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, thank you for all that you do in sharing your fertility knowledge. I have learned a lot from your articles and questions/comments. I was also hoping to get your advice:
I am 32 almost 33 and my fiance is 27. We just got engaged and are ready to start building our family. I was thinking about freezing eggs so i have “backup insurance” for myself before trying to conceive naturally. But my initial consultation on day 6 showed: AFC 7, AMH .98, FSH 9, LH 2.8, estradiol 38, normal trilaminar endometrium. The clinic advised that my numbers were too low for egg freezing and to only do embryos, especially given that we want 3-5 kids.
I have had consults with 2 local REIs. Protocol from REI 1: estrogen and HGH priming. clomid 100 mg, gonal 150 + menopur 150 + cetrotide 250, hcg trigger 10k (Pregnyl / Novarel / Chorionic Gonadotropin). Protocol from REI 2: estrogen priming (no HGH), 300 gonal + 150 menopur + dexamethasone + cetrotide, dual trigger Lup4/hCG10K. One recommended PGTA testing and the other did not.
1) What protocol would you advise for me?
2) What do you think of specific variations with the following: estrogen priming, HGH priming, Clomid 100, and dexamethasone?
3) Do you recommend PGTA testing?
4) What do you think for eggs vs embryos?
5) How many embryos should we aim to bank given our family size goals, and how many rounds do you think it will take to get there? Trying to prepare financially, mentally, and emotionally.
Thank you!
Indeed, using PGS tested embryos derived from your eggs would be preferable. However, if you have a desire to bank your own eggs for future dispensation, I do not see why this cannot be done, provided that:
a) you do not delay unduly, since you need to try to make hay while the sun still shines,
b) you are willing to undergo multiple harvests aimed at banking around 15 mature (MII) eggs and,
c) an individualized protocol is used for ovarian stimulation. I am not in favor of the suggested protocol where clomiphene or Letrozole is used and a 250mcg dosage of hCGr (Ovidrel) is proposed as a “trigger”)…see below.
You do have early onset diminished ovarian reserve however, it is largely age, rather than ovarian reserve that impacts egg quality, provided that an optimal protocol for ovarian stimulation is used given your young age, 2 out of every 3 eggs harvested should still be chromosomally normal….and it is egg , (rather than sperm competency) that is most important. (see below). .
It is primarily the egg (rather than the sperm) that determines the chromosomal integrity (karyotype) of the embryo, the most important determinant of egg/embryo competency”. A “competent” egg is therefore one that has a normal karyotype and has the best potential to propagate a “competent” embryo. In turn, a “competent embryo is one that possesses the highest potential to implant and develop into a normal, healthy, baby.
When it comes to reproductive performance, humans are the least efficient of all mammals. Even in young women under 35y, at best only 1 out of 2 eggs are chromosomally numerically normal (euploid). The remained have an irregular number of chromosomes (aneuploid) and are thus “incompetent”. The incidence of egg aneuploidy increases with age such by age 39 years, 3 in 4 are competent, and by the mid-forties, less 8 to 9 out of 10 are aneuploid. The fertilization of an aneuploid egg will inevitably lead to embryo aneuploid and an aneuploid embryo cannot propagate a normal pregnancy
Within hours of the spontaneous pre-ovulatory luteinizing hormone (LH) surge, and also following administration of the human chorionic gonadotropin (hCG) “trigger” shot (given to induce ovulation after ovarian stimulation with fertility drugs), the egg embarks on a rapid maturational process that involves halving of its 46 chromosomes to 23. During this process, (known as meiosis) 23 chromosomes are retained within the nucleus of the egg while the remaining (now redundant) 23are expelled, enveloped by a thin membrane. This small structure comes to lie immediately below the “shell” of the egg (the zona pellucida) and is known as the 1st polar body or PB-1. The spermatozoon, in the process of its maturation also undergoes meiosis at which time it too reduces its chromosomes by half. Thus in the process of fertilization the sperm divides into two separate functional gametes, each containing 23 chromosomes such that with subsequent fertilization, the 23 chromosomes in the egg, fuse with the 23 chromosomes of the mature sperm resulting in the development of an embryo that has 46 chromosomes (the normal human genome) comprising a combination of the genetic material from both partners. For the embryo to have exactly 46 chromosomes (the euploid number), both the mature egg and mature spermatozoon must contain exactly 23 chromosomes. Only euploid embryos are “competent” (capable of developing into healthy babies). Those with an irregular number of chromosomes (aneuploid embryos) are “incompetent” and are incapable of developing into healthy babies. While embryo “incompetence” can result from either egg or sperm aneuploidy, it usually stems from egg aneuploidy. However, in cases of moderate or severe male factor infertility, the sperm’s contribution to aneuploidy of the embryo increases significantly.
While embryo ploidy (numerical chromosomal integrity) is not the only determinant of its “competency, it is by far the most important and in fact is rate-limiting factor in human reproduction. It is causal in most cases of “failed implantation” which in turn is responsible for most cases of failed IVF. It causes early miscarriages and is responsible for many chromosomal birth defects such as X-monosomy and Down’s syndrome. . In most cases, embryos that develop too slowly as well as those that grow too fast (i.e. ones that by day 3 post-fertilization comprise fewer than 6 cells or more than 9 cells) and/or embryos that contain a large amount of cell debris or “fragments” are usually aneuploid and are thus “incompetent”. Additionally, embryos that fail to survive in culture to the blastocyst stage are also almost always aneuploid/”incompetent”. At a certain point in the later stage of a woman’s reproductive career, the number of remaining eggs in her ovaries falls below a certain threshold, upon which she is unable to respond optimally to fertility drugs. Often times this is signaled by a rising day 3 blood follicle stimulating hormone (FSH) level. Such women with diminishing ovarian reserve produce fewer eggs in response to ovarian stimulation. While diminished ovarian reserve is most commonly encountered in women over 40 years of age it can and indeed sometimes does occur in much younger women. A few important (but often overlooked concepts should be considered in this regard: 1. Age: It is advancing chronologic age and NOT declining ovarian reserve (as evidenced by abnormal blood AMH or FSH that results in an increased incidence of egg/embryo “incompetence” due to aneuploidy 2. DOR: The ovaries and developing eggs of women with diminished ovarian reserve (regardless of age) are highly susceptible to the adverse effect of excessive Luteinizing Hormone (LH)-induced overproduction of male hormones (mainly testosterone). A little testosterone produced by the ovary promotes normal follicle growth and orderly egg development but too much testosterone has the opposite effect. That is why (especially in women with diminished ovarian reserve who often have high LH and increased ovarian testosterone production , the use of ovarian stimulation protocols that fail to down-regulate LH production prior to initiating stimulation with gonadotropins, often prejudices egg/embryo quality and IVF outcome. Simply stated, while age is certainly the most important factor in determining the incidence of egg/embryo aneuploidy, women with diminished ovarian reserve (regardless of their age), unless they receive customized/individualized protocols of ovarian stimulation are less likely to propagate euploid (competent) eggs/embryos.
Selection of the ideal protocol for controlled ovarian stimulation: While NOTHING can be done to lower the incidence of age related aneuploidy, it is indeed possible to avoid a further increase in egg/embryo aneuploidy by individualizing the protocols of ovarian stimulation used.
•My preferred protocols for women who have relatively normal ovarian reserve:
a)The conventional long pituitary down regulation protocol: BCP are commenced early in the cycle and continued for at least 10 days. Starting 3 days before the BCP is to be discontinued, it is overlapped with an agonist such as Lupron 10U daily for three (3) days and continued until menstruation begins (which should ensue within 5-7 days of stopping the BCP). At that point an US examination is done along with a baseline measurement of blood estradiol to exclude a functional ovarian cyst. Simultaneously, the Lupron dosage is reduced to 5U daily and an FSH-dominant gonadotropin such as Follistim, Puregon or Gonal-f daily is commenced for 2 days. On the 3rd day the gonadotropin dosage is reduced and a small amount of daily menotropin (Menopur 75U daily) is added. Daily ultrasound and blood estradiol measurements are done starting on the 7th or 8th day of gonadotropin administration and continued until daily ultrasound follicle assessments indicate that most follicles have fully developed. At this point egg maturation is “triggered” using an intramuscular injection of 10,000U hCG. And an egg retrieval is scheduled for 36h later.
b)The agonist/antagonist conversion protocol (A/ACOP): This is essentially the same as the conventional long down regulation protocol (as above), except that with the onset of post-BCP menstruation, the agonist is supplanted by daily administration of a GnRH antagonist (e.g. Ganirelix, Cetrotide or Orgalutron) at a dosage of 125mcg daily until the day of the hCG trigger
•My preferred protocol for women who have relatively diminished ovarian reserve (DOR):
When it comes to women who have DOR I favor the use of the A/ACP, adding supplementary human growth hormone (HGH). In some cases where the DOR is regarded as severe, I also augment the process with estrogen priming, preferring twice weekly intramuscular administration of estradiol valerate (Delestrogen), starting with the commencement of antagonist injection and continuing for 1 week before commencing gonadotropins and continued until the hCG “trigger. I further recommend that such women be offered access to preimplantation genetic screening (PGS) for4 embryo selection and in some cases, for embryo banking (stockpiling). This is followed in a later hormone replacement cycle with the selective transfer of up to two (2) PGS-normal, euploid blastocysts. In this way we are able to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” , significantly enhancing the opportunity to achieve a viable pregnancy
•The following Ovarian stimulation protocols are in my opinion best avoided in women with DOR:
a)Microdose agonist (e.g. Lupron) “flare” protocols
b)High doses of LH/hCG-containing fertility drugs (E.G. Menopur).
c)Protocols that incorporate supplementation with male hormones (e.g. testosterone)
d)Supplementation with DHEA
e)Clomiphene citrate or Letrozole which cause an elevation in LH and thus increase ovarian male hormone (testosterone and androstenedione output.
f)“Triggering” egg maturation using too low a dosage of hCG (e.g. 5,000U rather than 10,000U) or Ovidrel e.g. 250mcg of Ovidrel rather than 500mcg)
g)“Triggering” women who have large numbers of follicles using an agonist such as Lupron, Superfact or Buserelin.
•Preimplantation Genetic Screening (PGS):
The introduction of preimplantation genetic screening (PGS) for the first time permits identification of all the chromosomes in the egg and embryo such that we can now far better identify “competent” (euploid) embryos for selective transfer to the uterus. This vastly improves the efficiency and success of the IVF process. This additional tool has better equipped us to manage cases with DOR. In my opinion, next generation gene sequencing (NGS), currently represents the most reliable method for performing PGS
Please visit my Blog on this very site, http://www.DrGeoffreySherIVF.com, 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
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
•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.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
•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
•Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
•Preimplantation Genetic Testing (PGS) in IVF: It Should be Used Selectively and NOT be Routine.
•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
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•Traveling for IVF from Out of State/Country–
•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
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
•IVF Egg Donation: A Comprehensive Overview
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ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.
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).
PLEASE SPREAD THE WORD ABOUT SFS!
Geoff Sher
Hello,
My wife and I have been trying to conceive for 2.5 years – 27 natural cycles and 2 IVF cycles. We have never had a positive pregnancy test result in this time. I am now 37.5 and she is 30.5.
My sperm analysis, DNA fragmentation, male hormone test and reactive oxygen species (MiOXSYS) results are all within the fertile range, also have had testicular ultrasound which was fine. My wife has had a HyCoSy test (both tubes are clear), at least 3 baseline ultrasounds (good endometrial lining thickness and antral follicle count noted) , AMH test (13.3 pmol/L, approximately 25th percentile for her age), detailed thyroid assessment (no anti thyroid antibodies, TSH was 3.42 at last blood test so bit high), regular ovulation tests using clear blue monitor to confirm she ovulate each month, FSH of 8.1 IU/L and LH of 4.2 IU/L on day 3, oestradiol of 451 pmol/L and progesterone of 47.5 nmol/L on day 21, dhea of 5.4 umol/L and testosterone of 1.64 nmol/L, coeliac negative but possibly gluten intolerant, vitamin d and vitamin b12/folate optimal.
In our ivf cycles we have had the following results:
Cycle 1 = long protocol, ovaleap used to stimulate =5 eggs retrieved, 4 eggs fertilised normally, no embryos at >5 cells on day 3 and no blastocysts on day 5 so transfer cancelled. High fragmentation noted at day 3.
Cycle 2 = long protocol, menopur used to stimulate = 10 eggs retrieved, 6 eggs fertilised normally, 1 egg at > 5 cells on day 3 (1 at 8 cells) and 2 at 4 cells, 1 expanded blastocyst on day 5 (very few cells) that was transferred and 1 blastocyst on day 6 (very few cells so not frozen as wouldn’t survive thawing). High fragmentation noted at day 3 in all except 8 cell embryo.
Evidently, while our infertility is unexplained our ivf cycles have indicated a problem with cleavage stage embryo arrest and fragmentation. My wife has had symptoms of endometriosis (painful periods that have led her to seek emergency room attention at times, fatigue, GI issues, light brown spotting from 4-6 days before her period) but has never had a laparoscopy before – we are wondering whether this could be a factor? However from research papers we have seen that endometriosis patients typically have similar day 3/5 embryo quality results but lower clinical pregnancy and live birth rates, ie embryo morphology looks OK but something is affecting quality. In our case embryo morphology doesn’t look good.
Another factor we are thinking of is genetic issues leading to early embryo arrest – a company called Igenomix have a test that checks for this. We are thinking though that since 2 embryos got to blastocyst stage in our 2nd cycle maybe this suggests environmental issues rather than genetic as in papers we have seen on this patients don’t even get to blastocysts stage.
What do you think could be a factor? Given that it is a pre day 3 problem we think it more likely to be on my wife’s side but had to know for sure without using donor eggs and given her age we don’t want to resort to this yet.
There are 2 broad issues to address: The 1st is egg quality which is to a large extent, linked to the protocol,being used for ovarian stimulation. This will n3eed to be reviewed carefully and probably, revised.
The second is the possibility of an anatomical or immunologic implantation dysfunction (IID).
We really should talk. Might I recommend that you contact my assistant, Patti Converse and set up an online consultation with me .
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 15y 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
e.Ureaplasma Urealyticum (UU) Infection of cervical mucous and the endometrial lining of the uterus, can sometimes present as unexplained early pregnancy loss or unexplained failure following intrauterine insemination or IVF. The infection can also occur in the man, (prostatitis) and thus can go back and forth between partners, with sexual intercourse. This is the reason why both partners must be tested and if positive, should be treated contemporaneously.
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?
______________________________________________________
ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.
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).
PLEASE SPREAD THE WORD ABOUT SFS!
Geoff Sher
Hi Dr. Sher, I’m currently 5w2d with my first. I’m considered high risk with my medical history (I’m a type 1 diabetic but VERY well controlled) and my cycles are irregular so I was initially brought in for an early ultrasound to determine gestational age and try to confirm viability. They saw a gestational sac with no yolk sac or fetal pole and said I was measuring at 4w6d, but they did confirm it’s in my uterus & decided they wanted to draw an hcg level which was 3340 that day. 48 hours later they had me come back in for a repeat hcg level and ultrasound. My hcg that day was 4378, which is really only a 30% increase. However, they said that my ultrasound looked perfect for where I’m measuring. Based on the hcg numbers though they told me I was more than likely going to miscarry. At this point they’re sending me home to wait 2 weeks and we’ll do a repeat ultrasound at that time to see if there has been any progression. They told me I can come have my hcg drawn again in 48 hours but that it wouldn’t really be beneficial at this point because they’re pretty certain it’s an impending miscarriage. I’ve had zero pain or bleeding, and my husband and I are absolutely devastated right now. My question is this… based on those numbers and the normal looking ultrasound, do you think there is any possibility at all that this baby could be ok? Do you think it’s worth getting the 3rd hcg drawn? Any insight is appreciated. Thank you in advance!
There is a possibility that all will turn out fine….BUT, I must agree with everything your doctor said and advised!
Sounds like you are in very good hands!
Good luck!
Geoff Sher
My first day of last period was dec 3. 2021. My first positive was 1/3/22. My first hcg was 1/6/22 at 98. The next one was done 1/7/22 came back as 135. I did my third period one on 1/11/22 came back as 663. And my ultrasound showed a gestational sac only. Is this still a viable pregnancy. ? My next US isn’t until feb 8 2022.
It is still early. Do an US at 6-7 weeks for a definitive answer!
Geoff Sher
In your experience, can progesterone suppositories cause bleeding in early pregnancy? I had a frozen IVF transfer in December, got a positive test after the 2ww, and had heavy bleeding at 5.5 weeks and again at 7 weeks. After both, we have seen the heartbeat and “everything looks fine” according to the doctor (who is not a fertility specialist, just an OBGYN). I’m taking 200 mg of progesterone 2 times a day through vaginal suppositories. From what I’ve read online, it sounds like it may be the suppository irritating my cervix and bleeding. Do you think that’s possible or is that a known issue with these kinds of suppositories?
Yes I have on numerous occasions seen significant bleeding resulting from local irritation due to suppositories.
Good luck!
Geoff Sher