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. Geoffrey,
Hello Dr. Geoffrey,
I am 38 years old an 2 years in fertlity treatments. 4 AI with one pregnancy ended in MC 6 weeks. All studies showed infertility as unknown cause. Chromosomal analysis also normal, only my housband with a 46, XYqh-. Apparenntly, should not affect.
1st IVF Gonal F 150+ merapur 150 ; 10 days. 7 eggs retrieved; 7 fertlized; 3 reached blastocyst stage. 2 of them apparently good quality. This cycle ended in chemical pregnancy.
2nd cycle (change in protocol).
Lupron 7 days prior to my next period 0.1 mg/day. Gonal F 100ui+ merapur 150 and lupron 0.05mg 2nd day after my period begins. This cycle was cancelled only 2 follicles at 5 days stimulation
3rd IVF cycle.
Lupron 0.1mg first 2 days after my period
Gonal F 100 ui + merapur 225
5 eggs retrieved; 2 fertilized; none made it to blastocyst. TRANSFER CANCELLED
Based in this results, first IVF protocol was repeated: Gonal F 200 ui + merapur 150 each day during 10 days. Cetrotide after 6 days of stimulation and ovitrel 250 for trigger.
Result: 3 blastocist (one ok, am two notado good). Beta negative
For next treatment muy doctor is suggesting egg donation. However, I saw one of your videos and seems that the protocols were not the best to my age, so I want to know if changing the protocol can I get better eggs.
Thanks!!!
Dear Dr. Sher,
Thank you so much for answering my question yesterday about timing for lipid infusions! You had replied that the lipid infusion should be infused 10-14 days prior to anticipated embryo transfer. After reading your response I was wondering …
1. How long then does the lipid infusion stay “active” in my system for?
2. Since you advise to do the first infusion almost 2 weeks before the transfer, when should I then have my second lipid infusion done? My plan originally was to do the 2nd infusion after a positive pregnancy test (so that would be about 3 1/2 weeks after the first infusion), but should I do it earlier than that?
Thank you again so much for your time!
Randi
1. How long then does the lipid infusion stay “active” in my system for?
A: 4-6 weeks!
2. Since you advise to do the first infusion almost 2 weeks before the transfer, when should I then have my second lipid infusion done? My plan originally was to do the 2nd infusion after a positive pregnancy test (so that would be about 3 1/2 weeks after the first infusion), but should I do it earlier than that?
A: No that would be fine!
Good luck!
Geoff Sher
Dear Dr Sher,
I have contacted you before but I would very much value your opinion on my recent failed second round of IVF. I am 31 and have a low AMH (just under 5). During my first failed cycle, there were 5 follicles all containing eggs – 4 out of the 5 fertilized and the 2 better ones were transferred but failed to implant. Therefore on my second round of IVF (and due to the discovery of my high levels of antibodies-
352 IU/ml), I was given the dose of Prednisolone 20mg daily, starting on the first day of my FSH stimulation. I received a Prostap injection for down reg but I discovered my thyroid was too high after getting it tested myself. The clinic then upped my dosage of thyroxine by 25ml as they weren’t happy with my TSH level being 3.39. Therefore I started on 125ml for 2 weeks which brought my TSH level down.
I received a second prostap without a bleed as they said that was fine and a week later started my stims. This time, on the first and second day of stims I had 2 injections (350IU), after that I just had one injection per day alongside taking steroids. I was very disappointed to discover I only had 2 follicles on my first scan and then a possible 3 follicles on my second scan. I received intralipids after my second scan in line with your advice to have them 10-14 days before transfer. On the day of egg collection there was only 1 egg. It fertilized abnormally and so there was nothing for transfer. I was told my case would be reviewed as urgent. I’m very confused as to why this second round failed so miserably? Could it be the double prostap with no bleed after the second injection or the late change in thyroxine meds? Could the steroids have had a negative impact on follicle growth? I would love to hear your opinion before I have the meeting with my clinic. Many thanks again.
You have two issues: 1. possibility of an autoimmune immunologic implantation dysfunction (IID) and 2) Diminished ovarian reserve
1. Immunologic:
Between 2% and 5% of women of the childbearing age have reduced thyroid hormone activity (hypothyroidism). Women with hypothyroidism often manifest with reproductive failure i.e. infertility, unexplained (often repeated) IVF failure, or recurrent pregnancy loss (RPL). The condition is 5-10 times more common in women than in men. In most cases hypothyroidism is caused by damage to the thyroid gland resulting from of thyroid autoimmunity (Hashimoto’s disease) caused by damage done to the thyroid gland by antithyroglobulin and antimicrosomal auto-antibodies.
The increased prevalence of hypothyroidism and thyroid autoimmunity (TAI) in women is likely the result of a combination of genetic factors, estrogen-related effects and chromosome X abnormalities. This having been said, there is significantly increased incidence of thyroid antibodies in non-pregnant women with a history of infertility and recurrent pregnancy loss and thyroid antibodies can be present asymptomatically in women without them manifesting with overt clinical or endocrinologic evidence of thyroid disease. In addition, these antibodies may persist in women who have suffered from hyper- or hypothyroidism even after normalization of their thyroid function by appropriate pharmacological treatment. The manifestations of reproductive dysfunction thus seem to be linked more to the presence of thyroid autoimmunity (TAI) than to clinical existence of hypothyroidism and treatment of the latter does not routinely result in a subsequent improvement in reproductive performance.
It follows, that if antithyroid autoantibodies are associated with reproductive dysfunction they may serve as useful markers for predicting poor outcome in patients undergoing assisted reproductive technologies.
Some years back, I reported on the fact that 47% of women who harbor thyroid autoantibodies, regardless of the absence or presence of clinical hypothyroidism, have activated uterine natural killer cells (NKa) cells and cytotoxic lymphocytes (CTL) and that such women often present with reproductive dysfunction. We demonstrated that appropriate immunotherapy with IVIG or intralipid (IL) and steroids, subsequently often results in a significant improvement in reproductive performance in such cases.
The fact that almost 50% of women who harbor antithyroid antibodies do not have activated CTL/NK cells suggests that it is NOT the antithyroid antibodies themselves that cause reproductive dysfunction. The activation of CTL and NK cells that occurs in half of the cases with TAI is probably an epiphenomenon with the associated reproductive dysfunction being due to CTL/NK cell activation that damages the early “root system” (trophoblast) of the implanting embryo. We have shown that treatment of those women who have thyroid antibodies + NKa/CTL using IL/steroids, improves subsequent reproductive performance while women with thyroid antibodies who do not harbor NKa/CTL do not require or benefit from such treatment.
2. DOR:
In my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”.
Older women as well as those who (regardless of age) have diminished ovarian reserve (DOR) tend to produce fewer and less “competent” eggs, the main reason for reduced IVF success in such cases. The compromised outcome is largely due to the fact that such women tend to have increased LH biological activity which often results in excessive LH-induced ovarian testosterone production which in turn can have a deleterious effect on egg/embryo “competency”.
Certain ovarian stimulation regimes either promote excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), augment LH/hCG delivered through additional administration (e.g. high dosage menotropins such as Menopur), or fail to protect against body’s own/self-produced LH (e.g. late antagonist protocols where drugs such as Ganirelix/Cetrotide/Orgalutron that are first administered 6-7 days after ovarian stimulation has commenced).
I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of a modified, long pituitary down-regulation protocol (the agonist/antagonist conversion protocol-A/ACP) augmented by adding supplementary human growth hormone (HGH). I further recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing/NGS)-normal blastocysts in such cases. This type of approach will in my opinion, optimize the chance of a viable pregnancy per embryo transfer procedure and provide an opportunity to capitalize on whatever residual ovarian reserve and egg quality still exists, allowing the chance to “make hay while the sun still shines”.
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.
•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 Aproach
•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)
•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?
•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
•Implications of “Empty Follicle Syndrome and “Premature Luteinization”
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
•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!
If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .
*FYI
The 4th edition of my book,”In Vitro Fertilization, the ART of Making Babies” is now available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoffrey Sher MD
Hello Dr. Sher,
I’m 35 next month and had my AMH tested a few days ago. It’s 15.3 pmol/L I believe that’s about 2.1 ng/ml. Do I need a donor egg with this level or is it still possible to use my own eggs. Thanks.
No , in my opinion, you do not!
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.
•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
•Why did my IVF Fail
•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
•Cervical Ureaplasma Urealyticum Infection: How can it Affect IUI/IVF Outcome?
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas
•Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
•A personalized, stepwise approach to IVF
•How Many Embryos should be transferred: A Critical Decision in IVF.
If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com.
*FYI
The 4th edition of my newest book ,”In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoffrey Sher
That’s great. I feel hopeful and just in the process of setting up skype with you!
Hi Dr. Sher,
I apologize that this may be a slightly long post since I’m trying to cover all the bases. I have questions regarding the timing of lipid infusions before an embryo transfer.
This is the first time I am doing lipid infusions. I have done one 5 day transfer and four 3 day transfers for previous IVF cycles. So I am trying to time the lipid infusions this IVF cycle for either a 3day or a 5day transfer, but I don’t know which it will be.
How many days before the transfer is the optimum timing for a lipid infusion? (I would be doing the infusion around 6 o’clock at night after work and my transfers have usually been done in the morning hours) I have heard 10-7 days before a transfer and I have heard 5-7 days before a transfer. Then, when I was discussing not knowing if my transfer would be a 3 day or 5 day transfer, one of the doctors at my practice said to do the infusion the day after the retrieval (which would only be about 2 days before a 3 day transfer, especially with my doing the infusion at night after work and the transfers are done at my practice during morning hours).
Does the lipid infusion need to be in your system for a certain amount of days before the transfer to suppress an autoimmune reaction? When I mentioned this to the nurse giving me the instructions from the doctor, the nurse said the doctor said it would be fine to do the infusion a day or two before the transfer, which left me feeling confused. Is this correct?
I also have questions about the lipid infusion interactions with medications… I usually do my trigger shot around 9 o’clock at night, and 36hrs later in the morning time is the retrieval, so I was also wondering please:
1. Can I do a lipid infusion around 6pm the same night I do my trigger shot around 9pm, or will that somehow impede the trigger shot?
2. Can I do my lipid infusion (around 6pm) the night before my retrieval (around 9am the next morning) or again will that somehow impede the trigger shot that’s been in my system at that point for about 20hrs?
3. I was told not to do my lipid infusion on the day I have the retrieval done since the propofol they give for the retrieval has lipids, is this correct?
As you can see I’m quite confused when the best timing is, and what interactions with medications may/or may not occur… I would really appreciate your help in answering these questions and in making the timing issue more clear for me.
Thank you,
Randi
IL should be infused 10-14 days prior to anticipated ET. That means if you infuse on the 3rd or 4th day of gonadotropin stimulation (well before ER), you should be fine, regardless of whether it is a day 3 or day-5 transfer.
Questions:
1. Can I do a lipid infusion around 6pm the same night I do my trigger shot around 9pm, or will that somehow impede the trigger shot?
A: Too late (see above).
2. Can I do my lipid infusion (around 6pm) the night before my retrieval (around 9am the next morning) or again will that somehow impede the trigger shot that’s been in my system at that point for about 20hrs?
A:Too late.
3. I was told not to do my lipid infusion on the day I have the retrieval done since the propofol they give for the retrieval has lipids, is this correct?
A: See above:
Geoff Sher