s blood. Unfortunately, there’s no easy way to recognize which DNA is from me and which is from baby.

It is, however, possible to extract the DNA soup (including mine and baby’s) from my blood, and then make copies of certain portions of DNA from certain chromosomes. (For any biology types, they use quantitative PCR for this.) To detect Down syndrome, they make copies of a piece of DNA that only appears on chromosome 21, along with copies specific to several other chromosomes. Then they compare the amount of chromosome 21-specific copied DNA to the amount of other chromosome-specific copied DNA.

  • If the amounts are the same, it suggests that there weren’t ‘extra’ copies of chromosome 21 floating around to begin with, and that my baby probably does not have Down syndrome.
  • If there is an excess of chromosome 21-specific DNA, it suggests there were extra copies of chromosome 21 in our combined blood. Since we are pretty sure I don’t have Down syndrome, the most likely explanation is that my baby does.

This test catches a higher percentage of Down syndrome cases than the California screen (99% versus 90-95% for the combined CA screen), and has a much lower false-positive rate. (The detection rate is a bit lower for some of the other chromosomal disorders, for reasons that I haven’t taken the time to investigate.) It doesn’t, however, give any information about neural tube defects (which the California screen does), and it still does not give a definitive yes or no answer. For that, one would have to do chorionic villus sampling (CVS) or amniocentesis, both of which actually look at the full set of chromosomes in baby’s cells.

 

What I did

So, if you’ve been reading this blog for long, you know that I’m a sucker for data, so perhaps it comes as little surprise that I requested both tests. I gave blood for part A of the California Prenatal Screening right after my first OB visit three weeks ago. No doubt my results are sitting on a computer somewhere, but they won’t release them until I’ve completed my nuchal translucency ultrasound (part B)…which I’ll do bright and early tomorrow morning.

Last Thursday, after my meeting with the genetic counselor, I gave a blood sample for the NIPT. I’m told the results of that test should come back to me within a week. (Oh, and did I mention, the NIPT will also tell us baby’s gender?!)

Given that the NIPT is so much more accurate than the California screen, one might argue (as the genetic counselor sort of did) that the NT ultrasound is a waste of time. For one thing, there’s a decent chance that the CA screen may indicate an abnormality, while the NIPT may come back normal. If that happens, it may indicate that baby has a chromosomal disorder but is in the very small percentage of cases that are missed by the NIPT. Or, it may mean that baby has no chromosomal disorder, but has an unrelated congenital heart defect (giving rise to the thicker-than-usual nuchal translucency). Or (most likely) it may mean that baby is fine and the CA screen gave a false positive.

The uncertainty could easily cause a lot of stress, which is why the genetic counselor was careful to make sure I didn’t choose it blindly. I’m probably being a bit naïve (or arrogant?), but I’d like to believe that I could think logically about the likelihood of each possibility and handle any ambiguity that might arise.

Also, I really want to see my baby in high resolution.

 

What if?

In all this talk about the science behind these screening tests, I’ve conveniently avoided the most important question that all this brings up.

Namely, what will we do if the screening tests (particularly the NIPT) show a chromosomal abnormality?

The short answer is, I don’t know.

After all that we’ve been through, it’s hard to imagine choosing to terminate this pregnancy under any circumstances. In particular, I don’t think I’d terminate if faced with any of the ‘mild’ abnormalities (Turner or Klinefelter Syndrome). I don’t even think I’d terminate in the case of Down syndrome. (The way I see it, this may be my only chance at genetic parenthood, and I’d rather be mom to a child with Down syndrome than to no child at all…)

The decision gets harder for the ‘severe’ chromosomal abnormalities – trisomy 13 or 18. Could I continue with all the emotional and physical pains of pregnancy and childbirth, knowing that my baby would in all likelihood not survive infancy?

On the other hand, could I choose to end a life – my baby’s life – even knowing that it wouldn’t live long anyway?

I just don’t know.

And then there’s the fact that this isn’t just my decision. This decision would affect C too, and we’d need to somehow arrive at a plan together.

It’s enough to make me think that the people who refuse to test are on to something. Perhaps mothers like me – who aren’t prepared to terminate yet do decide to test – are just betting on a negative test result so that we can enjoy rest of our pregnancies with one less thing to worry about…

Well, I’ve already placed my bet, so all I can do now is wait and hope that my big gamble pays off.

I’ll keep you posted.

Tired

Thank you all so much for your kind response to my news. I’m sorry it’s taken me so long to provide an update. Lest you think ‘No news is bad news’, I’ll spoil the punchline by telling you that all is well (as far as we know).

I hate to use a lame pregnancy excuse, but I am so tired that I can barely keep up with my work responsibilities, which is why working on a blog post has been out-of-the-question…

Suffice it to say that I am having some pregnancy symptoms:

  • Extreme exhaustion (coupled with difficulty sleeping…awesome!)
  • Moodiness (poor C has been dealing with some serious crankiness, punctuated by tearing up every morning during some story on the Today show…)
  • Acne (enormous, sore, pressurized zits…possibly worse than when I was a teenager)
  • Constipation (‘nuff said)
  • Unsettled stomach (I wouldn’t call it nausea per se, but more an uncomfortable feeling and general lack of enthusiasm for food)

As those of you who have miscarried can appreciate, I’m actually grateful for every symptom. (I had very few and very mild symptoms last time…) But nonetheless, it feels like all I do is work, sleep, and go to appointments (acupuncture or RE’s office)…

Here are some pictures to fill out this post:

ImagePhoto from the black-tie wedding in Chicago where we made a baby! (Well, an embryo anyway. Doesn’t C look handsome in a tux?)

ImageEating a Chicago Dog at Wrigley Field with my buddy R. (Meanwhile, my little embryo was on its way to becoming a blastocyst…)

Image“Umm. Wake up, C! Wanna hear something weird?!…”

ImageWhen my temperature didn’t drop by 10,11,12 dpo, I thought something was up. Then when it did drop at 15 dpo, I. FREAKED. OUT!

ImageBut I kept going in for blood tests, and my betas looked good…

ImageWhen I got to work the day of the ultrasound, I found these from my thoughtful colleague K! Notice the graduated cylinder ‘vase’.

ImagePrayed a lot to St. Gerard, and wore my lucky socks to the first ultrasound appointment. By my estimate, baby should be ~ 5 weeks 5 days old…

C and I were blown away to see this. “Baby Lou” (as my mom has taken to calling it in her nightly prayers) measured 5 weeks 6 days, with a steady heartbeat! (You can see the yolk sac ~6 seconds.)

This was HUGE news for us. Last time, we learned at our 8 week ultrasound that the baby was only measuring 5 weeks 5 days (no heartbeat). I miscarried naturally about a week later. That one extra day means that we’ve at least made it farther than last time.

And we’ve got a heartbeat.

We know that we are still so far from out of the woods, but we’ve decided to be hopeful. I even went out and bought another copy of The Belly Book to stick our ultrasound pics in.

And now, we wait.

Fortunately, a ‘perk’ of being an IF patient with Kaiser is that I get weekly ultrasounds until I ‘graduate’ to the OB (~9 weeks). So we’ll do it again on Friday (6w6d)…

A funny thing happened on the way to Colorado…

But first, I want to apologize for the radio silence. It started because I was so busy with the start of the school year…

  • We traveled to Chicago Labor Day weekend (8/31-9/2) for a good friend’s wedding. (I got my positive OPK there, so, once again, our plans for natural cycle IUI were foiled…)
  • Fall classes started that Wednesday (9/4).
  • My promotion portfolio was due Friday (9/6).
  • Then on Saturday (9/7), I flew to Indianapolis for a whirlwind trip the American Chemical Society meeting.
  • Then back Monday (9/9) to teach the second week of classes…

And then on Friday (9/13), I found myself…

a little bit.

pregnant.

 

 

As most of you know, I’ve been diagnosed with diminished ovarian reserve (AMH 0.19, FSH 13). I was a poor responder in both menopur + IUI and low-stim + IVF cycles. We were told by three different doctors that our chances of success with my eggs were slim.

We spent the last couple months doing (well, intending to do…) natural cycle IUI and taking a laundry list of supplements in the hope that they might improve egg quality, in preparation for a ‘last ditch’ high-stim IVF cycle at CCRM.

We had our CCRM phone consult a couple weeks ago, and scheduled our one day workup for this coming Tuesday (9/24).

As most of you also know, I’m a religious BBT charter. As a result, I know that I have a short luteal phase (usually only 10 days or so). When I got to 11, 12, 13dpo without a temperature drop (and noticed that my boobs were almost filling the cups of my bra…), I started to hope. Then a week ago Friday, I caved and used an old home pregnancy test I had lying around.

It was positive.

I called Dr. Y’s office and the advice nurse ordered a blood test.

  • Beta #1 (at 13dpo) was 110.

Then on Saturday, the spotting started. Red at first, then brown. On Sunday my BBT dropped half a degree and we just knew that we were miscarrying again. That morning I also realized that I had somehow FORGOTTEN to use the progesterone suppositories that the nurse told me to use when I called on Friday!! (You have no idea how completely out of character it is for me to ‘forget’ instructions from my healthcare provider…especially about something this important!!!) So I cried in bed for over an hour on Sunday, reading and rereading supportive comments on the online forum for my local Resolve support group, sure that I had killed our miracle baby with my thoughtlessness.

 

But I went in on Monday for Beta#2.

  • Beta #2 (at 16dpo) was 380.

I continued spotting for six days, but I kept going in for blood tests.

  • Beta #3 (at 18dpo) was 980.
  • Beta #4 (at 21dpo) was 3512.

Thankfully, the spotting seems to have stopped for now.

 

 

So now I’m feeling a bunch of things:

1) Elated. This is what we’ve been praying for the past 19 months. What we paid about $12K for so far, with nothing to show for it. What we were prepared to shell out another $25-30K more for at CCRM… And somehow we hit the jackpot ‘the old-fashioned way’?!

2) Terrified. Last time we got a BFP (nearly a year and a half ago), we miscarried at 9 weeks after seeing no heartbeat at our 8 week ultrasound. We were sad, but that was just the start of our infertility journey. At the time we were so sure that we would be pregnant again in a month or two. We’ve had a roller coaster year of infertility, a DOR diagnosis, a life-threatening injury, and two failed ART cycles since then. I can only imagine what a miscarriage would be like now that we know what is at stake… We are so far from out of the woods, and I’m really scared.

3) Embarrassed. I know it sounds really stupid, but I feel like a big fat infertility fraud. Like all the wonderful people I’ve met through this journey will resent me. (I could hardly blame them, as I’ve resented my share of pregnant women.) I feel bad for even saying that I feel this way. I’m sure you’re all like “Boo hoo for the poor pregnant girl.” But it’s weird. Infertility has become a part of my identity somehow. If this pregnancy sticks, does that part of me just die?

 

 

So we canceled the trip to Colorado. (Well, for fear of jinxing it, I waited until Beta #2, and used the word “postpone” rather than “cancel” when I called CCRM…)

Our first ultrasound is on Friday.

We are cautiously hopeful…

*******

To our friends IRL, I’m sorry that you’re hearing our news for the first time like this. Given our history and how early it is in the pregnancy (just 5 weeks today), we’re not ready to share far and wide yet… But I didn’t want to leave you hanging! C & I would appreciate your discretion for now.

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.

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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!

*****

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!