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.
hello,can doxyl and fragyl alone open blocked fallopian tubes?
I am afraid NOT!
Dear Dr. Sher,
I apologise.. i don’t think my message posted properly. I would be very grateful for your advice on the below. Thank you so much!
Dear Dr. Sher, We have been advised that we will have difficulties with gestational surrogacy, based upon studies undertaken in Spain. My HLA-C type is C2/C2 and my husband is C1/C2. According to our IVF clinic, we would need to find a surrogacy agency that has tested the surrogate to be KIR AB or KIR BB (ie. the gestational carrier cannot be a KIR AA type) because of our HLA-C types, otherwise the likelihood of implantation is miniscule/slim-to-none. The surrogacies agencies we have contacted are not even aware of the KIR testing. We would be grateful for your advice Dr. Sher. We would be very grateful to know if there is any other explanations on this topic as to why implantation in a gestational surrogate would or wouldn’t work for embryos that are C1/C2 or C2/C2, and if KIR testing is really necessary or not?
Thank you for getting back to me.
As I tried to indicate, I do NOT concur with that opinion. In my opinion there would be a problem with implantation, as long as the GS does not have activated uterine natural killer cells (NKa).
Hi! I wanted to. find out you would ever see someone for the following: I froze eggs last year not because of problems but for precaution. I got an infection after procedure and it was never treated adequately. I have developed all the horrible complications that result, including frequent new infections on top of the existing chronic problems…that I also have struggled beyond belief trying to get diagnosed and treated. I have pre-existing problems and struggle to fight infection to begin with and now the problems are very deep seated. This has been going on for over a year, I have been seriously unwell w/ pelvic problems and have lost my ability to function completely. No one seems to treat or be knowledgable about non-STI related pelvic infections. I was wondering if you would ever treat this kind of problem even though, very sadly, I am not in a position to get pregnant (and never will if this doesn’t get resolved – I’ve literally lost my life going on year 2). I am desperate, if you couldn’t tell. If not, do you know anyone who specifically treats things like chronic endometritis in patients without sex-related problems and not in a life circumstance to be getting pregnant?
I am so sorry for you. However, it is not possible for me to advise or treat this at a distance. You should see an OB/GYN in conjunction with a specialist in internal medicine!
Good luck!
Hi Dr. Sher,
I have a history of endometriosis (stage 4 in 2017 lap surgery/cold excision). My husband and I began trying to conceive and after no luck for almost a year were told we needed to do IVF . So we moved along with a well known clinic in our state and the results as follows:
After two rounds of ER we had 6 PGT tested embryos frozen.
Treatment plan suggested before transfer was Orilissa for three months to suppress endo, surgery not recommended to avoid scar tissue.
Took Orilissa for three months (YIKES) and began prep for transfer which included estrogen and PIO 1ml. PIO 5 days before transfer.
First transfer: March 17, 2022- positive HPT 6dp5dt (faint line). Lines stopped progressing, first beta 9dp5dt= 27. Told to prepare for possible biochemical pregnancy. Second beta 28 hours, HCG. 14. Cycle failed.
Treatment plan suggested: Same protocol. The Orilissa raised my TSH (I think)- it was always normal but went high and then put on Synthroid. We also pushed for biopsy to test for endometritis and bacterial issues. He agreed. Completed uterine biopsy and an HSG. HSG normal. Biopsy showed chronic endometritis and bad bacteria. Treated with two weeks of two antibiotics. Repeated biopsy and all clear. Began having really bad side effects from Orilissa, he added Aygestin in the last few weeks before transfer prep. We also asked for bloodwork to rule out clotting factors (my mother has factor V). He ran a repeat loss panel for us, came back showing MTHFR (I had been taking mentholated folate for years with my prenatal). Said no further action needed on that. No clotting or autoimmune issues (not sure all the tests he did run on this).
No issues with lining growth, responded well to stims, lining around 11.1 for both transfers, triple layer, no notable issues- both transfers went very smooth, though I did bleed from my cervix the second time, he said likely due to the speculum, but assured it was not from internal. The only issue I had this cycle was around the third month on Orilissa this time I began spotting for a few days. He said it was likely due to the lining being so thin and friction?
Second transfer: June 28th another positive HPT 6dp5dt that same day I began spotting brown (like I do before a period). He said it could be implantation bleeding, upped my progesterone to 1.5ML, it stopped a day later. The positive beta came 9dp5dt but level of 29.4, the second beta at 11dp5dt was 18, so another chemical pregnancy.
Wondering if need another lap surgery to address endo (if the reason for the repeat early losses). My RE is against the ERA test (but would do it if we wanted). He also is against trying things like medrol or aspirin, etc. He is against the idea of possible immunological causes. His suggestion is to up the dose and timing on the progesterone and try again. My progesterone levels were all fine during the process is it true that endometriosis makes it harder to absorb progesterone? Any thoughts on another lap or if it’s time for a second opinion?
This is a complex issue that could well involve an implantation dysfunction which could be linked to an anatomical or an immunologic cause. I think that we should talk. Might I suggest that you call my assistant, Patti Converse (702-533-2691 and set up an online consultation with me.
In the interim, please see below
Implantation dysfunction is unfortunately often overlooked as an important cause of IVF failure. In the pursuit of optimizing outcome with IVF, the clinician has a profound responsibility to meticulously assess and address this important issue if IVF success is to be optimized. This is especially relevant in cases of “unexplained IVF failure, Recurrent Pregnancy Loss (RPL) and in women suspected of having underlying anatomical and immunologic factors. Doing so will not only maximize the chance of a viable pregnancy but enhancing placentation, will at the same time promote the noble objective of optimizing the quality of life after birth.”
IVF success rates have been improving over the last decade. The average live birth rate per embryo transfer in the U.S.A for women under 40y using their own eggs, is currently better than 1:3 women. However, there is still a wide variation from program to program for IVF live birth rates, ranging from 20% to near 50%. Based upon these statistics, most women undergoing IVF in the United States require two or more attempts to have a baby. IVF practitioners in the United States commonly attribute the wide dichotomy in IVF success rates to variability in expertise of the various embryology laboratories. This is far from accurate. In fact, other factors such as wide variations in patient selection and the failure to develop individualized protocols for ovarian stimulation or to address those infective, anatomical and immunologic factors that influence embryo implantation are at least equally important.
About 80% of IVF failures are due to “embryo incompetency” that is largely due to an irregular quota of chromosomes (aneuploidy) which is usually related to advancing age of the woman and is further influenced by other factors such as the protocol selected for ovarian stimulation, diminished ovarian reserve (DOR)m and severe male factor infertility. However, in about 20% of dysfunctional cases embryo implantation is the cause of failure.
Anatomical Endo-uterine Lesions: This blog article will focus on implantation dysfunction and IVF failure due to:
•Anatomical abnormalities in the uterine cavity (e.g. scarring, polyps and encroaching fibroid tumors)
•A thin endometrial lining
•Immunologic rejection of the embryos
Several studies performed both in the United States and abroad have confirmed that a dye X-Ray or hysterosalpingogram (HSG) will fail to identify small endouterine surface lesions in >20% of cases. This is significant because even small uterine lesions have the potential to adversely affect implantation. Hysteroscopy is the traditional method for evaluating the integrity of the uterine cavity in preparation for IVF. It also permits resection of most uterine surface lesions, such as submucous uterine fibroids (myomas), intrauterine adhesions and endometrial or placental polyps. All of these can interfere with implantation by producing a local “inflammatory- type” response similar in nature to that which is caused by an intrauterine contraceptive device. Hysterosonography (syn HSN/ saline ultrasound examination) and hysteroscopy have all but supplanted HSG to assess the uterine cavity in preparation for IVF. HSN which is less invasive and far less expensive than is than hysteroscopy involves a small amount of a sterile saline solution is injected into the uterine cavity, whereupon a vaginal ultrasound examination is performed to assess the contour of the uterine cavity.
Endometrial Thickness: As far back as in 1989 I first reported on the finding that ultrasound assessment of the late proliferative phase endometrium following ovarian stimulation in preparation for IVF, permits better identification of those candidates who are least likely to conceive. We noted that the ideal thickness of the endometrium at the time of ovulation or egg retrieval is >9 mm and that a thickness of less than 8 mm bodes poorly for a successful outcome following IVF.
Then in 1993, I demonstrated that sildenafil (Viagra) introduced into the vagina prior to hCG administration can improve endometrial growth in many women with poor endometrial development. Viagra’s mechanism of action is improvement in uterine blood flow with improved estrogen delivery…thereby enhancing endometrial development.
Immunologic factors: These also play a role in IVF failure. Some women develop antibodies to components of their own cells. This “autoimmune” process involves the production of antiphospholipid, antithyroid, and/or anti-ovarian antibodies – all of which may be associated with activation of Natural Killer (NK) cells in the uterine lining. Activated NK cells (NKa) release certain cytokines (TH-I) that if present in excess, often damage the trophoblast (the embryo’s root system) resulting in immunologic implantation dysfunction (IID). This can manifest as “infertility” or as early miscarriages). In other cases (though less common), the problem is due to “alloimmune” dysfunction. Here the genetic contribution by the male partner renders the embryo “too similar” to the mother. This in turn activates NK cells leading to implantation dysfunction. These IID’s are treated using combinations of medications such as heparin, Clexane, Lovenox, corticosteroids and intralipid (IL).
I strongly recommend that you visit http://www.SherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•A Fresh Look at the Indications for IVF
•The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
•Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
•IVF and the use of Supplementary Human Growth Hormone (HGH) : Is it Worth Trying and who needs it?
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Blastocyst Embryo Transfers Should be the Standard of Care in IVF
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•IVF: Approach to Selecting the Best Embryos for Transfer to the Uterus.
•Fresh versus Frozen Embryo Transfers (FET) Enhance IVF Outcome
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•Genetically Testing Embryos for IVF
•Staggered IVF
•Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
•Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
•IVF: Selecting the Best Quality Embryos to Transfer
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
•PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
•Endometrial Receptivity Array (ERA): Is There an actual “There, There”?
•IVF Failure and Implantation Dysfunction:
•Diagnosing and Treating Immunologic Implantation Dysfunction (IID)
•The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
•Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
•Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
•Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
•Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
•Intralipid (IL) Administration in IVF: It’s Composition How it Works Administration Side-effects Reactions and Precautions
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
•A Thin Uterine Lining: Vaginal Viagra is Often the Answer (update)
•Cervical Ureaplasma Urealyticum Infection: How can it Affect IUI/IVF Outcome?
•The Role of Nutritional Supplements in Preparing for IVF
•The Basic Infertility Work-Up
•Defining and Addressing an Abnormal Luteal Phase
•Male Factor Infertility
•Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in Favor
•Hormonal Treatment of Male Infertility
•Hormonal Treatment of Male Infertility
•Antisperm Antibodies, Infertility and the Role of IVF with Intracytoplasmic Sperm Injection (ICSI)
•Endometriosis and Infertily
•Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF
•Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
•Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
•Early -Endometriosis-related Infertility: Ovulation Induction (with or without Intrauterine Insemination) and Reproductive Surgery Versus IVF
•Deciding Between Intrauterine Insemination (IUI) and In Vitro Fertilization (IVF).
•Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & Con’s!IUI-Reflecting upon its Use and Misuse: Time for a Serious “Reality Check
•Mode of Action, Indications, Benefits, Limitations and Contraindications for its ue
•Clomiphene Induction of Ovulation: Its Use and Misuse!
1.
Dear Dr. Sher,
We have been advised that we will have difficulties with gestational surrogacy, based upon studies undertaken in Spain.
My HLA-C type is C2/C2 and my husband is C1/C2. According to our IVF clinic, we would need to find a surrogacy agency that has tested the surrogate to be KIR AB or KIR BB (ie. the gestational carrier cannot be a KIR AA type) because of our HLA-C types, otherwise the likelihood of implantation is miniscule/slim-to-none.
The surrogacies agencies we have contacted are not even aware of the KIR testing.
We would be grateful for your advice Dr. Sher. We would be very grateful to know if there is any other explanations on this topic as to why implantation in a gestational surrogate would or wouldn’t work for embryos that are C1/C2 or C2/C2, and if KIR testing is really necessary or not?