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 doctor,
I hope that you will help me. I am 40 years old and I was recently pregnant but had a missed miscarrige week 10. My hcg was low and had a doubling time of 5.5 days , first measured week 6 when it was about 1550 iu/l. Spot bleeding from week 7 but 2 scanns showed fine heart beat, intrauterine pregnancy, last scan week 8 when HR was 164. After abortion week 10 because no heart beat and induced by misoprostol, i had only very little bleeding for one day. The fetus looked normal. The control scan showed no remains and a thin endometrium 0.5 mm. I just wonder why the endometrium was so thin when I bled so little. They did not want to do chromosome at the hospital. I just want some answers about what could likely be the cause of my miscarrige. Thank you in advance for your answer.
In my opinion the thin lining was the result of a failed implantation…rather than the cause of it and, I agree with you that it would have been preferable had they done karyotyping of the products of conception as chromosomal aneuploidy is the likeliest explanation.
Geoff Sher
Hello Dr. Sher!
I did IVF with my own eggs in 2016 at the age of 41, got pregnant and miscarried at 10 weeks. I tried another FET in March, but didn’t get pregnant. I used donor eggs last year, 2017, and got pregnant with twins, but miscarried again at 7 weeks. In December 2017, I went to RIA in Simi Valley for immunology testing since my doctor couldn’t figure out why I miscarried. My tests showed I tested positive for auto-antinuclear antibodies. So, I tried again this March 2018 with the same batch of donor eggs, having an IVIg transfusion a week before my FET. Unfortunately, I didn’t get pregnant. I was shocked because since I got pregnant last summer with twins, I thought I’d get pregnant this time again! I was injecting 1 ml progesterone in the morning and evening. I was also taking estradiol and baby aspirin each cycle. I’m considering one last try…I have 5 embryos left. Should I do IVIg before FET or this time do it after my FET? My doctor is leaning towards surrogacy, but I can’t afford it. I’m single and doing this on my own. I feel like I’m never going to be a mom and running out of hope. Is there something you would recommend I do differently? Thanks in advance!
It is in my opinion important to first determine the cause of your recurrent pregnancy losses before transferring the frozen embryos.
When it comes to reproduction, humans are the poorest performers of all mammals. In fact we are so inefficient that up to 75% of fertilized eggs do not produce live births, and up to 30% of pregnancies end up being lost within 10 weeks of conception (in the first trimester). RPL is defined as two (2) or more failed pregnancies. Less than 5% of women will experience two (2) consecutive miscarriages, and only 1% experience three or more.
Pregnancy loss can be classified by the stage of pregnancy when the loss occurs:
•Early pregnancy loss (first trimester)
•Late pregnancy loss (after the first trimester)
•Occult “hidden” and not clinically recognized, (chemical) pregnancy loss (occurs prior to ultrasound confirmation of pregnancy)
•Early pregnancy losses usually occur sporadically (are not repetitive).
In more than 70% of cases the loss is due to embryo aneuploidy (where there are more or less than the normal quota of 46 chromosomes). Conversely, repeated losses (RPL), with isolated exceptions where the cause is structural (e.g., unbalanced translocations), are seldom attributable to numerical chromosomal abnormalities (aneuploidy). In fact, the vast majority of cases of RPL are attributable to non-chromosomal causes such as anatomical uterine abnormalities or Immunologic Implantation Dysfunction (IID).
Since most sporadic early pregnancy losses are induced by chromosomal factors and thus are non-repetitive, having had a single miscarriage the likelihood of a second one occurring is no greater than average. However, once having had two losses the chance of a third one occurring is double (35-40%) and after having had three losses the chance of a fourth miscarriage increases to about 60%. The reason for this is that the more miscarriages a woman has, the greater is the likelihood of this being due to a non-chromosomal (repetitive) cause such as IID. It follows that if numerical chromosomal analysis (karyotyping) of embryonic/fetal products derived from a miscarriage tests karyotypically normal, then by a process of elimination, there would be a strong likelihood of a miscarriage repeating in subsequent pregnancies and one would not have to wait for the disaster to recur before taking action. This is precisely why we strongly advocate that all miscarriage specimens be karyotyped.
There is however one caveat to be taken into consideration. That is that the laboratory performing the karyotyping might unwittingly be testing the mother’s cells rather than that of the conceptus. That is why it is not possible to confidently exclude aneuploidy in cases where karyotyping of products suggests a “chromosomally normal” (euploid) female.
Late pregnancy losses (occurring after completion of the 1st trimester/12th week) occur far less frequently (1%) than early pregnancy losses. They are most commonly due to anatomical abnormalities of the uterus and/or cervix. Weakness of the neck of the cervix rendering it able to act as an effective valve that retains the pregnancy (i.e., cervical incompetence) is in fact one of the commonest causes of late pregnancy loss. So also are developmental (congenital) abnormalities of the uterus (e.g., a uterine septum) and uterine fibroid tumors. In some cases intrauterine growth retardation, premature separation of the placenta (placental abruption), premature rupture of the membranes and premature labor can also causes of late pregnancy loss.
Much progress has been made in understanding the mechanisms involved in RPL. There are two broad categories:
1.Problems involving the uterine environment in which a normal embryo is prohibited from properly implanting and developing. Possible causes include:
•Inadequate thickening of the uterine lining
•Irregularity in the contour of the uterine cavity (polyps, fibroid tumors in the uterine wall, intra-uterine scarring and adenomyosis)
•Hormonal imbalances (progesterone deficiency or luteal phase defects). This most commonly results in occult RPL.
•Deficient blood flow to the uterine lining (thin uterine lining).
•Immunologic implantation dysfunction (IID). A major cause of RPL. Plays a role in 75% of cases where chromosomally normal preimplantation embryos fail to implant.
•Interference of blood supply to the developing conceptus can occur due to a hereditary clotting disorder known as Thrombophilia.
2.Genetic and/or structural chromosomal abnormality of the embryo.Genetic abnormalities are rare causes of RPL. Structural chromosomal abnormalities are slightly more common but are also occur infrequently (1%). These are referred to as unbalanced translocation and they result from part of one chromosome detaching and then fusing with another chromosome. Additionally, a number of studies suggest the existence of paternal (sperm derived) effect on human embryo quality and pregnancy outcome that are not reflected as a chromosomal abnormality. Damaged sperm DNA can have a negative impact on fetal development and present clinically as occult or early clinical miscarriage. The Sperm Chromatin Structure Assay (SCSA) which measures the same endpoints are newer and possibly improved methods for evaluating.
IMMUNOLOGIC IMPLANTATION DYSFUNCTION
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 relatively 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 NK cells and CTL 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:
a)Antiphospholipid antibody (APA) panel
b)Antinuclear antibody (ANA) panel
c)Antithyroid antibody panel (i.e., antithyroglobulin and antimicrosomal antibodies)
d)Reproductive immunophenotype
e)Natural killer cell activity (NKa) assay (i.e., K562 target cell test)
f)Alloimmune testing of both the male and female partners
TREATMENT OF RPL
Treatment for Anatomic Abnormalities of the Uterus: 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 IL/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:
1.When in addition to a history of RPL, another standard indication for IVF (e.g., tubal factor, endometriosis, and male factor infertility) is superimposed.
2.In cases where selective immunotherapy is needed to treat an immunologic implantation dysfunction.
The reason for IVF being a preferred approach in such cases is that in order to be effective, the 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 diagnosis (PGD), with tests such as CGH, can provide a valuable diagnostic and therapeutic advantage in cases of RPL. PGD requires IVF to provide access to embryos for testing.
There are a few cases of intractable alloimmune dysfunction due to absolute DQ alpha matching 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.
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.
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
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
•Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
•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
•IVF: How Many Attempts should be considered before Stopping?
•“Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
•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
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•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
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 MD
Hi Dr Sher
We recently had our first cycle of IVF and when we got to the egg collection stage, we were advised that there were no eggs.
Having read your blog, I believe there were eggs but they may have been tightly attached to the ovaries still.
My wife is 40 years old (41 in July) and she’s had a number of abortions in the past. More recently (in the last 3 years) we have been trying for a baby with no success.
Here’s our story so far:
NB: SW is me and VW is my wife
Ovaries
2015
– VW Ultra sound scan showed no signs of chocolate cyst (endometriosis) but it did show signs of ovarian follicles (follicular cyst?)
– VW Radiologist asked if any history of fibrosis (fibrosis can cause bloated feeling)
– VW Doctor advised fibroids on the ovary
– VW Refer to gynaecologist if further symptoms persist with ovaries
– VW Will need another scan in 12 weeks to check if collapsing corpus luteum
– VW All confirmed normal on 18/04/15 from scan at hospital
– VW Arrange appointment with doctor in one week
– VW All confirmed as clear
Fertility
– SW blood tests normal (testosterone levels higher than normal)
– VW Gynaecologist advised possible endometriosis or no eggs being produced from ovaries
– VW Gynaecologist advised fertility blood test, ultrasound scan, key hole surgery and possible IVF
– SW 02/08/2016 – Semen sample provided should be available with GP in 7-10 days
– SW 12/08/16 – need to arrange another blood test (for testosterone levels being high previously) this would need to be at 9am with no food
– VW 08/08/2016- Ultrasound scan showed possible cyst/blood on right ovary
– VW Possible Endometritis on womb
– VW No evidence so far to have impact on fertility/pregnancy all normal
– VW Endometritis in womb is likely to be causing pain during menstruation
– VW Laparoscopy (keyhole surgery) consented to:
– VW Diagnose if endometriosis is present with camera
– VW Remove uterine polyps (with laser)
– VW Remove endometriosis lesions on ovaries (with laser)
– SW 23/08/2016 – Semen analysis complete and all normal which is reassuring for child birth – now need another blood sample because testosterone levels were high on previous sample (need to fast i.e not eat after midnight and arrange a morning appointment the next day)
– VW 02/11/2016 – laparoscopy + hysteroscopy diagnosis – small amount of endometriosis, removal of uterine polyps and many ovarian adhesions (one ovary blocked) – gynaecologist/surgeon advised more tests needed (MRI scan) to see if there are fibroids on the uterus
– VW 21/11/2016 gynaecologist/surgeon advised that MRI scan not necessary because biopsy results confirmed no cancerous cells on ovary and fibroid cells were benign
– VW 21/11/2016 gynaecologist/surgeon advised against open surgery to remove fibroids as it wasn’t necessary for removal
– VW 21/11/2016 gynaecologist/surgeon advised to discuss next steps with GP for more fertility testing and IVF on NHS
– VW 24/01/2017 – referred to Hospital for fertility treatment
– VW 24/04/2017 – was advised we couldn’t have IVF on NHS
– SW 28/04/2017 – Semen sample provided
– VW 22/05/2017 – call doctors to discuss with CCG options for IVF referral
– VW 31/05/2017 – Ultra Sound at Hospital – scans were normal
– SW 06/06/2017 Semen results received – results were normal
– VW 08/06/2017 – Consultation with gynaecologist
– Make appointment for fertility appointment
– VW 03/07/2017 – ultra sound scan showed small fibroids on womb (no change from last scan), cyst on ovary seems to have gone since last scan and signs of endometriosis remain
– VW 20/01/2018 AMH 3.5 pmol
– VW 06/02/2018 Oestradiol 2.33 pmol/L
– VW 06/02/2018 FSH 5.4 iu/L
– VW 06/02/2018 LH 2.2 IU/L
– VW 01/03/2018 period starts and 1st day of IVF protocol
-VW 02/03/2018 Gonal-F 300
-VW 03/03/2018 Gonal-F 300
-VW 04/03/2018 Gonal-F 300
-VW 05/03/2018 Gonal-F 300
-VW 06/03/2018 Gonal-F 300
-VW 07/03/2018 Gonal-F 300
-VW 08/03/2018 Gonal-F 300
-VW 09/03/2018 Gonal-F 300 + Ultra Sound scan (1 x normal follicle 18mm, 1 x medium follicle 12mm, 2 x small follicles <10mm)
-VW 10/03/2018 Gonal-F 300
-VW 11/03/2018 Gonal-F 300
-VW 12/03/2018 Gonal-F 300 + Cetrotide 0.25 + Ultra Sound scan (1 x normal follicle 18mm, 1 x medium follicle 12mm, 1 x small follicles <10mm)
-VW 13/03/2018 Gonal-F 300 + Cetrotide 0.25
-VW 14/03/2018 Gonal-F 300 + Orgalutran 0.25 + Ovitrelle 0.5 (36 hours before egg retrieval)
-VW/SW 16/03/2018 egg and sperm retrieval – advised there were no eggs in any of the follicles. Next protocol setup to take contraception for next menstrual cycle then Menopur the following menstrual cycle.
The questions I have are:
Why were there no eggs?
Were there eggs but they were too difficult to retrieve or were there no eggs at all?
Did she ovulate early?
Were medication timings incorrect or they wasn’t strong enough?
Would taking contraceptive pills for longer increase chances of a mature egg?
When we did US scan in first clinic the sonographer located 4 follicles but in IVF clinic only located 3 follicles (only 7 days between scans) – why?
I’m hoping you can help or advise on this situation as we are devastated at the news of no eggs
Kind regards
Steve
In my opinion, this could all be at least in part be related to diminished ovarian reserve and the protocol used for ovarian stimulation and/or its implementation increasing the the chance of the eggs developing abnormally and being grossly chromosomally abnormal (complex aneuploidy). However to respond authoritatively, I would need access to more detailed and specific information.
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.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
•Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
•Optimizing Response to Ovarian Stimulation in Women with Compromised Ovarian Response to Ovarian Stimulation: A Personal Approach.
•Egg Maturation in IVF: How Egg “Immaturity”, “Post-maturity” and “Dysmaturity” Influence IVF Outcome:
•Commonly Asked Question in IVF: “Why Did so Few of my Eggs Fertilize and, so Many Fail to Reach Blastocyst?”
•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
•Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•Staggered IVF
•Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of 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 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
•IVF Egg Donation: A Comprehensive Overview
•“Empty follicle syndrome”
If you are interested in my advice or medical 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.
Also, my 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 MD
2. Were there eggs but they were too difficult to retrieve or were there no eggs at all?
Did she ovulate early?
2. Were medication timings incorrect or they wasn’t strong enough? I would need much more information to respond aurhoritatively
3. Would taking contraceptive pills for longer increase chances of a mature egg?
When we did US scan in first clinic the sonographer located 4 follicles but in IVF clinic only located 3 follicles (only 7 days between scans) – why?
I’m hoping you can help or advise on this situation as we are devastated at the news of no eggs
Kind regards
Hi both myself and my partner are 34. Our first ivf cycle has just failed in the UK. I was on buserelin, gonal f and then my trigger shot was ovitrelle. All results for me throughout the treatment were excellent and on egg collection day we had 15 eggs. We have to use ICSI and when they looked at the eggs and started to prepare them, they were all unusable. Noone at our clinic had seen this before. We are a healthy weight with a good diet. We will try again but with no answers it’s difficult to know what to do differently. Have you seen this before?
Hi Dr. Sher,
I am 25 weeks pregnant and experiencing anxiety and depression. I can’t sleep at night due to anxiety. The dr. Says that the racing heart and cortisol I’m producing isn’t good for the baby. He prescribed 0.5mg lorazepam for sleeping (which I started taking at 20 weeks), and now he wants to switch me to an SSRI called Citalopram. I’m reluctant to take it because I don’t want to cause harm to the baby, especially long term harm like intellectual disabilities while its brain is still forming in the womb, or physical disabilities, but I’m severely depressed and have insomnia. I don’t know how to survive the next 3 months with disrupted sleep and depression. I feel trapped. What is the right way to go? Please help me if you have any knowledge of this. The internet is full of conflicting information.
Thank you,
Michelle
In your situation you need to follow the advice of your OB. Also I suggest you also consider seeking some psychological counseling.
Good luck!
Geoff Sher