Ask Our Doctors – Archive
Our Medical Directors are outstanding physicians that you will find to be very personable and compassionate, who take care to ensure that you have the most cutting-edge fertility treatments at your disposal. This is your outlet to ask your questions to the doctors.
I have pcos and currently going through fertility treatment. My cycle ended monday and I took femara monday to friday. Today is day 2 for my menopur injections but I started bleeding Friday night into Saturday morning. The bleeding was scant so I thought it would go away but today Sunday I’m bleeding more like my regular day 2 of periods. I was wondering if I should stop the menopur until I talk to my RE tomorrow? The drug is expensive and I do not want to waste it. I’m supposed to go in for a scan Tuesday to see if I’m ovulating and prepare for iui. Please advise
If I were you I would continue with the treatment as directed by your RE and contact him/her tonight or tomorrow for further directions.
Good luck!
Geoff Sher
Hello Dr. Sher-
My husband and I are both 35, and I will be 36 next month. We’ve been trying to get pregnant since 5/2013. I’d been temping, and other than an average luteal phase of 11 days, everything looked fine. My initial labs were fine 12/2013 (FSH 6, lab messed up on AMH so wasn’t done) and normal HSG. We did a few cycles of femara 2.5mg with my OB/GYN, which didn’t work. My husband’s SA showed great numbers but morphology of 4%, so he started on supplements to improve it. Three months later in June 2015, his morphology was 5%, all other numbers were great. In July 2015, we saw an RE. He started me on cabergoline due to galactorrhea and did labs. My FSH was 6, AMH 0.2, prolactin 25, TSH 2.7, and NK cells 34.9%. He told me to start melatonin, DHEA, synthroid 25mcg, continued cabergoline, and had me take prednisone 20mg after ovulation. I added vitamin D, coQ10, and acupuncture. My initial AFC was 10. We did 2 IUIs with femara 5mg/ovidrel trigger- each had 1-2 good follicles, postwash sperm count was over 50 million. He had me do an ovidrel booster 5 days after trigger to improve my luteal phase. Progesterone was around 40 both times. We did another similar cycle with a planned IUI that we had trouble scheduling so did timed intercourse instead- negative. My AFC count on second cycle was 15, and has since been 15-20. We then did a third IUI with femara 5mg, added gonal F 25units on CD8, had several good follicles and my RE decreased it to 12.5units so that we wouldn’t have too many follicles. He said I should ovulate 2-3 eggs. Sperm count and progesterone were both great, but it was negative.
We proceeded to IVF. My doc said 50% chance of success, and 50% chance of having some frozen, and estimated we’d get 10-15 eggs. I have focal migraines and haven’t done well on estrogen, so we did 2-3 weeks of micronor. The first week I didn’t understand how important it was to take it in the same timeframe and missed a dose or two. My doc did a saline uterine ultrasound which was normal. After micronor, I did estradiol 2mg BID for 4 days. I had a scan done at this time which showed an ovarian cyst 1.6cm, my estrogen was 80, that he said was elevated due to the cyst and the estradiol, and that it was ok to proceed. After estradiol, I immediately started gonal F 375units and menopur 75. Day 3 estrogen (after 2 days of stims) was 47. He continued same dose. day 5, estrogen was 90.6. I had five good ones on left, 1 good on right and several smaller ones. Largest one was 11cm. He changed his estimate to 5-10 eggs retrieved and mentioned we were seeing my “low AMH.” Day 7, Estrogen 285. Six good on left, four good on right, largest 13mm. Estimate 8-12 retrieved, “plenty to work with,” I Started ganirelix, and continued menopur 75 and gonal F 375. Day 8-Estrogen 466. Seven good on left, four good on right, some maybes. Estimated 7-10 mature eggs. We did Intralipids (20%, 1000cc). Day 10-Estrogen 827.1, 10-11 follicles. Lining 11- “fantastic.” Day 11- Estrogen 1010, Progesterone 2.7. 7 on left, 4 on right, mostly 18-19mm, uniform, Lining 13- “fantastic.” I triggered that night with pregnyl 10,000 units SQ. ER got 8 eggs, 6 mature, 5 fertilized with ICSI. After ER, I started prednisone 20mg, prometrium 200mg BID vaginally, and 0.5cc PIO IM daily. 2 days after ER, we did another dose of intralipids and I did acupuncture. On day 3, two looked great- one 8 cell, with great compaction, that “looks better than all the other day 3 eggs of the other patients,” one 9 cell starting to compact that looked good. The other three were four cells and didn’t look as good. We had a day 3 transfer with the 8 and 9 cell embryos. Transfer was very smooth, and my doc estimated 65% chance of success. I did acupuncture an hour afterward. RE had me do a second HCG 10,000 unit booster 5 days after trigger since my estrogen was borderline. I had strange uterine sensations 5 days after transfer that I thought was implantation. HCG 15 days after ER was 2.3, repeated 18 days after ER was 0.83. My doc recommended one cycle off with micronor, then starting again. He has mentioned adding growth hormone, and still feels I have a favorable prognosis. We are adding alpha-lipoic acid, pycnogenol, royal jelly, and PQQ for me, as well as adding pycnogenol and vitamin E for my husband. We stopped DHEA since it is controversial.
My questions:
1. Do you think failure was due to embryo quality, NK cells, or something else?
2. Do you think I was oversuppressed, and if so, what would you do differently? Could the early menopur have caused problems? I left a note about an agonist/antagonist conversion protocol and the nurse said he said no. We have an appointment in a few days to ask why not and questions on protocol.
3. For the NK cells, we are planning on doing intralipids 1 month before transfer, at the start of stims, and again 7-10 days before transfer, in addition to prednisone 20mg after retrieval. Is this sufficient? Am I likely to need IVIG or a gestational carrier?
4. How likely is the growth hormone going to help?
5. Do you think the beta of 2.3 was implantation that didn’t stick or the booster injection?
Thank you so much- I REALLY appreciate your help!
In most cases such as yours where (given your very low AMH) you clearly have DOR, it becomes a matter of carefully reevaluating and possibly revising the protocol for ovarian stimulation. In my opinion. you need a modified, robust, long pituitary down-regulation protocol. I would use an agonist/antagonist conversion protocol with human growth hormone (HGH) augmentation and would recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing)-normal blastocysts, to make hay while the sun still shines.
As for the NKa+ it is important to make certain that this is autoimmune in origin and not alloimmune (DQ alpha/HLA genetic matching) which needs a different approach to management (see below).
Please visit my new Blog on this very site, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Frozen Embryo Transfer (FET): What Does it Involve?
•Hereditary Clotting Defects (Thrombophilia)
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•Why did my IVF Fail?
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
•Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
•Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•The Role of Nutritional Supplements in Preparing for IVF
I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoff Sher
Dear Dr, Sher,
Is there any current way to retrieve an immature egg and grow it in the lab to correct size to mature it and fertilize?
There have been many suggestions with regard to deliberately harvesting immature oocytes and then maturing them in the lab and taking them to blastocyst for transfer. In my opinion, this, like so many initial claims, has NOT panned out. Some eggs harvested at ER during regular IVF, turn out to me immature (M1’s) and upon being left in culture for a few hours prior to fertilization, mature into M2 eggs…but not many do so.
Geoff Sher
Dear Dr. Sher,
My husband and I have been trying for a baby for two years and have been in treatment for just over one year (five IUIs and two IVFs-with-ICSI to date, although we had zero fertilisation on the last).
The tests I have had so far came back fine, all but one – I have high thyroid antibodies (TPOs). They have been measured twice and were in the 1000s. My doctor was concerned but the endocrinologist at the hospital said that I was “fine” as my TSH was around 1.5, and that I could contact her again when I fell pregnant. Therefore I’ve been left untreated. In the meantime I have had two miscarriages. The first one I lost naturally at 5+5 and the second one was a silent miscarriage – I should have been 7+4 at my early scan but the baby only measured 5+3. One week after this scan the heart had stopped beating and I had to take medicine to allow my body to miscarry. I had seen the endocrinologist when I thought was 6 weeks pregnant and she said I was “fine”. Later I find out that she only measured my TSH and not my TPOs.
I have read a lot about this and I suspect I have Hashimotos. Nobody has spoken to me about this where I live (Copenhagen, Denmark). I mentioned it again to my fertility clinic and they said they’d put me on Predisone for the next treatment, although it’s undocumented. I feel my concerns are being brushed aside. I’m trying a gluten free diet as I’ve read this may help, but I have no idea whether it will or not.
I’m now 35 and am in the ‘high end’ of the low AMH range. I’m so worried.
Do you have any initial thoughts on this? Could high TPOs indicate another auto immune disorder that I could be tested for? I am willing to pay privately for this over here.
Many thanks in advance for your response.
Nicola Strand
Between 2% and 5% of women of the childbearing age have reduced thyroid hormone activity (hypothyroidism). Women with hypothyroidism often manifest with reproductive failure i.e. infertility, unexplained (often repeated) IVF failure, or recurrent pregnancy loss (RPL). The condition is 5-10 times more common in women than in men. In most cases hypothyroidism is caused by damage to the thyroid gland resulting from of thyroid autoimmunity (Hashimoto’s disease) caused by damage done to the thyroid gland by antithyroglobulin and antimicrosomal auto-antibodies.
The increased prevalence of hypothyroidism and thyroid autoimmunity (TAI) in women is likely the result of a combination of genetic factors, estrogen-related effects and chromosome X abnormalities. This having been said, there is significantly increased incidence of thyroid antibodies in non-pregnant women with a history of infertility and recurrent pregnancy loss and thyroid antibodies can be present asymptomatically in women without them manifesting with overt clinical or endocrinologic evidence of thyroid disease. In addition, these antibodies may persist in women who have suffered from hyper- or hypothyroidism even after normalization of their thyroid function by appropriate pharmacological treatment. The manifestations of reproductive dysfunction thus seem to be linked more to the presence of thyroid autoimmunity (TAI) than to clinical existence of hypothyroidism and treatment of the latter does not routinely result in a subsequent improvement in reproductive performance.
It follows, that if antithyroid autoantibodies are associated with reproductive dysfunction they may serve as useful markers for predicting poor outcome in patients undergoing assisted reproductive technologies.
Some years back, I reported on the fact that 47% of women who harbor thyroid autoantibodies, regardless of the absence or presence of clinical hypothyroidism, have activated uterine natural killer cells (NKa) cells and cytotoxic lymphocytes (CTL) and that such women often present with reproductive dysfunction. We demonstrated that appropriate immunotherapy with IVIG or intralipid (IL) and steroids, subsequently often results in a significant improvement in reproductive performance in such cases.
The fact that almost 50% of women who harbor antithyroid antibodies do not have activated CTL/NK cells suggests that it is NOT the antithyroid antibodies themselves that cause reproductive dysfunction. The activation of CTL and NK cells that occurs in half of the cases with TAI is probably an epiphenomenon with the associated reproductive dysfunction being due to CTL/NK cell activation that damages the early “root system” (trophoblast) of the implanting embryo. We have shown that treatment of those women who have thyroid antibodies + NKa/CTL using IL/steroids, improves subsequent reproductive performance while women with thyroid antibodies who do not harbor NKa/CTL do not require or benefit from such treatment.
Please visit my new Blog on this very site, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
•IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Unexplained IVF Failure
•Why did my IVF Fail?
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
•Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
•Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report)
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•The Role of Nutritional Supplements in Preparing for IVF
•Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & Con’s!
I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoff Sher
Sana says:
January 28, 2016 at 5:49 am
Hello doctor
Got my Bhcg done today I. E 28-1-16 is 2970. Adnexa is normal in scan . A gestational sac of 2 cm is seen in uterus. What precautions should be taken.. The size of sac is very small as compared to 6 wk size of embryo. Sir, what is your suggestion?
Regards,
Sana
Geoffrey Sher says:
January 28, 2016 at 9:08 am
Hi Sana,
This in fact could all work out fine. The only thing to do is to wait and repeat the USin week.
Good luck!
Geoff Sher
Sana says:
February 7, 2016 at 12:21 am
Hello doctor,
I had bleeding 2 days back. Got my scan so there was no pregnancy. Got my Hcg the levels have fallen from 4500 to 350. I’d a miscarriage. Doctor has told me to put misoprostol. I’d got D&C done an year back also same 7 week miscarriage. What should I do tk tab or get D&C. When should I plan for next FET.
Regards. .5
So sorry to hear this news!
I would make sure that the endometrial cavity is totally empty by having an US done. If it is not…I would do a D&C sooner rather than later to avoid a risk of endometritis damaging the endometrium.
G-d bless!
Geoff Sher