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.
Dear Dr Sher
Despite almost undetectable AMH levels (1.5pmol/l) at the age of 34, I got a magnificent 17 eggs and 5 blasts, of which one AA blast was transferred and 4 frozen.
I was overjoyed when I got a positive pregnancy test, saw a heartbeat at 7+1, and again at 8+5, however very sadly at my 10w scan last week we discovered I had suffered a missed miscarriage, as the baby measured 9+3 with no fetal heartbeat
I had a D&C and the products of conception have been sent for histological and cytogenetic testing, which will hopefully give us an indication whether the miscarriage was due to the seed or the soil.
I am awaiting results of immune testing (Immunophenotyping,NK cytotoxicity assay & Th1/Th2 cytokine ratio), however we plan to treat empirically for immunes with prednisolone, intralipids & clexane to cover our bases in any case
With the benefit of hindsight I wish we had gone for PGS (my clinic CARE in London has an established genetics programme), however we were advised that at 34, they did not recommend PGS testing for a first cycle.
We have 4 blasts on ice, but I would like to have another crack at fresh cycles, embryo banking with the intention of PGS testing to ensure we only transfer a competent embryo. My clinic does array CGH on day 5 blastocysts, with transfer taking place in a subsequent FET cycle
How many blastocysts would you recommend a 34 year old should stockpile, to make PGS testing worthwhile?
We would like to have 2 children – whilst also bearing in mind we do still have 4 frozen blasts to make use of at a later date. The are however untested, and to thaw / biopsy / freeze / thaw would presumably put tremendous strain on the embryos.
Any thoughts you may have on how many blasts we should be aiming to bank would be very gratefully appreciated
Many thanks in advance
Katy
Clearly the AMH result was in error. I think at your age, about 6 blastocysts is a good number to bank.
Good luck!
Geoff Sher
Hi Dr. Sher,
One more question… What are your thoughts on Wobenzym N during pregnancy? I was taking it up until pregnancy, but stopped before transfer because I knew I would also be on prednisone. Now that I will be tapering off prednisone completely, would it be reasonable to take the Wobenzym N to help keep my inflammation under control? Is there any harm in this? Thank you, again so much!
Michelle
Sorry…I am not familiar with this.
Geoff Sher
About seventeen years ago, after reporting on the benefit of vaginal Sildenafil (Viagra) for to women who had implantation dysfunction due to thin endometrial linings I was proud to announce the birth of the world’s first “Viagra baby.” For those of you who aren’t familiar with the use of Viagra in IVF, allow me to provide some context.
It was as far back as 1989, when I first published a study that examined the correlation between the thickness of a woman’s uterine lining (the endometrium), and the subsequent successful implantation of embryos in IVF patients. This study revealed that when the uterine lining measured <8mm in thickness by the day of the “hCG trigger” (in fresh IVF cycles), or at the time of initiating progesterone therapy (in embryo recipient cycles, e.g. frozen embryo transfers, egg donation-IVF etc.) , pregnancy and birth rates were substantially improved. Currently, it is my opinion, that an ideal estrogen-promoted endometrial lining should ideally measure at least 9mm in thickness and that an endometrial lining measuring 8-9mm is “intermediate”. An estrogenic lining of <8mm is in most cases unlikely to yield a viable pregnancy.
A “poor” uterine lining is usually the result of the innermost layer of endometrium (the basal or germinal endometrium from which endometrium grows) ) not being able to respond to estrogen by propagating an outer, “functional” layer thick enough to support optimal embryo implantation and development of a healthy placenta (placentation). The “functional” layer ultimately comprises 2/3 of the full endometrial thickness and is the layer that sheds with menstruation in the event that no pregnancy occurs.
The main causes of a “poor” uterine lining are:
1.Damage to the basal endometrium as a result of:
a.Inflammation of the endometrium (endometritis) most commonly resulting from infected products left over following abortion, miscarriage or birth
b.Surgical trauma due to traumatic uterine scraping, (i.e. due to an over-aggressive D & C)
2.Insensitivity of the basal endometrium to estrogen due to:
a.Prolonged , over-use/misuse of clomiphene citrate
b.Prenatal exposure to diethylstilbestrol (DES). This is a drug that was given to pregnant women in the 1960’s to help prevent miscarriage
3.Over-exposure of the uterine lining to ovarian male hormones (mainly testosterone): Older women, women with diminished ovarian reserve (poor responders) and women with polycystic ovarian syndrome -PCOS tend to have raised LH biological activity.. This causes the connective tissue in the ovary (stroma/theca) to overproduce testosterone. The effect can be further exaggerated when certain methods for ovarian stimulation such as agonist (Lupron/Buserelin) “flare” protocols and high dosages of menotropins such as Menopur are used in such cases.
4.Reduced blood flow to the basal endometrium:
Examples include;
a.Multiple uterine fibroids - especially when these are present under the endometrium (submucosal)
b.Uterine adenomyosis (excessive, abnormal invasion of the uterine muscle by endometrial glands).
“The Viagra Connection”
Treatments such supplementary estrogen therapy, aspirin administration and/or administration of high dosage gonadotropin fertility drugs, aimed at improving endometrial development have all yielded disappointing results.
It was in the 90’s that Sildenafil (brand named Viagra) was gaining popularity as a treatment for erectile dysfunction. The mechanism by which it acted was through increasing penile blood flow through increasing nitric oxide activity. This prompted me to investigate whether Viagra administered vaginally, might similarly improve uterine blood flow and in the process cause more estrogen to be delivered to the basal endometrium and thereby increase endometrial thickening. We found that when Viagra was administered vaginally it did just that! However oral administration was without any significant benefit in this regard. We enlisted the services of a compound pharmacy to produce vaginal Viagra suppositories. Initially, four (4) women with chronic histories of poor endometrial development and failure to conceive following several advanced fertility treatments were evaluated for a period of 4-6 weeks and then underwent IVF with concomitant Viagra therapy. Viagra suppositories were administered four times daily for 8-11 days and were discontinued 5-7 days prior to embryo transfer in all cases.
Our findings clearly demonstrated that vaginal Viagra produced a rapid and profound improvement in uterine blood flow and that was followed by enhanced endometrial development in all four cases. Three (3) of the four women subsequently conceived. . I expanded the trial in 2002 and became the first to report on the administration of vaginal Viagra to 105 women with repeated IVF failure due to persistently thin endometrial linings. All of the women had experienced at least two (2) prior IVF failures attributed to intractably thin uterine linings. About 70% of these women responded to treatment with Viagra suppositories with a marked improvement in endometrial thickness. Forty five percent (45%) achieved live births following a single cycle of IVF treatment with Viagra The miscarriage rate was 9%. None of the women who had failed to show an improvement in endometrial thickness following Viagra treatment achieved viable pregnancies.
Following vaginal administration, Viagra is rapidly absorbed and quickly reaches the uterine blood system in high concentrations. Thereupon it dilutes out as it is absorbed into the systemic circulation. This probably explains why treatment is virtually devoid of systemic side effects
Since the introduction of this form of treatment, thousands of women with thin uterine linings have been reported treated and many have gone on to have babies after repeated prior IVF failure.
It is important to recognize that Viagra will NOT be effective in improving endometrial thickness in all cases. In fact, about one third of women treated fail to show any improvement. This is because in certain cases of thin uterine linings, the basal endometrium will have been permanently damaged and left unresponsive to estrogen. This happens in cases of severe endometrial damage due mainly to post-pregnancy endometritis (inflammation), chronic granulomatous inflammation due to uterine tuberculosis (hardly ever seen in the United States) and following extensive surgical injury to the basal endometrium (as sometimes occurs following over-zealous D&C’s).
To be effective, Viagra must be administered vaginally. It is NOT effective when taken orally. We prescribe 20mg vaginal suppositories to be inserted four times per day. Treatment is commenced soon after menstruation ceases and is continued until the day of the “hCG trigger.” While ideally the treatment should be sustained throughout the first half of the cycle, most women will respond within 48-72 hours. For this reason, Viagra can be used to “rescue” a poor lining after the cycle has already started, provided that there is enough time remaining prior to ovulation, egg retrieval or progesterone administration.
Please visit my new 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
•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)
•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?
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
•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
•Measuring and Interpreting Blood hCG to Assess Pregnancy Viability Following ART Treatments.
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
.
Thank you so much! Can you please remove my last name from my post? I included it inadvertently as it was autofilled. Thank you!
Hi Dr. Sher, thank you for having such an informative website and blog. My husband (34) and I (32) have been trying to conceive for 23 cycles now, with no luck. I have high fsh (from 10 to as high as 14, I believe), and my husband has borderline morphology (5% normal). We’ve done 3 IUIs with clomid (1 at 100mg dose and 2 at 50mg dose, each time I made 2-4 follicles). I dominantly produce eggs from my right ovary almost exclusively. HSG was completely normal. We also did an IVF with injectables (no downreg before) and I only produced 4 retrievable eggs: 2 over mature, 1 under mature and one that fertilized with ICSI. After 24 hours it stopped dividing and was never transferred. It’s been 6 months since our last round and we’re hoping to do IVF again. We live in the Middle East so we only have one fertility clinic- but the meds are subsidized and much cheaper, so the IVF is much more affordable (a definite positive!).
I am currently taking DHEA, flaxseed oil, CoQ10 and prenatals in preparation for the next IVF.
As such a poor responder to stims, do you think I could do an IVF with clomid only? Or another alternative to the injectables? Are you available for a consult with my RE here to provide your expertise? We know we are short on time and each failure is heartbreaking. Thank you so much in advance for your help!
Unfortunately, I cannot be involved in your cycle with another doctor. However, it sounds as if you have diminished ovarian reserve (DOR). If so…you should in my opinion not be using clomiphene (see below). I would also stay away from DHEA which in women with DOR can be harmful to egg development and embryo quality (see below).
If it were up to me, I would probably use 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.
Please visit my new 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
•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)
•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?
•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 Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Implications of “Empty Follicle Syndrome and “Premature Luteinization”
•Premature Luteinization (“the premature LH surge): Why it Happens and how it can be Prevented.
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
Dr. Sher,
I am just over 15 weeks pregnant with girl/girl twins after our first IVF (frozen) transfer with genetic testing. I have Raynaud’s phenomenon, I am hypothyroid, borderline PCOS and have had a positive ANA and 2 clinical miscarriages of chromosomally normal males (at around 6 1/2 weeks). I am currently taking synthroid 112mcg, Metformin 1000mg, Lovenox 40mg, low dose aspirin, Vitamin D, Calcium, fish oil, prenatal, Metanx, 10mg prednisone BID, claritin, Pepcid 20mg BID and Benadryl at bedtime (antihistamine protocol and I also have allergies so I have stayed on it). I was also on estrogen and progesterone until 12 1/2 weeks. I am worried to stop anything. My endocrinologist suggested tapering off the prednisone very slowly, soon. Would it hurt the babies to stay on a low dose of prednisone until atleast the end of the 2nd trimester or the whole pregnancy, like 5-10 mg daily? I just want to do what’s best for the babies. Thank you,
Michelle
Congratulations to both you and your obviously competent RE…Well done!!
I would taper the prednisone down and stop. Steroids taken in the 2nd and third trimesters can in my opinion be potentially risky for the babies.
Good luck!
Geoff Sher
I just wanted to add, my fear is if I stop the prednisone completely that my body could harm the babies. Is here a point in the pregnancy where the babies can protect themselves and if so, when? What is your suggestion with tapering and when? With my last miscarriage (Dec 2014) I was on Lovenox and low dose aspirin, the prednisone 20mg is the main new medication.
Thank you, again! 🙂
Michelle