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 dr!
I just found out that I’m pregnant from a fet cycle. I was on Estrace starting at day 4, endometriin 3x a day starting at day 15 and transfer day 19. Meds continue the same. I had blood work yesterday at 12 days after 3 day transfer. Hcg was 300, estrogen was 1,700 and progesterone was 11.1. I am worried about my progesterone level. Is it indicative of an unhealthy pregnancy? With my first pregnancy, also a fet, my progesterone at this stage was 17.4 but I had a twin pregnancy. I ended up losing one at 9 weeks so I am nervous.
I do not think that a progesterone alone is a real problem. I however would supplement by adding progesterone by injectio or suppositories. Only time will tell if the pregnancy is progressing normally. Do another beta hCG in 2 days, measure the progesterone in a wek and do an US examination in 2 weeks from now. The3n you will have more certainty.
Good luck!
Geoff Sher
Dear Dr Sher,
We had few failed IVFs. During next FET we want to do everything and anything that could increase our chanses…
What do you think about HCG 10,000 five days before transfer and then another 5,000 of HCG two days after transfer to make lining more receptive?
I would also do Intralipid, steroids and heparyne.
Thank you so much for all the info from this site.
Zuza
I do not believe in double dosing on hCG. It has no proven benefit and only clouds the ability to diagnose pregnancy on the basis of measuring hCG as early on as possible.As for Intralipid/steroids, it is only indicated if you have NK cell activation and heparin…if you have a certain type of thrombophilia or antiphospholid antibodies.
Please visit my new Blog on this very site, 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.
•Hereditary Clotting Defects (Thrombophilia)
•IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
•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)
Geoff Sher
Dr Sher,
My daughter was diagnosed with Complete Molar Pregnancy in June 2015. This is a first pregnancy at age 38.
There seems to be differing opinions as to whether there is a fetus (for however little time) prior to the egg’s genetic material being destroyed by the sperms’ genetic material, or if the egg was “empty” (devoid of genetic material) prior to fertilazation by 2 sperm. Since the eggs resulting in molar pregnancies are not examined prior to implantation, how is it determined if an egg was “empty” prior to fertilization?
In all the evaluations of retrieved eggs from IVF patients, are there any instances of eggs devoid of genetic material (prior to fertilization)?
Thank you,
Ann Y Stokes
A complete Hydatidiform Molar Pregnancies” occur when an egg that has no functional chromosomal material (anuclear) is fertilized by a sperm and thereupon divides in two and propagates haphazard tissue growth. And yes indeed, we do on occasion see eggs that are “empty”.
Please visit my new Blog on this very site, find the “search bar” and type in “Molar Pregnancy: What is it and How Should it be Treated?”, “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.
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
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Hi Dr Sher. Thank you for reading this. I just turned 31 and my husband is 36. In 2013 I was diagnosed with mild PCOS (28 yrs) and my doctor gave me metformin because my periods cycles were 35 -40 days. We successfully conceived naturally in June 2013 but miscarriaged at 8 weeks (didn’t find out until week 11 when I started having some spotting). Since then we haven’t fallen pregnant. Early 2015 we did three unsuccessful rounds of IUI (but using no hormones) because my husband’s sperm had 43% SpermMar IGG and 2% morphology. His other results were good with 85million sperm concentration and 77% motility.
I’m still taking metformin and ovulate every month – my Fallopian tubes have also been checked and they are not blocked. My AMH levels are high.
We were trying another IUI this month on clomiphene but I produced 6 eggs so our doctor postponed it. My question is: is IUI with sperm washing our best alternative if my husband has antibodies? Also, could you please advise if there are other tests my husband can do or which specialist can look into this matter further? Thank you kindly for your time!!
*Intrauterine insemination (IUI), (sometimes referred to as artificial insemination) of processed sperm is contraindicated in cases if moderate or severe male immunologic infertility because it does NOT improve pregnancy rates over NO TREATMENT AT ALL….You need IVF/ICSI in my opinion.
The presence of sperm antibodies reduces male fertility significantly, but does not usually prevent conception altogether. Rather, the effects are graduated; i.e., the larger the immunologic response (concentration of antibodies), the less likely it is that a pregnancy will occur and when the blood level rises above 40%, natural conception is highly unlikely to occur.
Like any other kind of antibody manufactured by the body, sperm antibodies are formed in response to antigens. These antigens are proteins, which appear on the outer sperm membranes as the young sperm cells, develop within the male testes. In the man’s own body, his sperm are regarded as foreign invading proteins and as such would normally be targeted for attack However, under normal conditions, direct contact between the man’s blood and sperm is prevented by a cellular structure in the testes called the blood/testis barrier. This barrier is formed by so-called, Sertoli cells, which abut very closely against each other, forming tight junctions that separate the developing sperm cells from the blood and prevent immunologic stimulation. However, the blood/ testis barrier can be broken by physical or chemical injury or by infection. When this barrier is breached, sperm antigens escape from their immunologically protected environment and come in direct contact with blood elements that launch an immunologic attack.
Once sperm and blood come in contact, whether in the male or female, specific antibodies are produced against them by specialized blood cells call T- and B-lymphocytes. The three main types of sperm antibodies produced are Immunoglobulin G (IgG), Immunoglobulin A (IgA) and Immunoglobulin M (IgM). These antibodies bind to the proteins (antigens) on the sperm head, midpiece or tail. The antibodies formed may be of the circulatory type (in the blood serum) or secretory type (in the tissue). This is important because high levels of antibodies in the blood serum do not invariably mean that the antibodies will find their way to the semen where they can affect the sperm. For example, the concentration of IgG is much lower in secretions of the reproductive tract that it is in the blood. Conversely, the local level of IgA is higher in the reproductive secretions than in the blood. This is an important point, which we will return to later.
Once sperm antibodies have formed, they can affect sperm in several different ways. Some antibodies will cause sperm to stick together or agglutinate. Agglutinated sperm clump together in dense masses and thus are unable to migrate through the cervix into the uterus. Other antibodies mark the sperm for attack by Natural killer (NK) cells of the body’s immune system (ie; opsonizing antibodies). Some antibodies cause reactions between the sperm membrane and the cervical mucus preventing the sperm from swimming through the cervix (ie; immobilizing antibodies). Antibodies can also block the sperm’s ability to bind to the zona pellucida of the egg, a prerequisite for fertilization (ie; blocking antibodies). Finally, there is recent evidence that the fertilized egg shares some of the same antigens that are found on the sperm. It is possible that sperm antibodies present in the mother can react with the early embryo, resulting in its destruction by phagocytic (ie; phagocytic antibodies) cells.
There are a number of diagnostic tests available to detect the presence of sperm antibodies. These are performed by flow cytometry and the ELISA (enzyme-linked immunoabsorbent assay), the Franklin-Dukes sperm agglutination assay or the Immunobead Binding Test (IBT), to name a few. SIRM, the indirect Immunobead Binding Test (IBT) is used to detect antibodies present in the blood serum, in cervical mucus or on the sperm surface.
In the male, IgA and IgG are found in the semen although there is controversy as to whether they originate locally (secreted by testicular cells) or cross over from the circulation. Antibodies of the IgM class are not found in semen.
Like the source of some antibodies, the question of the critical levels of sperm antibodies is also hotly debated among clinicians. There seems to be general agreement that blood levels above 30% by the IBT are associated with significant fertility problems.
Studiers have shown that pregnancy is highly unlikely following natural intercourse or intrauterine insemination when either the woman or the man harbors significant antisperm antibodies.
While , there have been isolated reports that administration of corticosteroids (eg; prednisone) will temporarily suppress antibody production pregnancy rates are poor. Besides, corticosteroid therapy carries with it the risk of significant side, some of which (although infrequent) can be serious. As an example, in the man spontaneous fractures (especially of the neck of the femur) have been reported in 2 % of cases. I do not recommend this treatment.
In Vitro Fertilization (IVF) with intracytoplasmic Sperm injection (ICSI) is the best option . Here each egg is injected with a single sperm and whether there are antibodies attached to the outer surface of the sperm becomes irrelevant.. In fact, pregnancy and birth rates are the same as in cases where IVF is performed for reasons other than male factor infertility. IVF/ICSI success rates are also .not unaffected by the concentration of antisperm antibodies.
The presence of sperm antibodies reduces male fertility significantly, but does not usually prevent conception altogether. Rather, the effects are graduated; i.e., the larger the immunologic response (concentration of antibodies), the less likely it is that a pregnancy will occur and when the blood level rises above 40%, natural conception is highly unlikely to occur.
Like any other kind of antibody manufactured by the body, sperm antibodies are formed in response to antigens. These antigens are proteins, which appear on the outer sperm membranes as the young sperm cells, develop within the male testes. In the man’s own body, his sperm are regarded as foreign invading proteins and as such would normally be targeted for attack However, under normal conditions, direct contact between the man’s blood and sperm is prevented by a cellular structure in the testes called the blood/testis barrier. This barrier is formed by so-called, Sertoli cells, which abut very closely against each other, forming tight junctions that separate the developing sperm cells from the blood and prevent immunologic stimulation. However, the blood/ testis barrier can be broken by physical or chemical injury or by infection. When this barrier is breached, sperm antigens escape from their immunologically protected environment and come in direct contact with blood elements that launch an immunologic attack.
Once sperm and blood come in contact, whether in the male or female, specific antibodies are produced against them by specialized blood cells call T- and B-lymphocytes. The three main types of sperm antibodies produced are Immunoglobulin G (IgG), Immunoglobulin A (IgA) and Immunoglobulin M (IgM). These antibodies bind to the proteins (antigens) on the sperm head, midpiece or tail. The antibodies formed may be of the circulatory type (in the blood serum) or secretory type (in the tissue). This is important because high levels of antibodies in the blood serum do not invariably mean that the antibodies will find their way to the semen where they can affect the sperm. For example, the concentration of IgG is much lower in secretions of the reproductive tract that it is in the blood. Conversely, the local level of IgA is higher in the reproductive secretions than in the blood. This is an important point, which we will return to later.
Once sperm antibodies have formed, they can affect sperm in several different ways. Some antibodies will cause sperm to stick together or agglutinate. Agglutinated sperm clump together in dense masses and thus are unable to migrate through the cervix into the uterus. Other antibodies mark the sperm for attack by Natural killer (NK) cells of the body’s immune system (ie; opsonizing antibodies). Some antibodies cause reactions between the sperm membrane and the cervical mucus preventing the sperm from swimming through the cervix (ie; immobilizing antibodies). Antibodies can also block the sperm’s ability to bind to the zona pellucida of the egg, a prerequisite for fertilization (ie; blocking antibodies). Finally, there is recent evidence that the fertilized egg shares some of the same antigens that are found on the sperm. It is possible that sperm antibodies present in the mother can react with the early embryo, resulting in its destruction by phagocytic (ie; phagocytic antibodies) cells.
There are a number of diagnostic tests available to detect the presence of sperm antibodies. These are performed by flow cytometry and the ELISA (enzyme-linked immunoabsorbent assay), the Franklin-Dukes sperm agglutination assay or the Immunobead Binding Test (IBT), to name a few. SIRM, the indirect Immunobead Binding Test (IBT) is used to detect antibodies present in the blood serum, in cervical mucus or on the sperm surface.
In the male, IgA and IgG are found in the semen although there is controversy as to whether they originate locally (secreted by testicular cells) or cross over from the circulation. Antibodies of the IgM class are not found in semen.
Like the source of some antibodies, the question of the critical levels of sperm antibodies is also hotly debated among clinicians. There seems to be general agreement that blood levels above 30% by the IBT are associated with significant fertility problems.
Studiers have shown that pregnancy is highly unlikely following natural intercourse or intrauterine insemination when either the woman or the man harbors significant antisperm antibodies.
While , there have been isolated reports that administration of corticosteroids (eg; prednisone) will temporarily suppress antibody production pregnancy rates are poor. Besides, corticosteroid therapy carries with it the risk of significant side, some of which (although infrequent) can be serious. As an example, in the man spontaneous fractures (especially of the neck of the femur) have been reported in 2 % of cases. I do not recommend this treatment.
In Vitro Fertilization (IVF) with intracytoplasmic Sperm injection (ICSI) is the best option . Here each egg is injected with a single sperm and whether there are antibodies attached to the outer surface of the sperm becomes irrelevant.. In fact, pregnancy and birth rates are the same as in cases where IVF is performed for reasons other than male factor infertility. IVF/ICSI success rates are also .not unaffected by the concentration of antisperm antibodies.
Please visit my new Blog on this very site, 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)
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•The Role of Nutritional Supplements in Preparing for IVF
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
My question is: can oocytes fertilized abnormally produce a baby. I have heard yes from Google. What’s your opinion on this matter?
Thank you!!!
Dee
I fully recognize that this article will raise eyebrows because so many doctors have been brainwashed to believe that it is preferable to perform Preimplantation Genetic Sampling (PGS ) biopsies on blastocysts than on day 3 cleaved embryos. In my opinion this is incorrect and here is why:
For Preimplantation Genetic Sampling (PGS) using array CGH (aCGH) to be reliable and accurate, it requires access to more DNA than is available from a single cell biopsied from a day 3 embryo or from the 1st polar body of an egg. Presently, accurate PGS using single cell (blastomeres) is best performed using Next Generation Gene Sequencing (NGS). Biopsying a multicellular (>100cells) blastocysts by allowing aces to several cells at a time, provides much safe access to much more DNA than when a single cell (blastomere) is extracted from a 5-10 cell day 3 embryo. This serves to explain why those that champion PGS/ aCGH, favor blastocyst biopsies over day 3 biopsies, but does doing this enhance the reliability of PGS. I suggest not…
Consider the fact most numerical chromosomal aberrations (aneuploidy) in day 3 embryos originate during maturational division (meiosis) in the egg and that many such meiotically aneuploid embryos never survive to the blastocyst stage. Embryos affected by meiotic aneuploidy are permanently “incompetent”. They cannot recover. In contrast, much aneuploidy detected in the hypercellular blastocyst, originates during post-fertilization cell replication (mitosis). In the latter situation, some blastocyst cells are aneuploid while others are chromosomally normal (i.e. mosaicism). While mitotic aneuploidy can reverse (autocorrect) with such embryos developing into chromosomally normal concepti. In contrast, as stated, meiotic aneuploidy is irreversible. Since it is presently not possible to reliably differentiate between mitotic and meiotic aneuploidy, it follows that in the process of discarding aneuploid blastocyst we could well (albeit unintentional) be destroying potentially normal concepti.
Since events that occur during meiosis in the final maturation of the egg inevitably lead to “irreversible” egg/embryo “incompetence”, it is meiotic aneuploidy that needs to be identified. It follows that the closer to egg retrieval that we perform PGS/biopsies, the greater will be the likelihood that detected aneuploidy detected will be meiotic in origin. It is another e reason why I believe that day 3 PBS embryo biopsy is preferable to blastocyst biopsy.
Finally, we recently observed that a blastocyst which is ultrarapidly frozen ( vitrified) immediately following biopsy for PGS , will have reduced viability as compared to cleaved embryos biopsied on day 3 and are then allowed to recover for a few days before being vitrified.
Please visit my new Blog on this very site, 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.
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•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?
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
Dear dr Sher,
Perhaps my question was misunderstood.
I’m talking about eggs right after retrieval some may not fertilize and some may fertilize abnormally. Can these eggs that were fertilized abnormally produce a viable embryo?? I’m not talking about the ones that are tested as abnormal. I’m specifically referring to eggs that were fertilized abnormally soon after retrieval. And you get that phone call 24 hours after retrieval; about how many fertilized, how many fertilized abnormally, and how many fertilized normally. so I’m specifically again speaking of eggs that were fertilized abnormally after egg retrieval.
Thanks again dee
Thanks again Dee