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! I was wondering if I have/have had ureaplasma if it will do anything to my fertility in the future?

    • Ureaplasma urealyticum is a bacterium that belongs to the mycoplasma family. It can be detected in the reproductive tract of as many as 40% of individuals (male and female). Ureaplasma probably does not prevent normal conception in the majority of cases, because the uterine cavity remains sterile even in women whose cervical mucous cultures positive for the organism. However, when present in the woman’s cervical secretions, the organism can be unintentionally dragged into the uterine cavity through introduction of a catheter into the uterus at the time of embryo transfer (ET) or intrauterine insemination (IUI). Molecular biologists have shown that contamination of rapidly growing cell cultures, by this organism and its close “relative”, mycoplasma hominis rapidly destroys such cells. The implanting embryo is indeed an example of an organism that comprises rapidly growing cells in a biological culture medium (the uterine lining), and as such, the cells of the trophoblast that form the “root system” of the embryo are vulnerable to intrauterine infection with Ureaplasma. However, even if the uterine cavity were to become infected, the infection willl be purged with the shedding of the infected lining at the time of the next menstruation.
      While infection with Ureaplasma rarely produces symptoms in the woman, it sometimes causes symptomatic prostatitis or epydidimitis in men. Although ureaplasma can be transmitted from one partner to the other by sexual intercourse, it may also be acquired by other means, since a large percentage of couples in monogamous relationships will culture positive for the organism. It is very difficult for the organism to grow in the laboratory. Accordingly, the reproductive secretions of both partners should be evaluated (sperm and cervical mucus) individually. Successful culturing of ureaplasma requires a specialized media in which the specimens can be transported safely from the physician’s office to the microbiology laboratory.
      If both partners culture negative, we can assume that there is no infection present. However, if one partner cultures positive and the other negative, we would err on the side of caution, by assuming that the negative result was caused by the difficulty in culturing the organism. When ureaplasma is detected in the reproductive secretions of either partner, both should be treated concurrently with the appropriate antibiotic (doxycycline, zithromax, erythromycin, ciprofloxin, or metranidazole).
      Unfortunately, in approximately 30-40% of couples infected ureaplasma urealyticum, the bacteria will have built resistance to mainstay traditional antibiotics such as tetracyclines (e.g. doxycycline) and erythromycin (e.g. Zythromax) derivatives. In such cases, ciprofloxin or metronidazole (Flagyl) therapy might be needed. This is the reason that we prefer to document cure by reculturing each partner prior to beginning ovarian stimulation for an IVF cycle.
      Several authors have shown a difference in pregnancy rates among patients with ureaplasma infection who were treated with antibiotics and those who were not. Other reports have not been able to identify an effect on outcome from ureaplasma infection. Thus, until the final verdict is in regarding the roll of ureaplasma with regard to its effect on IVF implantation, we prefer to err on the side of caution and ensure that this organism is absent in cervical secretions and semen before transferring embryos. To this end, my patients all receive prophylactic antibiotic therapy around the time of embryo transfer. This is administered as oral ciprofloxin. A day or two prior to embryo transfer, vaginal cleomycin suppositories are added.

      Good luck!

      Geoff Sher

  2. Hi Dr, I just turn 34 and we have been trying to conceive for the last 2 years, all my studies look great also my husband´s. I had an IUI last may with my own cycle egg 19mm and good lining, sample of 44mill but wasn’t successful, now the doctor says I might have endometriosis even if I have no symptoms at all, my cramps are mild and no heavy menstrual flow but now he is suggesting to have laparoscopic surgery, We are thinking that because I have no symptoms, even if I might have endometriosis isn’t is better to consider IVF? I don’t want to have a surgery that might not even help to get pregnant. I will appreciate your advice. Thanks!

    • When women with infertility due to endometriosis seek treatment, they are all too often advised to first try ovarian stimulation (ovulation Induction) with intrauterine insemination (IUI) ………as if to say that this would be just as likely to result in a baby as would in vitro fertilization (IVF). Nothing could be further from reality It is time to set the record straight. And hence this blog!

      Bear in mind that the cost of treatment comprises both financial and emotional components and that it is the cost of having a baby rather than cost of a procedure. Then consider the fact that regardless of her age or the severity of the condition, women with infertility due to endometriosis are several fold more likely to have a baby per treatment cycle of IVF than with IUI. It follows that there is a distinct advantage in doing IVF first, rather than as a last resort.

      So then, why is it that ovulation induction with or without IUI is routinely offered proposed preferentially to women with mild to moderately severe endometriosis? Could it in part be due to the fact that most practicing doctors do not provide IVF services but are indeed remunerated for ovarian stimulation and IUI services and are thus economically incentivized to offer IUI as a first line approach? Or is because of the often erroneous belief that the use of fertility drugs will in all cases induce the release (ovulation) of multiple eggs at a time and thereby increase the chance of a pregnancy. The truth however is that while normally ovulating women (the majority of women who have mild to moderately severe endometriosis) respond to ovarian stimulation with fertility drugs by forming multiple follicles, they rarely ovulate > 1 (or at most 2) egg at a time. This is because such women usually only develop a single dominant follicle which upon ovulating leaves the others intact. This is the reason why normally ovulating women who undergo ovulation induction usually will not experience improved pregnancy potential, nor will they have a marked increase in multiple pregnancies. Conversely, non-ovulating women (as well as those with dysfunctional ovulation) who undergo ovulation induction, almost always develop multiple large follicles that tend to ovulate in unison. This increases the potential to conceive along with an increased risk multiple pregnancies.

      So let me take a stab at explaining why IVF is more successful than IUI or surgical correction in the treatment of endometriosis-related infertility:
      1.The toxic pelvic factor: Endometriosis is a condition where the lining of the uterus (the endometrium) grows outside the uterus. While this process begins early in the reproductive life of a woman, with notable exceptions, it only becomes manifest in the 2ndhalf of her reproductive life. After some time, these deposits bleed and when the blood absorbs it leaves a visible pigment that can be identified upon surgical exposure of the pelvis. Such endometriotic deposits invariably produce and release toxins” into the pelvic secretions that coat the surface of the membrane (the peritoneum) that envelops all abdominal and pelvic organs, including the uterus, tubes and ovaries. These toxins are referred to as “the peritoneal factor”. Following ovulation, the egg(s) must pass from the ovary (ies), through these toxic secretions to reach the sperm lying in wait in the outer part the fallopian tube (s) tube(s) where, the sperm lie in waiting. In the process of going from the ovary(ies) to the Fallopian tube(s) these eggs become exposed to the “peritoneal toxins” which alter s the envelopment of the egg (i.e. zona pellucida) making it much less receptive to being fertilized by sperm. As a consequence, if they are chromosomally normal such eggs are rendered much less likely to be successfully fertilized. Since almost all women with endometriosis have this problem, it is not difficult to understand why they are far less likely to conceive following ovulation (whether natural or induced through ovulation induction). This “toxic peritoneal factor impacts on eggs that are ovulated whether spontaneously (as in natural cycles) or following the use of fertility drugs and serves to explain why the chance of pregnancy is so significantly reduced in normally ovulating women with endometriosis.
      2.The Immunologic Factor: About one third of women who have endometriosis will also have an immunologic implantation dysfunction (IID) linked to activation of uterine natural killer cells (NKa). This will require selective immunotherapy with Intralipid infusions, and/or heparinoids (e.g. Clexane/Lovenox) that is much more effectively implemented in combination with IVF.
      3.Surgical treatment of mild to moderate endometriosis does not usually improve pregnancy potential:. The reason is that endometriosis can be considered to be a “work in progress”. New lesions are constantly developing. So it is that for every endometriotic seen there are usually many non-pigmented deposits that are in the process of evolving but are not yet visible to the naked eye and such evolving (non-visible) lesions can also release the same “toxins that compromise fertilization. Accordingly, even after surgical removal of all visible lesions the invisible ones continue to release “toxins” and retain the ability to compromise natural fertilization. It also explains why surgery to remove endometriotic deposits in women with mild to moderate endometriosis usually will fail to significantly improve pregnancy generating potential. In contrast, IVF, by removing eggs from the ovaries prior to ovulation, fertilizing these outside of the body and then transferring the resulting embryo(s) to the uterus, bypasses the toxic pelvic environment and is therefore is the treatment of choice in cases of endometriosis-related infertility.

      I am not suggesting that all women with infertility-related endometriosis should automatically resort to IVF. Quite to the contrary…. In spite of having reduced fertility potential, many women with mild to moderate endometriosis can and do go on to conceive on their own (without treatment). It is just that the chance of this happening is so is much lower than normal.

      In young ovulating women (< 35 years of age ) with endometriosis, who have normal reproductive anatomy and have fertile male partners, expectant treatment is often preferable to IUI or IVF. However, for older women, women who (regardless of their age) have any additional factor (e.g. pelvic adhesions, ovarian endometriomas, male infertility, IID or diminished ovarian reserve-DOR) IVF should be the primary treatment of choice. 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?
      •The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
      • “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!
      •Traveling for IVF from Out of State/Country–
      •Endometriosis and Infertily
      •Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
      •Treating Ovarian Endometriomas with Sclerotherapy.

      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 have one frozen embryo that I will soon be transferring. I was told it is a Grade 5CB. From what I read that doesn’t sound very good. Is it worth a try in your opinion?

    • Sorry Sue,

      Different programs use different grading systems and I am not familiar with the one used on your embryo.

      Geoff Sher

  4. Hi Dr Sher! I was a patient of yours until you moved away and am now seeing Dayal at the St Louis office (she’s great btw). After three failed IVF attempts, I’m hoping you have some new/experimental research or advice I can try for IID?

    -Cycle 1: My egg (fresh), donor sperm, treated with dex, intralipids – negative
    -Cycle 2: Donor egg , donor sperm, (fresh cycle, PGS normal (got PGS results after implantation of course)), treated with dex, intralipids – negative
    -Mock Cycle for ERA, not enough tissue to perform test
    -Cycle 3: Donor egg , donor sperm, (frozen, PGS normal), treated with prednisone, double intralipids, Lovenox – negative

    All the other regular tests for pollups and such were done of course. I do show an elevated level of NK Cells and an elevated ratio of TH1/TH2 (but the steriods and intralipids should be treating these).

    Thanks!

    • I mean I got the PGS results after transfer already happened, not after implantation as I haven’t had any implant.

    • I really would need to review your records thoroughly to determine a) If you have been using the same sperm donor, whether he and you might share a DQ alpha/HLA match because that would alter treatment and b) whether or not there is another uterine factor being overlooked such as an intrauterine surface lesion. This would require a hysteroscopy. If everything is normal then with your next cycle I would recommend switching from intralipid to IVIG.

      Good luck!

      Geoff Sher

  5. So.. Can polyps grow back fast? I had two polyps removed in March of this year… Could they have grown back already? I also had a tiny cyst that was on my left ovary (they said it was not hurting anything or producing any estrogen.) When we did our first FET .. I have another hysteroscopy on next Thursday.. If there are no polyps then could I possibly just have cysts? because like I said yesterday my period this month was crazy.. Two days of heavy bleeding then barely anything. How will my Dr be able to see if I have an ovarian cysts while doing a hysteroscopy?

    • The polyps can grow back quickly and the hysteroscopy will not detect a cyst…only polyps and other intrauterine surface lesions. Ultrasound will diagnose cysts.

      Good luck!

      Geoff Sher