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. Dr. Sher,
    Leading up to my past FETs, my lining has been on the thinner side (6-7.5mm) but always trilaminar. I have chronic mild endometritis but all else looks good.

    Today I went in for my Mid-cycle check and this is the FIRST time in all my cycles that it has ever NOT been trilaminar.

    What might be the cause of this and would you recommend canceling the cycle? What would you suggest doing to fix the trilaminar issue?

    • Regardless of cause, , a lining of <8mm is inadequate. The absence of a trilaminar pattern does not really alarm me at all.

      It was as far back as 1989, when I first published a study that examined the correlation between the thickness of a woman’s uterine lining (the endometrium), and the subsequent successful implantation of embryos in IVF patients. This study revealed that when the uterine lining measured <8mm in thickness by the day of the “hCG trigger” (in fresh IVF cycles), or at the time of initiating progesterone therapy (in embryo recipient cycles, e.g. frozen embryo transfers-FET, egg donation-IVF etc.) , pregnancy and birth rates were substantially improved. Currently, it is my opinion, that an ideal estrogen-promoted endometrial lining should ideally measure at least 9mm in thickness and that an endometrial lining measuring 8-9mm is “intermediate”. An estrogenic lining of <8mm is in most cases unlikely to yield a viable pregnancy.

      A “poor” uterine lining is usually the result of the innermost layer of endometrium (the basal or germinal endometrium from which endometrium grows) ) not being able to respond to estrogen by propagating an outer, “functional” layer thick enough to support optimal embryo implantation and development of a healthy placenta (placentation). The “functional” layer ultimately comprises 2/3 of the full endometrial thickness and is the layer that sheds with menstruation in the event that no pregnancy occurs.

      The main causes of a “poor” uterine lining are:

      1.Damage to the basal endometrium as a result of:
      a.Inflammation of the endometrium (endometritis) most commonly resulting from infected products left over following abortion, miscarriage or birth
      b.Surgical trauma due to traumatic uterine scraping, (i.e. due to an over-aggressive D & C)
      2.Insensitivity of the basal endometrium to estrogen due to:
      a.Prolonged , over-use/misuse of clomiphene citrate
      b.Prenatal exposure to diethylstilbestrol (DES). This is a drug that was given to pregnant women in the 1960’s to help prevent miscarriage
      3.Over-exposure of the uterine lining to ovarian male hormones (mainly testosterone): Older women, women with diminished ovarian reserve (poor responders) and women with polycystic ovarian syndrome -PCOS tend to have raised LH biological activity.. This causes the connective tissue in the ovary (stroma/theca) to overproduce testosterone. The effect can be further exaggerated when certain methods for ovarian stimulation such as agonist (Lupron/Buserelin) “flare” protocols and high dosages of menotropins such as Menopur are used in such cases.
      4.Reduced blood flow to the basal endometrium:
      Examples include;
      a.Multiple uterine fibroids - especially when these are present under the endometrium (submucosal)
      b.Uterine adenomyosis (excessive, abnormal invasion of the uterine muscle by endometrial glands).

      “The Viagra Connection”

      Eighteen years ago years ago, after reporting on the benefit of vaginal Sildenafil (Viagra) for to women who had implantation dysfunction due to thin endometrial linings I was proud to announce the birth of the world’s first “Viagra baby.” Since the introduction of this form of treatment, thousands of women with thin uterine linings have been reported treated and many have gone on to have babies after repeated prior IVF failure.

      For those of you who aren’t familiar with the use of Viagra in IVF, allow me to provide some context. It was in the 90’s that Sildenafil (brand named Viagra) started gaining popularity as a treatment for erectile dysfunction. The mechanism by which it acted was through increasing penile blood flow through increasing nitric oxide activity. This prompted me to investigate whether Viagra administered vaginally, might similarly improve uterine blood flow and in the process cause more estrogen to be delivered to the basal endometrium and thereby increase endometrial thickening. We found that when Viagra was administered vaginally it did just that! However oral administration was without any significant benefit in this regard. We enlisted the services of a compound pharmacy to produce vaginal Viagra suppositories. Initially, four (4) women with chronic histories of poor endometrial development and failure to conceive following several advanced fertility treatments were evaluated for a period of 4-6 weeks and then underwent IVF with concomitant Viagra therapy. Viagra suppositories were administered four times daily for 8-11 days and were discontinued 5-7 days prior to embryo transfer in all cases.

      Our findings clearly demonstrated that vaginal Viagra produced a rapid and profound improvement in uterine blood flow and that was followed by enhanced endometrial development in all four cases. Three (3) of the four women subsequently conceived. I expanded the trial in 2002 and became the first to report on the administration of vaginal Viagra to 105 women with repeated IVF failure due to persistently thin endometrial linings. All of the women had experienced at least two (2) prior IVF failures attributed to intractably thin uterine linings. About 70% of these women responded to treatment with Viagra suppositories with a marked improvement in endometrial thickness. Forty five percent (45%) achieved live births following a single cycle of IVF treatment with Viagra The miscarriage rate was 9%. None of the women who had failed to show an improvement in endometrial thickness following Viagra treatment achieved viable pregnancies.

      Following vaginal administration, Viagra is rapidly absorbed and quickly reaches the uterine blood system in high concentrations. Thereupon it dilutes out as it is absorbed into the systemic circulation. This probably explains why treatment is virtually devoid of systemic side effects

      It is important to recognize that Viagra will NOT be effective in improving endometrial thickness in all cases. In fact, about 30%-40% of women treated fail to show any improvement. This is because in certain cases of thin uterine linings, the basal endometrium will have been permanently damaged and left unresponsive to estrogen. This happens in cases of severe endometrial damage due mainly to post-pregnancy endometritis (inflammation), chronic granulomatous inflammation due to uterine tuberculosis (hardly ever seen in the United States) and following extensive surgical injury to the basal endometrium (as sometimes occurs following over-zealous D&C’s).

      Combining vaginal Viagra Therapy with oral Terbutaline;
      In my practice I sometimes recommend combining Viagra administration with 5mg of oral terbutaline. The Viagra relaxes the muscle walls of uterine spiral arteries that feed the basal (germinal) layer of the endometrium while Terbutaline, relaxes the uterine muscle through which these spiral arteries pass. The combination of these two medications interacts synergistically to maximally enhance blood flow through the uterus, thereby improving estrogen delivery to the endometrial lining. The only drawback in using Terbutaline is that some women experience agitation, tremors and palpitations. In such cases the terbutaline should be discontinued. Terbutaline should also not be used women who have cardiac disease or in those who have an irregular heartbeat.
      About 75% of women with thin uterine linings see a positive response to treatment within 2-3 days. The ones that do not respond well to this treatment are those who have severely damaged inner (basal/germinal) endometrial linings, such that no improvement in uterine blood flow can coax an improved response. Such cases are most commonly the result of prior pregnancy-related endometrial inflammation (endometritis) that sometimes occurs post abortally or following infected vaginal and/or cesarean delivery.
      Viagra therapy has proven to be a god send to thousands of woman who because of a thin uterine lining would otherwise never have been able to successfully complete the journey “from infertility to family”.

      To be effective, Viagra must be administered vaginally. It is NOT effective when taken orally. We prescribe 20mg vaginal suppositories to be inserted four times per day. Treatment is commenced soon after menstruation ceases and is continued until the day of the “hCG trigger.” While ideally the treatment should be sustained throughout the first half of the cycle, most women will respond within 48-72 hours. For this reason, Viagra can be used to “rescue” a poor lining after the cycle has already started, provided that there is enough time remaining prior to ovulation, egg retrieval or progesterone administration.

      Geoff Sher

  2. hi dr Sher
    i had my first beta hcg last friday( sept 14) at 1300. but my progesteron level 7.4. my doctor said that it’s good number considering i’m still 4 weeks pregnant. she put me on crinone once a day, duphaston 2 pills orally, and femoston. and she said that vaginal suppositories goes directly to uterus so it doesn’t show up in blood test. this week my doctor will do blood test again to check for second beta and progesteron level.
    my question is how do i know if i get enough progesteron to support my pregnancy? what is your best advice? i’m just worried about the progesteron level since this is my first baby and my only normal pgs tested embryo.

    Best Regard
    Sandy

    • Unfortunately, only time will tell. There is not anything more you can do.

      Good luck!

      Geoff Sher

  3. Dr I just want to find out, what is going on. I had 5 day trf 25 Aug 2018. My blood work came back negative on the 4 September 2018. I stopped all medication and accepted a negative. But since then I still have pregnancy symptoms, I am just worried that it could be a cyst. Do I do another blood test, or make appointment for ultra sound. Thank you

    • I would do a repeat test and then if -ve do an US.

      Geoff Sher

  4. Hi Dr sher, what is your opinion on transferring the following mosaic embryo: -15p15.33-15.2(12mb,50%)??

    • I would!

      Geoff Sher

  5. I have had a devastating year and a half and I hope you can give me some advice.

    I have been recently diagnosed with lean PCOS which I’m slight skeptical about. I am not your typical candidate. I’m in shape (44kg/151cm), have regular periods and produce one egg every month (according to ultrasound and follicular tracking). I have undergone A LOT before being told that I’m a lean cyster . I’m a 24 year old who has been trying to conceive for a year and a half. Firstly, I started my journey with ovulation kits. The smiley face ALWAYS showed up giving me false hope. Then i went on with a little stimulates to increase the amount of follicles in my ovaries and release more eggs followed by the trigger shot. Every month, I had about 2 or 4 eggs tops because I was taking low dosages. When that failed, I did a round of IUI which also failed. I went on and had an HSG to check my tubes which were patent. I did another round of IUI which again failed. One of my doctors suggested that I do a laparoscopy, which I did. They found a tiny septum in the uterus which they resurrected. Assuming that was the problem, we tried naturally for months. Nothing worked. Then we tried another round of stimulates which failed. I decided to get into IVF. I produced 10 eggs and 8 blastocysts. 2 embryos transferred. No pregnancy. 19 doctors later and I was diagnosed with lean PCOS. He had one look at me and assumed I had PCOS. From my skin. My skin is not a pimple fest. But I do have some reoccurring pimples which are barely visible but you can see SLIGHT spotting or scarring. My hair sheds a lot too and I do have some bothersome body hair even after a million sessions of laser hair removal. Anyway, the doctor checked through the ultrasound and had a look at my ovaries and claimed that one had more follicles than it should. It had around 15 follicles I guess. So he ruled it as lean PCOS. He put me on 1000mg Metformin and ask asked me to cut sugar, gluten and dairy.

    Now I was dumbfounded because my periods are extremely regular and I was clearly ovulating. My weight was always more than fine. The thing that I completely dismissed was my diet and exercise. I have always been that person who eats EVERYTHING but never gains weight. So I never bothered dieting or exercising. Also I wasn’t insulin resistant so it didn’t make much sense. But apparently, lack of diet and exercise affects the eggs chromosomes. So even if I do make good looking embryos, they could be chromosomely faulty. I didn’t do a PGS testing on my embryos because I’m only 24 and my doctor didn’t think there was a need.

    Now, I’m just wondering if I do have high androgen levels (which I’m not sure of because I never tested for that) affect an embryo’s chromosome? My doctor claims that PCOS affects an embryo’s chromosomal formation. My FSH and LH levels are 1:1 ratio too. He asked me to follow almost vegan diet and exercise. The next 3 months we’ll try with IUI then if that fails we’ll get into IVF. I’m very skeptical and I hope you can give me some kind of answer to this?

    • Hi Rora,

      I too am very skeptical about the diagnosis of PGS in your case. With no alteration in FSH/LH ratio, regular (apparently) ovulating cycles), atypical body habitus…etc, I would hard pressed to make that diagnosis.

      I do not know what your underlying problem is and in order to provide you with an authoritative opinion, I would need to see all your old records, do a consultation with you and perhaps order other directed tests.

      If you are interested in my advice or medical services, I urge you to contact my patient concierge, ASAP to set up a Skype or an in-person consultation with me. You can also set this up by emailing concierge@sherivf.com or by calling 702-533-2691 and/or 800-780-743. You can also enroll for a consultation with me, 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 .

      Geoffrey Sher MD