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.

19,771 Comments

  1. Hi Dr. Sher,
    Is there anything you recommend for PCOS women with recurrent implantation failure and pregnancy loss? I am 28 and have non insulin resistant PCOS with no other health problems. I have now transferred 6 PGS normal embryos over 3 frozen cycles. Two of them resulted in negative betas, this last one resulted in a positive beta of 46.5 at 11dp5dt that only rose to 53 at 14dp5dt. I am waiting to miscarry. I have hetero MTHFR, all of my immune panels have come back clean. I’ve had a hysteroscopy to remove a polyp and adhesion. My protocol (in addition to vitamins) has included Heparin, baby aspirin, dexamethasone, Metanx prescription, as well as PIO 2mL/day and estradiol valerate 0.3mL 2x/week. My husband and I are at a loss as we assumed IVF with PGS was usually pretty successful, and we’ve now gone through 6 embryos with only one confirmed pregnancy that unfortunately is not viable. Does PCOS have an effect on implantation? Anything else you suggest for us?

  2. Hi Dr. Sher,

    I’m 38 years old and I’ve been TTC for 15 months. I’m from Toronto. I was diagnosed with Diminished ovarian reserve and though I’m 38, my doctors are telling me that my ovaries function as a 43 year old.

    During investigations I was told I have a polyp in the cavity of my uterus. I had an operation to have it removed.

    After I had the polyp removed, I did an IUI. I had one follicle at 20mm and my FSH was 25. I did not get pregnant from that IUI.

    After that, I was given clomid 150mg for five days, from days 3-7, and I did not respond to clomid whatsoever. Right after takin clomid they told me that i developed a cyst. Before this, I always had a 28 day cycle. When I took Clomid, I had 39-40 day cycles and I also missed one period.

    I naturally produce maximum three follicles and minimum one. It varies from cycle to cycle.

    My cyst has now shrunk to 0.9mm, and I was hoping to do an IUI except my fertility doctor doesn’t want to do it because he says that my FSH is too high this month at 18.5. But this month I have two follicles, one on each side, measured on day 4 at less than 10mm. I really wanted to do a medicated IUI, but my doctor refused and told me to wait till next month to see if my FSH changes and if I have more follicles next month. Why did my doctor refuse just because of my FSH? Prior to this, he used my cyst as an excuse to not give me an IUI.

    My diagnosis is diminished ovarian reserve, which, as I understand, my FSH will always be higher than normal and since I have sought treatment two years ago, I never never had more than 1-3 follicles each cycle. So if this is the case, why shouldn’t I do IUI this cycle? It seems to me, time is of the essence for me.

    My fertility doctors are recommending donor eggs for me, but if I have follicles, don’t I still have a chance to get pregnant with my own eggs?

    What would you recommend for me? Do you think I should do IUI or IVF? What’s the best course of action for me?

    Stacey

  3. Hello Dr. Sher,
    I am 30. Stage 3 endo. Male factor. My first ivf cycle resulted in 6 eggs, 5 mature, 4 fertilized. 2 embryos stopped growing. 0 eggs retrieved from left ovary. Chocolate cyst discovered on left ovary 5 months before ivf. Amh .55. Fsh 5.6. Afc 5-7 per ovary. 1 morula transferred on day 5. Negative pregnancy test. 1 day 7 hatching blast frozen. Graded 5bb.
    My new RE has me on the following protocol before my next ivf cycle. 2mg 3 times a day of estradiol. This is for 28 days. The last 10 days of being on the estradiol I’ll add progesterone 200mg twice a day. I’ll start my ivf meds 4 days after finishing the estrogen and progesterone. I don’t know yet what they will be. Can you explain this to me? I was on birth control pills before my first cycle. Hope to hear from you! Thank you!
    Erin

    • You have endometriosis and diminished ovarian reserve. You also have an endometrioma that in my opinion, needs to be addressed prior to ovarian stimulation for IVF. Finally, you should know that 1/3 of women who have endometriosis will (regardless of its severity) also have an immunologic implantation dysfunction (IID). All these issues need to be addressed.

      1. 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”.

      2. Endometriosis and immunologic implantation dysfunction:

      More than half of women who have endometriosis harbor antiphospholipid antibodies (APA) that can compromise development of the embryo’s root system (trophoblast). In addition and far more serious, is the fact that in about one third of cases endometriosis, regardless of its severity is associated with NKa and cytotoxic uterine lymphocytes (CTL) which can seriously jeopardize implantation. This immunologic implantation dysfunction (IID) is diagnosed by testing the woman’s blood for APA, for NKa (using the K-562 target cell test or by endometrial biopsy for cytokine activity) and, for CTL (by a blood immunophenotype). Activated NK cells attack the invading trophoblast cells (developing “root system” of the embryo/early conceptus) as soon as it tries to gain attachment to the uterine wall. In most cases, this results in rejection of the embryo even before the pregnancy is diagnosed and sometimes, in a chemical pregnancy or an early miscarriage. As such, many women with endometriosis, rather than being infertile, in the strict sense of the word, often actually experience repeated undetected “mini-miscarriages”.
      Women who harbor APA’s often experience improved IVF birth rates when heparinoids (Clexane/Lovenox) are administered from the onset of ovarian stimulation with gonadotropins until the 10th week of pregnancy. NKa is treated with a combination of Intralipid (IL) and steroid therapy: Intralipid (IL) is a solution of small lipid droplets suspended in water. When administered intravenously, IL provides essential fatty acids, linoleic acid (LA), an omega-6 fatty acid, alpha-linolenic acid (ALA), an omega-3 fatty acid.IL is made up of 20% soybean oil/fatty acids (comprising linoleic acid, oleic acid, palmitic acid, linolenic acid and stearic acid) , 1.2% egg yolk phospholipids (1.2%), glycerin (2.25%) and water (76.5%).IL exerts a modulating effect on certain immune cellular mechanisms largely by down-regulating NKa.
      The therapeutic effect of IL/steroid therapy is likely due to an ability to suppress pro-inflammatory cellular (Type-1) cytokines such as interferon gamma and TNF-alpha. IL/steroids down-regulates NKa within 2-3 weeks of treatment the vast majority of women experiencing immunologic implantation dysfunction. In this regard IL is just as effective as Intravenous Gamma globulin (IVIg) but at a fraction of the cost and with a far lower incidence of side-effects. Its effect lasts for 4-9 weeks when administered in early pregnancy.
      The toxic pelvic environment caused by endometriosis, profoundly reduces natural fertilization potential. As a result normally ovulating infertile women with endometriosis and patent Fallopian tubes are much less likely to conceive naturally, or by using fertility agents alone (with or without intrauterine (IUI) insemination. The only effective way to bypass this adverse pelvic environment is through IVF. I am not suggesting here that all women who have endometriosis require IVF! Rather, I am saying that in cases where the condition is further compromised by an IID associated with NKa and/or for older women(over 35y) who have diminished ovarian reserve (DOR) where time is of the essence, it is my opinion that IVF is the treatment of choice.

      3. Endometrioma:

      Women, who have advanced endometriosis, often have endometriotic ovarian cysts, known as endometriomas. These cysts contain decomposed menstrual blood that looks like melted chocolate…hence the name “chocolate cysts”. These space occupying lesions can cause chronic pelvic pain, pain with intercourse (dyspareunia) and painful menstrual periods, thus compromising quality of life. They can also activate ovarian connective tissue (stroma or theca) resulting in an overproduction of male hormones (especially testosterone). An excess of ovarian testosterone can severely compromise follicle and egg development in the affected ovary. Thus there are two reasons for treating endometriomas. The first is to alleviate symptoms and the second is to optimize egg and embryo quality.
      Conventional treatment of endometriomas involves surgical drainage of the cyst contents with subsequent removal of the cyst wall (usually by laparoscopy).Unfortunately, with surgery normal ovarian tissue can be inadvertently removed/damaged along with the cyst wall, thereby decreasing the number of available eggs for harvest. Since many women who have endometriomas also have advanced endometriosis and have had one or more previous surgeries, they often .have significant scarring and adhesions. This can compromise visualization of and access to anatomic structures during conventional laparoscopic surgical correction, increasing the risk of surgical complications.
      Many patients with recurrent ovarian endometriomas are uncomfortable with the prospect of repeat surgery and its avoidance is often a factor in their decision to proceed with IVF. We recently reported on a new, effective and safe outpatient approach to treating endometriomas in women planning to undergo IVF. We termed the treatment ovarian Sclerotherapy. The process involves; needle aspiration of the “chocolate colored liquid content of the endometriotic cyst, followed by the injection of 5% tetracycline hydrochloride into the cyst cavity. Such treatment will, more than 75% of the time result in disappearance of the lesion within 6-8 weeks. In some cases the injection of tetracycline into the endometrioma causes a reaction that results in clear or blood stained fluid collecting in the original cyst cavity where the endometrioma had been. Upon re-aspirating the fluid in the seroma, the lesion will usually disappears permanently most times. In a small number of cases, the endometrioma comes back and sclerotherapy must be repeated or surgical removal undertaken.
      Ovarian sclerotherapy can be performed under local anesthesia or under conscious sedation. It has the advantage of being an ambulatory in-office procedure, low cost, and has a low incidence of significant post-procedural pain or complications and the avoidance of the need for laparoscopy or laparotomy.
      Sclerotherapy is a safe and effective alternative to surgery for definitive treatment of recurrent ovarian endometriomas in a select group of patients planning to undergo IVF. Since the procedure is associated with a small, but yet realistic possibility of adhesion formation; its use should be confined to cases where IVF is the only treatment available to the patient. Women who intend to try and conceive through fertilization in their Fallopian tubes (e.g; following natural conception or intrauterine insemination) are better off undergoing laparotomy or laparoscopy for the treatment of endometriomas.

      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!
      •Endometriosis and Infertily

      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

  4. Dr. Geoffrey,

    Hello! I’m a 39-year old woman trying for pregnancy. I have a FSH 24,6 and AMH 0,362. Never had children before. Possible to get pregnant? Which method would you suggest?
    Please assist as I am so lost and desperate from informations I read all over.
    Thank you very much,
    Eva

  5. Hi Dr Sher,
    I had my first egg retrieval today and looks like I will need another. How long should I wait before starting stims? Thanks

    • In my opinion, you need one full resting cycle between egg retrievals.

      Geoff Sher