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.
The nurse (who tends to lean to the negative end of things) said she wished my hcg had doubled, but they’d just have to wait for my Next ultrasound next Friday. At 5 weeks my ultrasound measured exactly 5 weeks and a gestational sac. They had no concerns. Next Friday I’ll be 6w4d.
Apparently I’ve never had a 48 hour doubling time either. I put it all into a spreadsheet today. Sigh. None of my symptoms have changed. No spotting. Some occasional nausea, still exhausted, and pee all the time.
My progesterone is still in the 120’s as well.
I’ve gotten worried and not sure who to ask.
HCG |Date |Test time |Doubling time| 2 Day % Increase
First HCG 10 Days past ovulation = 40.72 | 1-Apr | 9:00 | (10DPO and 5DPT)
739 |7-Apr |9:00 |34.40 hrs |162.00%
1326| 9-Apr |9:00 |56.91 Hrs | 79.40%
3291|12-Apr|12:00 |57.19 Hrs |78.90%
5783| 15-Apr| 10:00 | 86 Hrs | 47.20%
Unfortunately, an US at 6-7 weeks is needed. You will have to be a littl;e patient!
Good luck and G-d bless!
Geoff Sher
Hello Dr. Sher,
I have an embryo 323 BL, 44xx Aneuploid mosaic -4 mosaic,-16 mosaic. Is this one I should stay clear of transferring because although it is mosaic is it 44 chromosomes? I do not understand what this means exactly.
Also, I recently miscarried due to subchorionic hemorrhage at 7 weeks. I was on lovenox and low dose aspirin, I have mthfr. My last successful pregnancy I also had a significant subchorionic bleed but it resolved. What should be done to minimize this risk next time?
I would transfer the “mosaic” embryo.
AS for the SCH, it is my opinion that you need to be evaluated for an implantation dysfunction before undergoing another ET.
Implantation dysfunction is unfortunately often overlooked as an important cause of IVF failure. In the pursuit of optimizing outcome with IVF, the clinician has a profound responsibility to meticulously assess and address this important issue if IVF success is to be optimized. This is especially relevant in cases of “unexplained IVF failure, Recurrent Pregnancy Loss (RPL) and in women suspected of having underlying anatomical and immunologic factors. Doing so will not only maximize the chance of a viable pregnancy but enhancing placentation, will at the same time promote the noble objective of optimizing the quality of life after birth.”
IVF success rates have been improving over the last decade. The average live birth rate per embryo transfer in the U.S.A for women under 40y using their own eggs , is currently better than 1:3 women. However, there is still a wide variation from program to program for IVF live birth rates, ranging from 20% to near 50%. Based upon these statistics, the majority of women undergoing IVF in the United States require two or more attempts to have a baby. IVF practitioners in the United States commonly attribute the wide dichotomy in IVF success rates to variability in expertise of the various embryology laboratories. This is far from accurate. In fact, other factors such as wide variations in patient selection and the failure to develop individualized protocols for ovarian stimulation or to address those infective, anatomical and immunologic factors that influence embryo implantation are at least equally important.
About 80% of IVF failures are due to “embryo incompetency” that is largely due to an irregular quota of chromosomes (aneuploidy) which is usually related to advancing age of the woman and is further influenced by other factors such as the protocol selected for ovarian stimulation, diminished ovarian reserve (DOR)m and severe male factor infertility. However in about 20% of dysfunctional cases embryo implantation is the cause of failure.
Anatomical Endo-uterine Lesions: This blog article will focus on implantation dysfunction and IVF failure due to:
•Anatomical abnormalities in the uterine cavity (e.g. scarring, polyps and encroaching fibroid tumors)
•A thin endometrial lining
•Immunologic rejection of the embryos
Several studies performed both in the United States and abroad have confirmed that a dye X-Ray or hysterosalpingogram (HSG) will fail to identify small endouterine surface lesions in >20% of cases. This is significant because even small uterine lesions have the potential to adversely affect implantation. Hysteroscopy is the traditional method for evaluating the integrity of the uterine cavity in preparation for IVF. It also permits resection of most uterine surface lesions, such as submucous uterine fibroids (myomas), intrauterine adhesions and endometrial or placental polyps. All of these can interfere with implantation by producing a local “inflammatory- type” response similar in nature to that which is caused by an intrauterine contraceptive device. Hysterosonography (syn; HSN/ saline ultrasound examination) and hysteroscopy have all but supplanted HSG to assess the uterine cavity in preparation for IVF. HSN which is less invasive and far less expensive than is than hysteroscopy involves a small amount of a sterile saline solution is injected into the uterine cavity, whereupon a vaginal ultrasound examination is performed to assess the contour of the uterine cavity.
Endometrial Thickness: As far back as in 1989 I first reported on the finding that ultrasound assessment of the late proliferative phase endometrium following ovarian stimulation in preparation for IVF, permits better identification of those candidates who are least likely to conceive. We noted that the ideal thickness of the endometrium at the time of ovulation or egg retrieval is >9 mm and that a thickness of less than 8 mm bodes poorly for a successful outcome following IVF.
Then in 1993, I demonstrated that sildenafil (Viagra) introduced into the vagina prior to hCG administration can improve endometrial growth in many women with poor endometrial development. Viagra’s mechanism of action is improvement in uterine blood flow with improved estrogen delivery…thereby enhancing endometrial development.
Immunologic factors: These also play a role in IVF failure. Some women develop antibodies to components of their own cells. This “autoimmune” process involves the production of antiphospholipid, antithyroid, and/or anti-ovarian antibodies – all of which may be associated with activation of Natural Killer (NK) cells in the uterine lining. Activated NK cells (NKa) release certain cytokines (TH-I) that if present in excess, often damage the trophoblast (the embryo’s root system) resulting in immunologic implantation dysfunction (IID). This can manifest as “infertility” or as early miscarriages). In other cases (though less common), the problem is due to “alloimmune” dysfunction. Here the genetic contribution by the male partner renders the embryo “too similar” to the mother. This in turn activates NK cells leading to implantation dysfunction. These IID’s are treated using combinations of medications such as heparin, Clexane, Lovenox, corticosteroids and intralipid (IL).
I strongly recommend that you visit http://www.SherIVF.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.
•A Fresh Look at the Indications for IVF
•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.
•Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
•IVF and the use of Supplementary Human Growth Hormone (HGH) : Is it Worth Trying and who needs it?
•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
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•IVF: Approach to Selecting the Best Embryos for Transfer to the Uterus.
•Fresh versus Frozen Embryo Transfers (FET) Enhance IVF Outcome
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•Genetically Testing Embryos for IVF
•Staggered IVF
•Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
•Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
•IVF: Selecting the Best Quality Embryos to Transfer
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
•PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
•Endometrial Receptivity Array (ERA): Is There an actual “There, There”?
•IVF Failure and Implantation Dysfunction:
•Diagnosing and Treating Immunologic Implantation Dysfunction (IID)
•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
•A Thin Uterine Lining: Vaginal Viagra is Often the Answer (update)
•Cervical Ureaplasma Urealyticum Infection: How can it Affect IUI/IVF Outcome?
•The Role of Nutritional Supplements in Preparing for IVF
•The Basic Infertility Work-Up
•Defining and Addressing an Abnormal Luteal Phase
•Male Factor Infertility
•Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in Favor
•Hormonal Treatment of Male Infertility
•Hormonal Treatment of Male Infertility
•Antisperm Antibodies, Infertility and the Role of IVF with Intracytoplasmic Sperm Injection (ICSI)
•Endometriosis and Infertily
•Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF
•Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
•Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
•Early -Endometriosis-related Infertility: Ovulation Induction (with or without Intrauterine Insemination) and Reproductive Surgery Versus IVF
•Deciding Between Intrauterine Insemination (IUI) and In Vitro Fertilization (IVF).
•Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & Con’s!IUI-Reflecting upon its Use and Misuse: Time for a Serious “Reality Check
•Mode of Action, Indications, Benefits, Limitations and Contraindications for its ue
•Clomiphene Induction of Ovulation: Its Use and Misuse!
ADDENDUM: PLEASE READ!!
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If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).
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Geoff Sher
Hi Dr.Sher
I had very very slight brown spotting on Saturday the 17th of April and was sent for a scan.I had a transvaginal scan.A gestitional sac was visible however no yolk sac was visible.I thought I was 5wk+6 days according to first day of last period.Doctor was not very helpful.Said he couldn’t give me an answer either way.That my dates may be wrong or just to early to see anything. He said I would to have my hcg levels taken over 48 hours and another scan in 7 days.First bloods came back reading 1080.Does not seeing a yolk sac at this stage mean a blighted ovium/non viable pregnancy?Thank you in advance.
Hi Dr. Sher,
Thank you for answering my questions.
1) I had a successful FET in 2019 of a pgs-tested embryo and now a failed FET of a pgs-tested embryo. My clinic recommends straight doing an ERA since they believe that I was lucky last time it somehow worked. I am wondering if it makes sense to try again without ERA in the sense of that this time we were unlucky.
What do you recommend?
2) My doc puts me on Lupron Depot 2 months before FET because of suspected Endometriosis. Should I be on Lupron Depot as well before ERA to have kind of the same conditions?
If yes, I would have 8 months between 2 FETS which is is a crazy wait. What are your insights?
Thanks
Perhaps we should talk Miriam. I do not personally advocate ERA and here is why:
The blastocyst and the endometrium are in a constant state of cross-talk. In order for successful implantation to take place, the blastocyst must be at the appropriate stage of development, and needs to signal a well synchronized endometrium to ‘accept it”. This dialogue between embryo and endometrium involves growth factors, cytokines, immunologic accommodations, cell adhesion molecules, and transcription factors. These are all mostly genetically driven but are also heavily influenced by numerous physiologic, pathophysiologic, hormonal and molecular mechanisms capable of profoundly affecting the receptivity of the secretory endometrium to the overtures made by the embryo, to implant.
Embryo implantation takes place 6-9 days after ovulation. This period is commonly referred to as the “window of implantation (WOI)”. In the past it was believed that as long as the embryo reached the uterus in this 4 day time frame, its chance of implanting would not be affected.
In 2013, after evaluating 238 genes in the secretory endometrium and applying bioformatics, Ruiz-Alonzo, et all introduced the Endometrial Receptivity Array (ERA) . Using this test, they categorized mid-secretory endometria into 4 categories: “a) proliferative, b) pre-receptive, c) receptive or d) post-receptive”. They claimed that women with pre-receptive or post-receptive endometria were more likely to experience failed implantation post-embryo transfer (ET).
It was in large part this research which suggested that the concept of a relatively “wide” (4day) WOI, was flawed, that an optimal WOI is likely much narrower and could be a critical factor in determining the success or failure of implantation post-ET. Ruiz-Alonzo also reported that about 25% of women with recurrent IVF failure (RIF), have pre, or post-receptive endometria. They presented data suggesting that viable IVF pregnancy rates could be enhanced,
by deferring FET by about 24 hours in women who had pre-receptive endometria and bringing ET forward by the same amount of time, in women with post-receptive endometria,
There is no doubt that ERA testing has opened the door to an intriguing arena for research. Presently however, available data is inconclusive. Here, following recent studies are 2 dissenting opinions regarding the value for ERA:
•Basil and Casper (2018) state: “Performing the ERA test in a mock cycle prior to a FET does not seem to improve the ongoing pregnancy rate in good prognosis patients. Further large prospective studies are needed to elucidate the role of ERA testing in both good prognosis patients and in patients with recurrent implantation failure”
•Churchill and Comstock (2017) conclude:” In our preliminary observations, the non-receptive ERA group had similar live birth rates compared to the receptive ERA group. It appears the majority of the pregnancies conceived in the non-receptive group occurred during ovulatory cycles and thus a non-receptive ERA in a medicated cycle likely does not have prognostic value for ovulatory cycles. Larger studies are needed to assess the prognostic value of ERA testing in the gen-eral infertility population.”
There are additional negatives that relate to the considerable emotional and financial cost of doing ERA testing:
1.First, the process costs $600-$1000 to undertake
2., Second, it requires that the patient undergo egg retrieval, vitrify (cryobank) all blastocysts, res for 1 or more cycles to allow their hormonal equilibrium to restore, do an ERA biopsy to determine the synchronicity of the endometrium, wait a few weeks for the results of the test and thereupon engage in undertaking an additional natural or hormonal preparation cycle for timed FET. This represents a significant time lapse, emotional cost and additional expense.
Presently, ERA testing is only advocated for women who have experienced several IVF failures. However, some authorities are beginning to advocate that it become routine for women undergoing all IVF.
The additional financial cost inherent in the performance of the ERA test ($600-$1000), the considerable time delay in getting results, the fact that awaiting results of testing and preparing the patient for FET, of necessity extends the completion of the IVF/ET process by at least a few months, all serve to increase the emotional and financial hardship confronting patients undergoing ERA. Such considerations, coupled with the current absence of conclusive data that confirm efficacy, are arguments against the widespread use of ERA . In my opinion, ERA testing should presently be considered as being one additional diagnostic and be confined to women with “unexplained” RIF.
Gold standard statistical analyses require that all confounding variables be controlled while examining the effect of altering the one under assessment. There is an obvious interplay of numerous, ever changing variables involved in outcome following ET, e.g. embryo competency, anatomical configuration of the uterus and the contour of the endometrial cavity, endometrial thickness, immunologic and molecular factors as well as the very important effect of technical skill/expertise in performing the ET procedure …(to mention but a few). It follows that it is virtually impossible to draw reliable conclusions from IVF-related randomized controlled studies that use outcome as the end-point. This applies equally to results reported following “ gold standard” testing on the efficacy of ERA and, is one of the main reasons why I question the reliability of reported data (positive or negative).
The fact is that IVF (and related technologies) constitute neither a “pure science” nor a “pure art”. Rather they represent an “art-science blend”, where scientific principles applied to longitudinal experience and technical expertise coalesce to produce a biomedical product that will invariably differ (to a greater or lesser degree) from one set of clinical circumstances to another.
Since, the ultimate goal of applied Assisted Reproductive Medicine is to safely achieve the birth of a viable and healthy baby, the tools we apply, that are aimed at achieving this end-point, are honed through the adaptation of scientific principles and concepts, experience and expertise, examined and tested longitudinally over time. Needless to say, the entire IVF/ET process is of necessity subject to change and adaptation as new scientific and technical developments emerge.
This absolutely applies to the ERA as well!
Geoff Sher
702-533-2691
Hi Dr sher,
I have Dor and want to transfer day 5 blast of my own egg embryo
Day 3 of donor egg + husbands sperm
Day 5 donor embryo.
Is this possible. My RE says the embryos must be same day.
Thank you
In my opinion, the blastocysts (day 5 and Day 6) could be transferred together by FET on the 6th day post progesterone initiation.
Geoff Sher
I have a history of 2 ectopic. I lonely have 1 fallopian tube which we thought was closed off after last ectopic 2 years ago. I surprisingly tested positive. My hcg at 13dpo was 167 and at 15 dpo it was 421. Could this one be another ectopic. I am scheduled for an ultrasound late next week.
The risk of another ectopic is about 1:6.
Good luck!
Geoff Sher