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.
What are your thoughts on luteal-phase stimulation? I’m doing FET so the timing of my uterine lining doesn’t matter anyway, so perhaps this can save time (by getting started quickly) and even allow for back-to-back stim in the follicular phase?
Articles for reference:
https://www.ncbi.nlm.nih.gov/pubmed/25154677
http://journals.sagepub.com/doi/pdf/10.1177/0300060516669898
https://www.sciencedirect.com/science/article/pii/S1028455915002910
Good Morning Doctor! I need some hope! I had my hcg levels tested 13 dpo (3 days before my period) and they came back at 70. Two days later (exactly 48 hrs later) they were at 112. I heard in early pregnancy they can take 72 hrs to double so I wasn’t extremely concerned. I went back for more blood draw 3 days later and they had only gone from 112 to 136. This was very upsetting. Two days later they went from 136 to 216. I go back tomorrow for more blood draw. My doctor said to hold out hope. I had an ectopic pregnancy a year ago so this is my fear again. I have no cramping or bleeding yet. I am only 5 Weeks 3 days today. My question is do I have hope? Is there anything that could cause my levels to barely go up over 72 hrs but still have a healthy pregnancy? This was my first round of Clomid 100mg. Thank you for hearing my case. Megan
This is troubling. It could be a chemical prfegnancy, an ectopic or a slowly implanting pregnancy. Only tgime will tell.
Needless to say, if you start experiencing pain or light headedness go straight to the ER.
Good luck!
Geoff Sher
Dear Dr,
First i’d like to thank you for having this website and always replying. I consulted you before as well. I had brighht red spotting one week ago but that was due to intercourse , im assuming. Now im in my 5th week and 2 days and experiencing some light pink to brownish red spotting since yesterday with one to two hour breaks and it only comes out when i go to pee and wipe a tissue. I have no cramping or whatsoever. I did beta hcg last week and the results were 176.6 and then after 2 days they were 455.5. Im extremely confused and worried . Kindly help.
Without cramping and heavy bleeding, I do not think this is significant.
Keep me in the loop please.
Good luck!
Geoff Sher
Dear Dr.
I am 35 yrs my husband is 40 yrs, he has 100% teratozoospermia, I am normal just i have common migriane.
Ihad 1 abortion after spontenous pregnancy in 4 wks. We had ICSI and fresh ET on D5, last Dec failed after 11 D. Then I had my menses(it was heavy 8 D bleeding) we started preparation for FTI in Jan 20 , us showed functional overian cyst 4cm whuch regressed in subsequent us to 2.5cm , Iwas started on climen on D 3 of period 2mg bid for 10 D , in us the thickness of endometrium was 5.5mm so dose increased to tid plan for 4 days but Ihad vaginal bleeding 2 days after increasing the dose it less than period bleeding but its significant.
Ihave called the clinic and they told me to stop climen and come next month when I have another period.
I am warried why Ihave this bleeding & when could i start next FET cycle? Should they use same protocol with me or no.
With such a thin lining, you are very likely having break through bleeding. In my opinion, your protocol needs to be reviewed and consideration should be given to changing it and adding vaginal Viagra.
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.
Good luck!
Geoff Sher
PH: 800-780-7437
Dear Dr Sher
Thank you v.much for your great effort helping us.
I have sent you my queries around 7 weeks back.
Last week another event occured i discovered ihave ectopic pregnancy , it was spontenous pregnancy , endometrial thickness this time was 1cm, and large overian cyst 5*7 mm (previously diagnosed as functional cyst ,it was regressing ) , laproscopic salpengectomy and cystectomy was done for me. My questions now : why this happened?
What is my chance to have spontenous pregnancy? Should i wait for that to happen? Or should i go directly for FET as i have 4 freezed?
Should i take contraception for few months?
Thanks dr.Sher i am so grateful for all of your explanation, but now i am doubtful shall i proceed to another ivf trial? Does having blunted empty follicle once mean my ovaries producing such a follicle repeatedly each cycle?
Not necessarily Dya. I would not give up.
Geoff Sher