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. Dear Dr. Sher—I was wondering if you could give me your opinion: I had eggs retrieved after COH three days ago, but at the time of the retrieval my RE saw that there was quite a lot of fluid in the endometrium (it hadn’t been there in any of the previous ultrasounds during stimulation). There is no easy pathological explanation for the fluid (no tubal blockage, no scarring in the uterus, no PCOS). My doctor said that there was a chance, with the pre-transfer progesterone and estrogen meds, that the fluid would be gone by day five, but even in that case, he’s reluctant to transfer as, while studies are limited (and seem to me to be a little mixed), he has had bad results with transfers into a uterus that had previous fluid in the same cycle (and his colleagues report similar misfortunes). We have today five embryos (2 8A graded and 3 8B graded), and he has recommended freezing those that thrive through day five at the blastocyst stage and trying again in two months after a transfer-only cycle with a FET. Do you have an opinion about transferring during cycles where there was endometrial fluid, if that fluid has disappeared by the transfer day? Or are the outcomes worse in such cases?
    A little more info in case it matters: I’m 37 years old, with excellent ovarian reserves according to AMH test, no previous pregnancies, this is my first IVF cycle (my husband has low sperm count following chemo in his 20s). Thanks so much for any advice! You provide so much useful information here which must help thousands of people.

    • Frances,

      In my opinion, the commonest cause of fluid in the uterus is the “backtracking” of estrogen-induced cervical mucous from the cervical, retrograde into thew cavity. My practice is to transfer blastocysts if the fluid absorbs spontaneously by day 5-6 post-fertilization and if not, to freeze the blastocysts for a “staggered” FET in a subsequent hormone replacement cycle. However, I do not fault your RE for taking a more cautious approach by freezing the blastocysts for a later FET.

      It is however important to know that sometimes, the presence of scar tissue or a surface lesion (polyp(s) or submucous fibroid(s) can also irritate the lining causing fluid collection. When this is suspected, it is wise to investigate by hysteroscopy or sonohysterogram and to correct the problem if it exists, before embarking on a Staggered FET.

      Good luck!

      Geoff Sher

  2. Hi Dr. Sher,
    I am hoping you can give me some direction. I am 32 years old. My husband is 31. We have two children who were conceived within 1-2 cycles naturally with no medication. Our first was unplanned. The youngest is 5. We have been trying for baby #3 for two years now. Sperm test was great all around. My husband tested positive for MTHFR but it wasn’t affecting his sperm in any way. My hormone levels are in the normal range. I ovulate like clockwork on day 14. I had a uterine polyp removed last year. The dr looked for endo and there was none. My left tube looked strange but the dye cleared just fine. My right tube looked fine but the dye didn’t clear. My dr doesn’t believe it was blocked though. He said my uterus and ovaries looked great. We have had autoimmune tests that were negative. My FSH was 2. My mycoplasma test was positive so next week I go in to test for Ureaplasma. The only thing that has changed is that I was diagnosed with Interstitial Cystitis after the birth of our 5 year old. We are both healthy. I’ve never had a miscarriage that I know of. My cycles are like clockwork. At this point, I’m at a loss for which direction to take. Are there any other tests we should have done? I have had Clomid sitting on my dresser for a while now but I don’t feel right about taking it when we don’t even know what’s wrong. Thank you.

    • For about 10% of all infertile couples, the cause of the infertility cannot be readily determined using conventional diagnostic methods. Such cases are often referred to as “unexplained infertility.” The truth however is that in most such cases, the diagnosis of “unexplained infertility is in fact “presumptive because a more in-depth evaluation would have revealed a cause. This having been said, people diagnosed with so called “unexplained infertility” fall into two broad groups: a)those couples who don’t have any biological problems interfering with pregnancy and, b) those who do but the reason cannot be found due to insufficient medical information or technology. It is in this latter group that improved testing techniques have made infertility easier to diagnose and treat.
      In order to make even a presumptive diagnosis of “unexplained infertility” the answers to the following questions must be in the affirmative.
      ?Is the woman ovulating normally?
      ?Is the couple having intercourse regularly in the periovulatory phase of the cycle?
      ?Are the fallopian tubes normal and open?
      ?Can endometriosis be excluded?
      ?Does the male partner have normal semen parameters (most specifically with regard to sperm count and motility?
      ?Is the post coital (Huhner) test (periovulatory examination of cervical mucous, done 6-18 hours after intercourse) normal?
      The definitive diagnosis of “unexplained infertility” has a lot to do with the thoroughness of the health care provider in excluding all possible causes. The fewer tests performed, the more likely a presumptive diagnosis
      For Example:
      ?Abnormalities of the fallopian tubes (adhesions or developmental defects) of the finger-like “petals” at their outer ends of the tubes that help sweep eggs inside (i.e. fimbriae). can prevent eggs from being collected and transported to the awaiting sperm
      ?Chromosomal abnormalities of eggs or embryos: Eggs must be euploid (contain the right number of chromosomes) to be successfully fertilized and embryos must also be euploid in order to implant successfully in the uterine lining. Until recently there was no reliable method for determining whether eggs and embryos were euploid. The recent introduction of genetic tests such as comparative genomic hybridization (CGH) now allows for identification of all chromosomes in the egg and embryo. As such CGH represents an important addition to the “infertility” diagnostic armamentarium.
      ?Luteinized Unruptured Follicle (LUF)Syndrome: Here, the eggs can become trapped in the follicle and not be released (trapped ovulation) In such cases routine tests done to detect ovulation ((temperature charting, Urine LH testing, Blood progesterone levels) may be normal resulting in false interpretation that ovulation is actually occurring.
      ?Ovulation (hormonal) Dysfunction: Abnormalities in ovarian hormone production in the preovulatory phase of the cycle (follicular phase defect) and/or in the postovulatory phase (luteal phase defect) can negatively affect preparation of the uterine lining (endometrium), thus thwarting normal implantation.
      ?Immunologic implantation dysfunction (IID): Sometimes, the woman’s or the man’s own immune system can attack sperm cells, killing them or causing them to become immobilized. Also, immunologic dysfunction involving the uterine lining can cause the implanting embryo to be rejected so early that the woman does not even recognize that she in fact had conceived.
      ?Cervical infection; Ureaplasma urealyticum infection of the cervical glands can prevent sperm from migrating through the cervix and uterus to reach the egg(s) in the fallopian tube(s). Such infection will usually not be detectable through routine examination and/or cervical culturing methods.
      ?Mild or Moderate Endometriosis: Endometriosis is in 100% of cases associated with the production of “pelvic toxins” that reduce the fertilization potential of otherwise normal eggs by a factor of 3-5. In addition, about 1/3 of woman with endometriosis (regardless of its severity) have immunologic implantation dysfunction (IID). Furthermore mild and often even moderately severe endometriosis can only be accurately diagnosed by direct visualization of the lesions through laparoscopy or laparotomy and, the detection of IID requires highly sophisticated tests that can only be adequately performed by a handful of Reproductive Immunology Reference Laboratories in the United States. Finally, a condition called nonpigmented endometriosis, in which the endometrium may be growing inside the pelvic cavity with many of the same deleterious effects as overt endometriosis, cannot be detected even by direct vision (at laparoscopy/laparotomy). The fertility of these patients may be every bit as compromised as if they had detectable endometriosis.
      ?Psychological Factors: The entire reproductive process is governed by the brain. Thus it should come as no surprise that stress and negativity can interfere with hormonal balance and decrease the ability to conceive.
      ?Mild Male Factor
      ?Antisperm antibodies in the man or woman.
      Management:
      Successful management of “Unexplained Infertility” requires that a very individualized approach be taken. Wherever possible the underlying cause should first be identified. Problems that involve ovulation dysfunction (hormonal imbalance) require ovulation induction with oral or injectible fertility drugs. Cervical mucous hostility due to infection with ureaplasma (which is transferred back and forth sexually to both partners) requires specific and concurrent antibiotic therapy. In other cases involving younger women (under 39 years) where there is a problem with sperm migration via the cervix and uterus to the fallopian tube(s) intrauterine insemination (IUI) with or without ovulation induction, is indicated. When these treatments fail, in cases, women over the age of 39 years, in women with IID, in men or women who harbor antisperm antibodies in significant concentrations and in cases associated with tubal abnormalities, in vitro fertilization (IVF) is needed. All cases of intractable, moderate or severe male infertility call for injecting sperm directly into the egg to achieve forced fertilization (intracytoplasmic sperm injection-ICSI).
      It is an indisputable fact that most causes of infertility can be diagnosed and it is a great pity that the diagnosis of “unexplained infertility” is often used as an excuse for not having performed a full and detailed evaluation of the problem. Couples should not simply accept a diagnosis of “unexplained infertility” at face value since treatment is most likely to be successful when the specific cause of the problem can be fully identified

      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)
      •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
      •Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & Con’s!
      •Micro-IVF: Often Preferable to Ovarian Stimulation with or Without IUI

      Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
      Julie Dahan
      •Email: Julied@sherivf.com
      •Phone: 702-533-2691
      ?800-780-7437

      Geoff Sher

      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.

  3. I’m 46 years old. My husband and I are trying to get pregnant over ten years now. We got 21 years old donor eggs and one egg made it to 4CC blastocyst and frozen. We would like to know if it is worth transferring it.

    Thank you so much,
    Kim

    • Yes! I think it is worthwhile trying.

      Geoff Sher

  4. Hi Dr. Sher, it has been challenging journey going through IVF with my wife, not to mention, trying to educate ourselves(I feel like we learn something new every week) to help increase the chances of us conceiving. We have gone through 2 IVF cycles and have had 4 transfers (2 fresh and 2 FET). The fresh embryo transfers did not take, but our last two FET’s were successfully until we miscarried(1st FET 38 hCG and 2nd 4,330 hCG, “we are getting closer!!”). Both fresh cycles produced 8 embryos with 4 fertilizing and making it to blast. I learned in one of your videos that, in your opinion there should not be a gap between BCP and FSH. Currently, our protocol entails a 6 day gap between BCP and gonadtrophins, then a antagonist (cetrotide) after the 10th day of gonadtrophins. In your opinion, would it be worth a try to adopt one of your protocols and start taking agonist 2 days before the last BCP and continue to take it until the menstrual cycle ends? Then start Gonadtrophins? Any input would be greatly appreciated, thank you!

    • For reasons outlined below, in my opinion it is less than optimal to initiate ovarian stimulation coming off a BCP unless there is an overlap with an agonist for the last few days of on the pill (see below).

      One often hears the expressed opinion that the BCP suppresses response to ovarian stimulation. This is not the case, provided that the BCP is overlapped with administration of an agonist (e.g. Lupron, Buserelin, Superfact) for several days leading up to the start of menstruation and the initiation of ovarian stimulation cycle with gonadotropin drugs. If the latter precaution is not taken, and the cycle of stimulation is initiated coming directly off the BCP the response will often be blunted and subsequent egg quality could be adversely affected.
      The explanation for this is that in natural (unstimulated) as well as in cycles stimulated with fertility drugs, the ability of follicles to properly respond to FSH stimulation is dependent on their having developed FSH-responsive receptors . Pre-antral follicles (PAF) do not have such primed FSH receptors and thus cannot respond properly to FSH stimulation with gonadotropins. The acquisition of FSH receptor responsivity requires that the pre-antral follicles be exposed to FSH, for a number of days (5-7) during which time they attain “FSH-responsivity” and are now known as antral follicles (AF). These AF’s are now able to respond properly to stimulation with administered FSH-gonadotropins. In regular menstrual cycles, the rising FSH output from the pituitary gland insures that PAPs convert tor AF’s. The BCP (as well as prolonged administration of estrogen/progesterone) suppresses FSH. This suppression needs to be countered by artificially causing blood FSH levels to rise in order to cause PAF to AF conversion prior to COS commencing, otherwise pre-antral-to –antral follicle conversion will not take place in an orderly fashion and the follicles will not readily respond to gonadotropins (FSH) , thereby delaying follicle development by up to 7 days and compromising egg quality. GnRH agonists (e.g. Lupron, Buserelin, Superfact) , cause an immediate surge in release of FSH by the pituitary gland thus causing conversion from PAF to SAF. This is why, women who take a BCP to launch a cycle of COS need to have an overlap of the BCP with an agonist.
      By overlapping the BCP with an agonist for a few days prior to menstruation the early recruited follicles are able to complete their developmental drive to the AF stage and as such, be ready to respond appropriately to optimal ovarian stimulation. Using this approach, the timing of the initiation of the IVF treatment cycle can readily and safely be regulated and controlled by varying the length of time that the woman is on the BCP.

      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
      •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?
      •Blastocyst Embryo Transfers Should be the Standard of Care in IVF
      •Blastocyst Embryo Transfers Done 5-6 Days Following Fertilization are Fast Replacing Earlier day 2-3 Transfers of Cleaved Embryos.
      •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.
      •Traveling for IVF from Out of State/Country–
      •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
      Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
      Julie Dahan
      •Email: Julied@sherivf.com
      •Phone: 702-533-2691
      ?800-780-7437

      Geoff Sher

      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.

  5. Dear Dr Sher,

    Could you please tell me what dosage of prontogest injections you would advise in the week before frozen transfer? My clinic doesn’t normally use it and is unsure whether it would be 5omg or 100mg daily.

    Thankyou so much

    • About 50-100mg daily but discuss with your own RE!

      Geoff Sher