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.
Hi Dr Sher I was wondering if you could possible help me. My husband and I have been trying to conceive our second child, first little girl born 3 and a half years ago with no problem at all. My periods stopped for around a year and came back just in December there. We have been seeing a fertility specialist who has put me on clomid for 6 months. Firstly on 50mg but on 4th month my periods stopped again and he put me onto 100mg which seemed to have brought them back again and it looked like I had ovulated this month. Just taken period today and about to start my last round of it. I got my day 21 bloods done last month and results are below:
Serum FSH level – 3.4 U/L
Serum LH level – 3.1 U/L
Serum Progesterone – 99.7 nmol/l
Serum Oestradiol – 599 pmol/L
Serum prolactin level (HI) – 413mU/L (102- 496)
I was wondering if you could please shed any light on these results as I am concerned that my prolactin level is high. Could this be one of the main reasons why I might not be getting pregnant and also is there anything that I can take to lower the level.
Any advice or help would be most grateful.
Kind Regards
Laura ( A desperate 35 year old wanting another child)
I do not think this is prolactin-related. It sounds like an hypothalamic dysfunction. Could you re-post this question but next time ad your blood AMH level?
If so I could better advise you.
Geoff sher
Hi Dr Sher. I am 23 weeks pregnant with B/G twins after my second round of IVF. My first pregnancy (natural) ended when my son was born at 24 weeks due to incompetent cervix. He did not survive. My cervix is already shortening and I am having contractions. My doctor is thinking about a cerclage but is saying there is a 50% chance that the cerclage can cause labour to proceed. Please please advise if you would recommend a cerclage for your patient in this scenario?
I would definitely advise you having a cerclage put in place stat. Also get advice from a high-risk OB (a perinatologist).
Geoff Sher
Hi Dr. Sher I am about to do my first FET with one of my PGS tested embryos. Because of my endometriosis diagnosis 2 years ago (did laproscopy to clear it out) my RE did immunology testing and it resulted in slightly elevated levels for Nk activation/AntiPhosEth IgM/Immunopheno Type. After watching one of your facebook videos you referred to the CD3 cells but those came back normal for me and only the CD56+/16+NK came back slightly elevated. What does this mean ? Also when looking at the test results it showed under NK Intralipid suppression to be 11. H % killing. The RE recommended IVIG (which I do not wish to do) I am wondering why he didn’t recommend Intralipids instead.
My question is since I have no history of a failed IVF as yet should go without the intralipid treatment on my first try and see how it goes first or knowing this information do I go ahead with treatment for my first FET.? Also if I choose to not do the intralipids on my first try would it be recommended that I transfer two PGS tested embryos or just one? The statistics show that if you transfer two PGS tested embryos it is 80% as opposed to a much lower rate for one PGS tested embryo. Is this correct ?
If your tests were done correctly at one of 5 Reproductive Immunology reference laboratories in the U.S.A, then it sounds as if you indeed do have an immunologic implantation dysfunction that needs to be causally identified (alloimmune versus autoimmune)…see below. I I am correct then I would advise against proceeding to FET without addressing a possible immunologic implantation dysfunction (IID) appropriately ion advance.
More than half of women who have endometriosis harbor antiphospholipid antibodies (APA) that can compromise development of the embryo’s root system (trophoblast). In addition and far more serious, is the fact that in about one third of cases endometriosis, regardless of its severity is associated with NKa and cytotoxic uterine lymphocytes (CTL) which can seriously jeopardize implantation. This immunologic implantation dysfunction (IID) is diagnosed by testing the woman’s blood for APA, for NKa (using the K-562 target cell test or by endometrial biopsy for cytokine activity) and, for CTL (by a blood immunophenotype). Activated NK cells attack the invading trophoblast cells (developing “root system” of the embryo/early conceptus) as soon as it tries to gain attachment to the uterine wall. In most cases, this results in rejection of the embryo even before the pregnancy is diagnosed and sometimes, in a chemical pregnancy or an early miscarriage. As such, many women with endometriosis, rather than being infertile, in the strict sense of the word, often actually experience repeated undetected “mini-miscarriages”.
Women who harbor APA’s often experience improved IVF birth rates when heparinoids (Clexane/Lovenox) are administered from the onset of ovarian stimulation with gonadotropins until the 10th week of pregnancy. NKa is treated with a combination of Intralipid (IL) and steroid therapy: Intralipid (IL) is a solution of small lipid droplets suspended in water. When administered intravenously, IL provides essential fatty acids, linoleic acid (LA), an omega-6 fatty acid, alpha-linolenic acid (ALA), an omega-3 fatty acid.IL is made up of 20% soybean oil/fatty acids (comprising linoleic acid, oleic acid, palmitic acid, linolenic acid and stearic acid) , 1.2% egg yolk phospholipids (1.2%), glycerin (2.25%) and water (76.5%).IL exerts a modulating effect on certain immune cellular mechanisms largely by down-regulating NKa.
The therapeutic effect of IL/steroid therapy is likely due to an ability to suppress pro-inflammatory cellular (Type-1) cytokines such as interferon gamma and TNF-alpha. IL/steroids down-regulates NKa within 2-3 weeks of treatment the vast majority of women experiencing immunologic implantation dysfunction. In this regard IL is just as effective as Intravenous Gamma globulin (IVIg) but at a fraction of the cost and with a far lower incidence of side-effects. Its effect lasts for 4-9 weeks when administered in early pregnancy.
The toxic pelvic environment caused by endometriosis, profoundly reduces natural fertilization potential. As a result normally ovulating infertile women with endometriosis and patent Fallopian tubes are much less likely to conceive naturally, or by using fertility agents alone (with or without intrauterine (IUI) insemination. The only effective way to bypass this adverse pelvic environment is through IVF. I am not suggesting here that all women who have endometriosis require IVF! Rather, I am saying that in cases where the condition is further compromised by an IID associated with NKa and/or for older women(over 35y) who have diminished ovarian reserve (DOR) where time is of the essence, it is my opinion that IVF is the treatment of choice.
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. 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.
•The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
•Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Blastocyst Embryo Transfers Should be the Standard of Care in IVF
•IVF: How Many Attempts should be considered before Stopping?
•“Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
•IVF Failure and Implantation Dysfunction:
•The Role of 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)
•Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
•Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
•Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•A personalized, stepwise approach to IVF
•How Many Embryos should be transferred: A Critical Decision in IVF.
•The Role of Nutritional Supplements in Preparing for IVF
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
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.
Dear Dr. Sher,
First of all I cannot thank you enough for all the uncountable help you provide to a lot of woman that read your blogs and books all over the world! – not only technically but also emotionally it helps us go thru all those difficult situations and help make informed decisions.
Today I am writing on behalf of my close friend:
She (38) had several failed IVF cycles with her own eggs achieving only one chemical pregnancy. The conclusion was drawn that her eggs were not good thus they moved to DE.
But now after few attempts with DE, total of four CCS tested blastocysts were transferred by now and still no success. Lining was good. Hysteroscopy was good.
She had previously checked NK at ReproSource and there was no activation.
Also, DQ-alpha test with Reprosource had no issues.
Currently she has three tested blastocysts (and one mosaic) from a new donor … but she doesn’t want to rush into another transfer only for the history to repeat itself! Her clinic thinks it was bad luck.
However, she did more testing on her own at Clinical Immunology Laboratory at RFUMS/The Chicago Clinical School
The below results came out of range:
1) Test immunophenotype:
CD4 (T-helper): Results: 63.3 (H) % (Range is 31.0-53.0)
2) Test Th1/Th2 Intracellular Cytokine Ratios:
TNF-a:IL-10 (CD3+CD4+). Results: 37.2. Range is 13.2-30.6
The remaining results were within the range:
CD3 (PanT Cell), CD8 (T-cytotoxic/suppr), CD+CG56+(NKT) [*], CD3/IL-2R [*], CD3-CD56+(NK cells)CG56+CD16 +cells, % CD19+cells, CD5+
Also. IFN-g:IL-10 (CD3+CD4+) was within a range.
Please help interpret what in your opinion she should do? – more investigations? Is there a protocol you would recommend for her case before next FET?
Not sure if it matters but during medicated cycles she gets break thru bleeding so last time they tried FET on natural cycle with no results either.
My Friend is very grateful for having this opportunity to ask your advise because she feels she is at a loss, she feels she did all she could and still no results.
Many, many thanks!
Zuza
Unfortunately I do not agree that based upon the immune tests cited here you can exclude an immunologic implantation dysfunction linked go NK cell activation. I do not see the results of a K-562 target cell test and the elevated TNF alpha indeed suggests that there is k likely NK cell activation (NKa). Also you do not report APA and ATA results, nor do you present DQ alpha/HLA for you and your husband.
I think you could be a classic case where the required tests were not ordered and the results of those cited might have been misinterpreted.
Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
1.Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
2.Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3.The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
4.Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
a.A“ thin uterine lining”
b.A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c.Immunologic implantation dysfunction (IID)
d.Endocrine/molecular endometrial receptivity issues
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. 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.
•The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
•Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Blastocyst Embryo Transfers Should be the Standard of Care in IVF
•IVF: How Many Attempts should be considered before Stopping?
•“Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
•IVF Failure and Implantation Dysfunction:
•The Role of 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)
•Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
•Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
•Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•A personalized, stepwise approach to IVF
•How Many Embryos should be transferred: A Critical Decision in IVF.
•The Role of Nutritional Supplements in Preparing for IVF
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
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.
Hi Dr. Sher- I’ve been writing you a lot the past few weeks. I’ve been in limbo, but just had a miscarriage after an FET of a 4AA blast. This is my first miscarriage, I had a successful pregnancy with my first FET. My hcg numbers were always great and doubling/ tripling how they were supposed to. My progesterone was always low, even on suppositories. It was 7 at 9dp5dt and went up to 11.5 but never higher. The gestational sack always measured a week behind and a fetal pole never developed, just the gestational sack and egg sack. Worth noting is my yolk sack was “big”. What do you think about this?
Do you think it sounds chromosomal?
Do you think the low progesterone was a cause or a symptom?
I’m an anxious person and this has thrown me through a loop. I feel like something is wrong with me that caused this. My dr isn’t so concerned. He thinks because I had a successful pregnancy that I will again and this was just a one off situation. What do you think? I really value your opinion. I have 11 blastocysts frozen, I stimned well, I’m 31, my eggs are 29 and my cause in unexplained. My husband has slight morphology. Thank you!
I tend to agree with your RE. It is more than likely that this was a case of “embryo incompetence that most often is due to chromosomal aneuploidy. I think that the the low progesterone was the effect rather than the cause of this failing pregnancy.
Good luck!
Geoff Sher