Hello,
What are your thoughts about using prednisone and/or prograv for a FET with donor eggs?
– Geoffrey Sher, MD
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Name: Bree M
Hello,
What are your thoughts about using prednisone and/or prograv for a FET with donor eggs?
In my opinion, the administration of low dosage steroids in embryo transfer cycles is always beneficial as it modulates uterine immune receptivity.
Geoff Sher
_________________________________________________________
PLEASE SHARE THIS WITH OTHERS AND HELP SPREAD THE WORD!!
Herewith are online links to 2 E-books recently co-authored with my partner at SFS-NY (Drew Tortoriello MD)……. for your reading pleasure:
I invite you to visit my very recently launched “Podcast”, “HAVE A BABY” on RUMBLE; https://rumble.com/c/c-3304480
If you are interested in having an online consultation with me, please contact my assistant, Patti Converse at 702-533-2691 or email her at concierge@sherivf.com\
Name: Bree M
Hello,
I recently had my first FET ever with a PGT tested normal donor egg embryo. I had such high hopes, but it unfortunately did not stick. When my lining was checked a week before the FET, it was 8.7. Do you think this was still too thin?
For this previous FET I was on 2mg estrace taken orally 3Xday and vaginally 1Xday. For progesterone, I was doing suppositories 2Xday and the PIO shot once per day. I was also taking baby aspirin and low dose naltrexone. I’m 44, normal weight and BMI and in good health. I do have an under active thyroid, but it is controlled with medication.
Do you have any ideas on what I can do differently (if anything) for my next transfer? Or did I just get unlucky in the numbers game this round?
Thanks so much!
Two decades ago, when women went through IVF (in vitro fertilization), they usually had their embryos put in the uterus right after the eggs were collected in the same cycle (known as “Fresh” Embryo Transfer). Freezing embryos at that time was risky, with about 30% not surviving the process, and those that did had lower chances of successfully implanting and growing a healthy pregnancy compared to fresh embryos. This was because the slow freezing process led to ice forming within the embryo’s cells, harming them.
But things changed with a new, faster freezing method called vitrification. With vitrification, embryos are frozen so quickly that ice crystals don’t have a chance to form. More than 90% of embryos survive this process in excellent condition, just like they were before freezing, giving them a better chance to develop into healthy pregnancies.
Modern advancements in frozen embryo transfers (FET) have shown great promise, possibly even surpassing the success rates of transferring “fresh” embryos. This improvement likely isn’t because of the freezing process itself, but rather due to two key factors:
Considering these factors, FET offers several clear advantages:
These advancements provide hope and options for couples seeking successful IVF journeys and healthy outcomes for growing families.
The advent of PGS/PGT heralded a major advance in IVF as it enables us to choose the healthiest embryos for transfer to the uterus, thereby significantly boosting the chances of a successful pregnancy. The performance of PGS/PGTA virtually mandates that advanced embryos ( blastocysts) be biopsied 5-6 days after fertilization and that an additional period of 10 days be allowed for genetic testing to be performed. It follows that such blastocysts be vitrified and stored for FET to be performed in a later cycle.
For women who are older or have a lower number of eggs (diminished ovarian reserve-DOR ), as well as those who have faced repeated pregnancy loss or IVF failure, PGS/ PGT-A can be a game-changer. It helps identify the best embryos for successful transfer. However, for younger women who tend to have normal egg reserves, and because of their youth produce a larger number of quality eggs/ embryos the benefits of PGS might not be necessary.
When it comes to creating a reserve of embryos through “Embryo Banking,” FET is mandatory and ground-breaking. Here, multiple IVF cycles are conducted over an extended period of time allowing for the collection and banking of a good number of advanced ( usually PGS/PGT-A tested) embryos ( blastocysts) for future dispensation. Once we’ve gathered a promising group of such embryos, well-timed FETs can be undertaken, significantly improving the chances of a successful pregnancy and reducing the risk of miscarriage.
Through these advancements, we are able to offer greater hope and possibilities to those on their journey to parenthood, making IVF an even more effective and accessible option.
Let’s break down the process to prepare the uterus for a frozen embryo transfer (FET) in simpler terms:
*Note: In cases where intramuscular progesterone administration is not well tolerated, we tend to use a vaginal gel known as Crinone8%. This gel is used twice a day (morning and evening) until the day of the embryo transfer.
Regime for Thawing and Transferring Cryopreserved Embryos/Blastocysts:
Patients undergoing FET with cryopreserved embryos/ blastocysts will have their embryos thawed and transferred by the following regimen.
Day 2 (P4) | Day 6 (P4) | |
PN | Thaw | ET |
Day 3 Embryo | Thaw | ET |
Blastocysts frozen on day 5 post-ER | Thaw-FET | |
Blastocysts frozen on day 6, post-ER | Thaw-FET |
_________________________________________________________________________________________________
PLEASE SHARE THIS WITH OTHERS AND HELP SPREAD THE WORD!!
Herewith are online links to 2 E-books recently co-authored with my partner at SFS-NY (Drew Tortoriello MD)……. for your reading pleasure:
I invite you to visit my very recently launched “Podcast”, “HAVE A BABY” on RUMBLE; https://rumble.com/c/c-3304480
If you are interested in having an online consultation with me, please contact my assistant, Patti Converse at 702-533-2691 or email her at concierge@sherivf.com\
Name: Sandra W
Dear Dr. Sher, five and a half years ago my husband and I conceived naturally in our first cycle. I gave birth to a healthy baby boy 9 month later. Two years after that we tried to have another child, after six cycles my gyn said I should go to a fertility clinic. I was 37 at that time and I had a low amh of 0,33 but regular menstrual cycles. 1,5 years later, with now 39, I am still within this journey. Summary of treatsments:
1) ICSI: Stimulation with Pergoeris 375 IE from day 3 to 10 -> two follices but no egg retrival
2) Natural ICSI few months later: 0,25mg Clomiphene from day 3 to 8 -> one follicel, 10 cell ambry transfer 3 days after punction, negative
3) Next cycle tried yet again with Clomiphene, same plan: more follicel than usual in both ovaries but no growth or even shrinking. After getting off of Clomiphene eventually one follicel did grow but persisted as my fsh and lh levels were high even due estrogen was high too
3) after pausing for few months we started now with a new stimulation cycle with 150 IE Menopur from day 3. As it looks for now just one follicel is growing and the other ones are not or some of them with smaller size disappear.
I am getting really frustarated with my clinic as they just have two possibilities high or “low” dosage of stimulation. I still have reagulary cycles with ovulation, high endometrium line (before ovulation approx. 9-10 mm, 7 days after ovulation approx. 13 mm), and in normal cycles my eggs will grow till approx. 12 mm and then stop to let the dominate follicle to grow further. But with stimulation starting on day3 everything changes and except the dominant follicel others just stop growing or shrink/disappear. I am always downregulating at day 7, never before that. I do not have much eggs and in most cycles 3-4 are visible on day 2.
Dr. Sher, what could be the reason for my body to react like what could be a better stimulation protocol for someone like me? I know that I will not produce many follicels, but I cannot understand why my body just refuses to accept any stimulation drugs.
Thanks in advance!
Best
Thanks for the inquiry. I think I can help here.
Might I suggest that you contact my assistant Patti Converse at 702-533-2691 and set up an online consultation with me to discuss in depth.
I would need a lot more information but my first thought is that there might be diminished ovarian reserve and if so, you will need a very individualized protocol for ovarian stimulation.
Geoff Sher
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Understanding the impact of age and ovarian reserve on the success of in vitro fertilization (IVF) is crucial when it comes to reproductive health. This article aims to simplify and clarify these concepts, emphasizing their significance in the selection of ovarian stimulation protocols for IVF. By providing you with this information, we hope to shed light on the importance of considering these factors and making informed decisions regarding fertility treatments.
Why IVF should be regarded as treatment of choice for older women an those who have diminished ovarian reserve ( DOR):
Understanding the following factors will go a long way in helping you to make an informed decision and thereby improve the chances of a successful IVF outcome.
Preimplantation Genetic Screening/Testing(PGS/T): PGS/T is a valuable tool for identifying chromosomal abnormalities in eggs and embryos. By selecting the most competent (euploid) embryos, PGS/T significantly improves the success of IVF, especially in older women or those with DOR.
Understanding the impact of advancing age and declining ovarian reserve on IVF outcomes is essential when making decisions about fertility treatments. Age-related factors can affect egg quality and increase the likelihood of aneuploid embryos with resultant IVF failure. Diminished ovarian reserve (DOR) further complicates the process. By considering these factors, you can make informed choices and work closely with fertility specialists to optimize your chances of success. Remember, knowledge is power, and being aware of these aspects empowers you to take control of your reproductive journey.
______________________________________________________________________________________
PLEASE SHARE THIS WITH OTHERS AND HELP SPREAD THE WORD!!
Herewith are online links to 2 E-books recently co-authored with my partner at SFS-NY (Drew Tortoriello MD)……. for your reading pleasure:
I invite you to visit my very recently launched “Podcast”, “HAVE A BABY” on RUMBLE; https://rumble.com/c/c-3304480
If you are interested in having an online consultation with me, please contact my assistant, Patti Converse at 702-533-2691 or email her at concierge@sherivf.com\
Name: Bronagh M
Hi Dr Sher, I’ve been getting mixed advice from consultants and I’m hoping you can help. I’m 40years old and have one child, conceived with no issues, and have had a number of chemical pregnancy losses. I’m conceiving very easily, almost every cycle I try, but losing each pregnancy soon after a positive pregnancy test. I have had some tests done which showed borderline antiphospholipid syndrome but everything else has come back normal.
One consultant has recommended an endometrial biopsy, and another consultant said this was to check for NK cells which can easily change and so it wasn’t a reliable test, and that the treatment would be Intralipids which is just ‘mayonnaise’! I know that you recommend intralipids so I would love to know your thoughts on this.
Another consultant suggested steroids but was concerned about the increased risk of cleft lip in baby, I wasn’t aware of this risk, is it something to be concerned about and to rule out the use of steroids for RPL?
Finally, the same consultant who felt intralipids offered no help, has prescribed hydroxychloroquine to help with RPL. I have been advised to take this for 3 months before trying to conceive, and when I do start trying to take aspirin until 6 weeks pregnancy, and to begin clexane with pregnancy also.
Would you suggest intralipids alongside the hydroxychloroquine, or is one preferred over the other for RPL?
Many thanks for any advice
B
Thanks for the inquiry. I think I can help here.
Might I suggest that you contact my assistant Patti Converse at 702-533-2691 and set up an online consultation with me to discuss in depth.
Geoff Sher
_____________________________________________________________________________
When it comes to reproduction, humans face challenges compared to other mammals. A significant number of fertilized eggs in humans do not result in live births, with up to 75% failing to develop, and around 30% of pregnancies ending within the first 10 weeks (first trimester). Recurrent pregnancy loss (RPL) refers to two or more consecutive failed pregnancies, which is relatively rare, affecting less than 5% of women for two losses and only 1% for three or more losses. Understanding the causes of pregnancy loss and finding solutions is crucial for those affected. This article aims to explain the different types of pregnancy loss and shed light on potential causes.
Types of Pregnancy Loss: Pregnancy loss can occur at various stages, leading to different classifications:
Causes of Recurrent Pregnancy Loss (RPL): Recurrent pregnancy loss refers to multiple consecutive miscarriages. While chromosomal abnormalities are a leading cause of sporadic early pregnancy losses, RPL cases are mostly attributed to non-chromosomal factors. Some possible causes include:
IMMUNOLOGIC IMPLANTATION DYSFUNCTION AND RPL:
Autoimmune IID: Here an immunologic reaction is produced by the individual to his/her body’s own cellular components. The most common antibodies that form in such situations are APA and antithyroid antibodies (ATA). But it is only when specialized immune cells in the uterine lining, known as cytotoxic lymphocytes (CTL) and natural killer (NK) cells, become activated and start to release an excessive/disproportionate amount of TH-1 cytokines that attack the root system of the embryo, that implantation potential is jeopardized. Diagnosis of such activation requires highly specialized blood test for cytokine activity that can only be performed by a handful of reproductive immunology reference laboratories in the United States. Alloimmune IID, (i.e., where antibodies are formed against antigens derived from another member of the same species), is believed to be a common immunologic cause of recurrent pregnancy loss. Autoimmune IID is often genetically transmitted. Thus, it should not be surprising to learn that it is more likely to exist in women who have a family (or personal) history of primary autoimmune diseases such as lupus erythematosus (LE), scleroderma or autoimmune hypothyroidism (Hashimoto’s disease), autoimmune hyperthyroidism (Grave’s disease), rheumatoid arthritis, etc. Reactionary (secondary) autoimmunity can occur in conjunction with any medical condition associated with widespread tissue damage. One such gynecologic condition is endometriosis. Since autoimmune IID is usually associated with activated NK and T-cells from the outset, it usually results in such very early destruction of the embryo’s root system that the patient does not even recognize that she is pregnant. Accordingly, the condition usually presents as “unexplained infertility” or “unexplained IVF failure” rather than as a miscarriage. Alloimmune IID, on the other hand, usually starts off presenting as unexplained miscarriages (often manifesting as RPL). Over time as NK/T cell activation builds and eventually becomes permanently established the patient often goes from RPL to “infertility” due to failed implantation. RPL is more commonly the consequence of alloimmune rather than autoimmune implantation dysfunction. However, regardless, of whether miscarriage is due to autoimmune or alloimmune implantation dysfunction the final blow to the pregnancy is the result of activated natural killer cells (NKa) and cytotoxic lymphocytes (CTL B) in the uterine lining that damage the developing embryo’s “root system” (trophoblast) so that it can no longer sustain the growing conceptus. This having been said, it is important to note that autoimmune IID is readily amenable to reversal through timely, appropriately administered, selective immunotherapy, and alloimmune IID is not. It is much more difficult to treat successfully, even with the use of immunotherapy. In fact, in some cases the only solution will be to revert to selective immunotherapy plus using donor sperm (provided there is no “match” between the donor’s DQa profile and that of the female recipient) or alternatively to resort to gestational surrogacy.
DIAGNOSING THE CAUSE OF RPL.
In the past, women who miscarried were not evaluated thoroughly until they had lost several pregnancies in a row. This was because sporadic miscarriages are most commonly the result of embryo numerical chromosomal irregularities (aneuploidy) and thus not treatable. However, a consecutive series of miscarriages points to a repetitive cause that is non-chromosomal and is potentially remediable. Since RPL is most commonly due to a uterine pathology or immunologic causes that are potentially treatable, it follows that early chromosomal evaluation of products of conception could point to a potentially treatable situation. Thus, I strongly recommend that such testing be done in most cases of miscarriage. Doing so will avoid a great deal of unnecessary heartache for many patients. Establishing the correct diagnosis is the first step toward determining effective treatment for couples with RPL. It results from a problem within the pregnancy itself or within the uterine environment where the pregnancy implants and grows. Diagnostic tests useful in identifying individuals at greater risk for a problem within the pregnancy itself include Karyotyping (chromosome analysis) both prospective parents Assessment of the karyotype of products of conception derived from previous miscarriage specimens Ultrasound examination of the uterine cavity after sterile water is injected or sonohysterogram, fluid ultrasound, etc.) Hysterosalpingogram (dye X-ray test) Hysteroscopic evaluation of the uterine cavity Full hormonal evaluation (estrogen, progesterone, adrenal steroid hormones, thyroid hormones, FSH/LH, etc.) Immunologic testing to include Antiphospholipid antibody (APA) panel Antinuclear antibody (ANA) panel Antithyroid antibody panel (i.e., antithyroglobulin and antimicrosomal antibodies) Reproductive immunophenotype Natural killer cell activity (NKa) assay (i.e., K562 target cell test) Alloimmune testing of both the male and female partners
TREATMENT OF RPL
This involves restoration through removal of local lesions such as fibroids, scar tissue, and endometrial polyps or timely insertion of a cervical cerclage (a stitch placed around the neck of the weakened cervix) or the excision of a uterine septum when indicated. Treatment of Thin Uterine Lining: A thin uterine lining has been shown to correlate with compromised pregnancy outcome. Often this will be associated with reduced blood flow to the endometrium. Such decreased blood flow to the uterus can be improved through treatment with sildenafil and possibly aspirin. sildenafil (Viagra) Therapy. Viagra has been used successfully to increase uterine blood flow. However, to be effective it must be administered starting as soon as the period stops up until the day of ovulation and it must be administered vaginally (not orally). Viagra in the form of vaginal suppositories given in the dosage of 25 mg four times a day has been shown to increase uterine blood flow as well as thickness of the uterine lining. To date, we have seen significant improvement of the thickness of the uterine lining in about 70% of women treated. Successful pregnancy resulted in 42% of women who responded to the Viagra. It should be remembered that most of these women had previously experienced repeated IVF failures. Use of Aspirin: This is an anti-prostaglandin that improves blood flow to the endometrium. It is administered at a dosage of 81 mg orally, daily from the beginning of the cycle until ovulation.
Treating Immunologic Implantation Dysfunction with Selective Immunotherapy:
Modalities such as intralipid (IL), intravenous immunoglobulin-G (IVIG), heparinoids (Lovenox/Clexane), and corticosteroids (dexamethasone, prednisone, prednisolone) can be used in select cases depending on autoimmune or alloimmune dysfunction. The Use of IVF in the Treatment of RPL In the following circumstances, IVF is the preferred option: When in addition to a history of RPL, another standard indication for IVF (e.g., tubal factor, endometriosis, and male factor infertility) is superimposed and in cases where selective immunotherapy is needed to treat an immunologic implantation dysfunction. The reason for IVF being a preferred approach when immunotherapy is indicated is that in order to be effective, immunotherapy needs to be initiated well before spontaneous or induced ovulation. Given the fact that the anticipated birthrate per cycle of COS with or without IUI is at best about 15%, it follows that short of IVF, to have even a reasonable chance of a live birth, most women with immunologic causes of RPL would need to undergo immunotherapy repeatedly, over consecutive cycles. Conversely, with IVF, the chance of a successful outcome in a single cycle of treatment is several times greater and, because of the attenuated and concentrated time period required for treatment, IVF is far safer and thus represents a more practicable alternative Since embryo aneuploidy is a common cause of miscarriage, the use of preimplantation genetic screening/ testing (PGS/T), with tests such as next generation gene sequencing (NGS), can provide a valuable diagnostic and therapeutic advantage in cases of RPL. PGS/T requires IVF to provide access to embryos for testing. There are a few cases of intractable alloimmune dysfunction due to absolute DQ alpha gene matching ( where there is a complete genotyping match between the male and female partners) where Gestational Surrogacy or use of donor sperm could represent the only viable recourse, other than abandoning treatment altogether and/or resorting to adoption. Other non-immunologic factors such as an intractably thin uterine lining or severe uterine pathology might also warrant that last resort consideration be given to gestational surrogacy. Conclusion:
Understanding the causes of pregnancy loss is crucial for individuals experiencing recurrent miscarriages. While chromosomal abnormalities are a common cause of sporadic early pregnancy losses, other factors such as uterine environment problems, immunologic implantation dysfunction, blood clotting disorders, and genetic or structural abnormalities can contribute to recurrent losses. By identifying the underlying cause, healthcare professionals can provide appropriate interventions and support to improve the chances of a successful pregnancy. The good news is that if a couple with RPL is open to all of the diagnostic and treatment options referred to above, a live birthrate of 70%–80% is ultimately achievable.
___________________________________________________________________________________
PLEASE SHARE THIS WITH OTHERS AND HELP SPREAD THE WORD!!
Herewith are online links to 2 E-books recently co-authored with my partner at SFS-NY (Drew Tortoriello MD)……. for your reading pleasure:
I invite you to visit my very recently launched “Podcast”, “HAVE A BABY” on RUMBLE; https://rumble.com/c/c-3304480
If you are interested in having an online consultation with me, please contact my assistant, Patti Converse at 702-533-2691 or email her at concierge@sherivf.com\
Name: Sandra W
Just to add some info I forgot with previous question:
– usually no high FSH levels on day 1-5. I had once after the first ICSI treatment an FSH level of 21 on day 3. One dominant follicel grew but the others remained small -> so similar to when starting stimulation treatment on day 3. In this particular menstrual cycle my ovulation was 2-3 days later than usual. Usually my ovulation takes place between day 11-13 of my menstrual cycle. 14 days after ovulation my period starts
– the quality of transferred embryo was B, if that in any case matters
Understood. The answer I gave earlier still holds!
Geoff Sher
Name: Edna U
Que documentos necesito para hacer donación de ovilos
Please re-post in English!
Geoff Sher