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.
Please I need help I had 3 blastocysts tea freed on the 23 rd of December 2 hours letter I had a stoping and later the sporting changed to a light red bleeding for 6 days it stoped on the 30th of dec and I don’t know if it was a miscarriage am meant to get my period yesterday but I still have not gotten it please help
You need to undergo tests through your RE to determine what is transpiring.
Geoff Sher
Hi Dr Sher,
I’m 35yo, and am 5 weeks 3 days pregnant with a grade 5 donor egg.
My first beta was (10dp5dt) 360 and 2nd was (17dp5dt) 4850, I have requested a 3rd this coming Friday where I will be 5 weeks 5 days due to a bleed I had at exactly 5 weeks. I experienced abdominal cramping at the same time, it was a light flow (runny bright red blood) and passed a very small clot, did not fill a pad, and did not last long, however that day I lost tenderness in my breasts.
The days since the bleed, I have had lower back pain, abdominal cramping, and my breasts are off and on tender/sensitive.
In most of the blogs I’ve read the signs aren’t looking very good – I’m really just wanting to prepare myself for tomorrow’s 3rd Beta if things are not going my way… I also experienced a missed miscarriage earlier in the year at 9 weeks – hence the worry.
Do you have any experience with patients who may have experienced similar symptoms?
Thank you in advance, and happy new year!
Mel
The symptoms are very subjective, I am afraid. You should wait about 10n days and do an ultrasound. That should be definitive.
Geoff Sher
I have low AMH (1.9pmol) , aged 41 and have been given different protocols from different clinics so don’t know how to decided which is best. I have had one successful ivf with one child who is now 3 years old. I am trying for my second child. I have been told my ivf success rates are low but would like to try with my own eggs.
I had PID in Nov 2018 which was treated with antibiotics. I also only have one ovary that is accessible for IVF.
My other stats are FSH 11.8, LH 3.3 AND Estradiol 97.
One protocol suggests a long agonist protocol with pergoveris and buserelin at day 21 of the preceding cycle.
Another suggests Gonal F starting 375 and then menopur at day 7.
Third protocol suggests short agonist with pergoveris and synarelle.
I would be most grateful for your advice and hope there is enough information for you to provide your views.
While I personally would modify option 1 and 2, these are in the my opinion preferable to option 3. Good luck!
Geoff Sher
Hello doc.
I’m about to start my second embryo transfer – first one had failed. I have been on birth control for 35 days. I took my last pill on the dec 30th and I am to start estradiol 3 mg bid on January 2nd for 10 days before I see my doctor for an ultrasound. Last time I didn’t get a period in between the birth control and the estradiol. I was wondering if that has any effect on the outcome of the transfer or the lining ?
In my opinion, it is important where ever possible to launch cycles coming off a BCP.
Happy 2020!
Geoff Sher
I have always had healthy periods with normal flow and length. I am now almost 34 yo, but a few years ago it was at the time of wanting to try to conceive my periods changed and got drastically shorter lasting one day with full flow and a few days of spotting, this has now been my norm for the last few years for no reason for the change. I have been generally healthy. I have never been pregnant. No miscarriages. 4 tries with IUIs without success. The thickest my lining has been is 7mm (since checking at the fertility clinic) but has been as thin as 5.4 as well. I have always had trilaminar. At the time of my egg retrieval my estrogen levels were extremely high and my lining was 7.4, the thickest it had ever been but I had to wait to transfer due to my blood estrogen levels. I have now tried one FET with the use of viagra suppositories. My lining was 6.4 a few days before transfer but bulked up to 7 on the day of transfer. I was using the viagra BID daily with additional estrogen supplements (estrace BID vaginally alternating day a with estrogen patches). The transfer was not successful. I will next do a scrapping and ERA since I only have 2 embryos left. Do you have any recommendations of what else I could be doing to help thicken my lining? Thank you.
I earnestly think we should talk!
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”.
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ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.
Patients are encouraged to share the information I provide, with their treating Physicians and/or to avail themselves of my personal hands-on services, provided through batched IVF cycles that I conduct every 3 months at Los Angeles IVF (LAIVF) Clinic, Century City, Los Angeles, CA.
If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).
PLEASE SPREAD THE WORD ABOUT SFS!
Geoff Sher
I am 30 years old and my husband is 28 years old. We have been trying to conceive for 1 1/2 years. We were diagnosed with unexplained infertility. I have a history of endometriosis, hypothyroidism, short luteal phase, ovulation dysfunction and a high amh 6.3. They ruled out PCOS. I also was diagnosed with CIN3 cells and had to have a LEEP done 2 1/2 months prior to transfer. I had an HSG and saline hysteogram which were both normal. My husband has no issues except his strict morphology was 2%, increased to 3% with supplements; but we were told this was not why we couldn’t get pregnant. We both had carrier screening completed as well and I carried risk for 2 things, but my husband’s was negative.
We tried on our own for 6 months and determined that my luteal phase was only 9-11 days. Once we started seeing our doctor, we tried timed intercourse with Femara and trigger shot and then moved on to IUI. I always responded well and had between 3-5 follicles that were the right size. But I never fell pregnant. We were advised to do IVF due to unexplained infertility and never being pregnant. I anticipated having great results but, contrary to my doctors opinion, I did not. My last ultrasound showed 18 follicles but we ended up retrieving only 11 follicles, as she said the others were “empty.” I feel they did not stimulate me enough as they were worried with ohss, which I did not develop. I was on a small dose of Lupron before retrieval, as well as transfer. We used gonal-f 150 and 75 of menopur for 8 days. Then decreased to 75 of both for day 9 and triggered on day 10. We used ICSI and ended up with 8 fertilized embryos. We sent 6, 5-day blasts off for PGS testing. Only 2 out of our 6 were normal, which was very unexpected for our age and lack of risk factors as we were originally advised that we did not need to do PGS.
We were advised to do FET due to my history of endometriosis and high risk for developing OHSS. We did two months of Lupron suppression for the endo. I had surgery to have it burned out 8 years ago but I was assured that the Lupron was just as effective as surgery. I was also diagnosed with CIN3 and had to have a LEEP done 2 1/2 months prior to transfer.
We recently got pregnant via a FET with a PGS tested normal male embryo. I was on Lupron prior to transfer, then on estradiol tablets 2mg and patches changed every 3 days. I was also on baby aspirin and 2.5 mg prednisone. She had me stop the prednisone 11/25, 6 days after our positive beta. My levels did not rise the way they were supposed to. We had a 55% rise, then a 67% rise and we were not checked again. My progesterone was only checked once, with the first HCG and was only 16. I was on 1 mL IM and 200mg vaginal suppository daily. I spotted dark brown for 1 1/2 weeks during week 5 and 6. I miscarried at 8 weeks and 3 days after hearing a heartbeat at 7 weeks and 2 days. We are heartbroken and being told that there is no explanation for our loss.
My doctor seems to like to throw things at the problem without finding the cause. For example, I suspected because of a short luteal phase, that my progesterone was low. She never checked it, just started giving me progesterone.
We only have one embryo left. I feel there are a lot of stones unturned. I feel it would be best to have a lap done to ensure my endo is at bay. I feel an ERA, just to ensure we were receptive on day 5 is worth the piece of mind. I feel a recurrent loss panel is needed to identify any blood clotting issues or immune issues. I feel these things should have been done prior to my first transfer since we had a limited amount of embryos and a lot of risk factors (endo, hypothyroidism, low progesterone). I also feel I should have been placed on an immune protocol.
How would you advise to move forward to give our last PGS normal, female embryo the best chance?