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.
Sir,
I was diagnosed with chocolate cyst in left ovary 4×3 cms approx, i was on birth control pills for 6 months and during the last month of the treatment i had bleeding between periods and had pain in my lower abdomen, which led to laprascopic excision of the cyst and mild adhesions removal in oct 2014, i was under depo provera shot and got married jun 2015, i took us scan and was diagnosed with bilateral polycystic ovaries,i was given birth control pills and my periods were regular and with usual cramps, i took scan after 6 months of treatment it showed normal ovaries freed of any cysts & practising yoga extensively for nearly an year, so i stopped the birth control pills for 3 months and was taking ayurvedic medicines & during the last month my periods was little painful,i replaced millets for rice, sipped green tea, now i m taking maca, bee propolis, flax seeds, cod liver oil pill, multivitamin, cinnamon powder and ayurvedic medicines & birth control pills as i am having pain during periods, i want to conceive soon, i m 26yrs old, my husband is 27 yrs old and he isnt interested for a baby now, he feels he is young now, please advise me not to fall ill with recurrent endo and to conceive soon…
Endometriosis is a progessive condition. prregnancy/hormonal/surgicallyinduced arrest of menses and ovarian activity will place it in remission, but resumption of estrogen activity (spontaneous or induced will cause it to resume.
Geoff Sher
Dr. Sher, I had a stem cell transplant 3 yrs ago for Leukemia, I have had 5 unsuccessful IVF cycles with donor eggs. My first cycle worked it took 32 days for my uterine lining to get to 8.1 all of my other cycles my uterine lining gets to about 4 then cycles cancelled. I have been on estrogen patches and vaginal estrace, My Dr wanted to do an ERA biopsy but how will that increase my lining? He said we can transfer with a thin lining but I think it’s too thin,what do you think ?
In my opinion, a lining of <8mm is unlikely to support a viable pregnancy.
The considerable emotional, physical and financial burden associated with infertility treatment in general and with IVF in specific, demand that factors known to affect outcome be identified and regulated prior to initiating treatment.
Just as a successful garden needs a ”good” seed properly planted in fertile soil to produce healthy plants, successful embryo implantation requires a good seed (genetically “normal” embryo) and fertile soil (receptive uterine lining) to make a healthy baby. I have long used this “Seed/Soil Relationship” analogy to help clarify the critical nature of the interaction between embryo and endometrium in the successful propagation of pregnancy..
There have in the last decade been numerous reports suggesting that certain drugs/supplements (e.g. GCSF) and endometrial receptivity testing/preparation might dramatically improve implantation. As yet, none of these have been proven to be effective. This article addresses the influence of the most relevant and important factors that are known to affect .endometrial receptivity and discusses approaches to treatment:
1. Endometrial thickness
In 1989, I first demonstrated that in both normal and "hormonally stimulated” cycles, preovulatory endometrial thickness as assessed by ultrasound examination, is partially predictive of embryo implantation (pregnancy) potential following IVF. Ideally the endometrium should measure at least 8.0mm in thickness, (but preferably >9mm).
A “poor” endometrial lining is most commonly due to: 1) inflammation of the uterine lining (endometritis) that usually occurs as a result of endometritis (inflammation of the uterine lining that can follow a septic delivery, partial retention of the placenta following delivery, abortion or miscarriage, 2) severe adenomyosis (gross invasion of the uterine muscle by endometrial glandular tissue), 3) multiple fibroid tumors of the uterine wall) 4) prenatal exposure to the synthetic hormone, diethylstilbestrol (DES) and, 5) following >3, consecutive, back to back cycles of clomiphene citrate ovulation induction.
Treatment with vaginal Sildenafil (Viagra): Hitherto, attempts to augment endometrial growth in women with poor endometrial linings by bolstering circulating estrogen blood levels (through the administration of increased doses of fertility drugs, aspirin administration and with supplementary estrogen therapy) have yielded disappointing results.
In the mid-90’s I first reported on the finding that thee vaginal administration of Viagra for several days prior to the “hCG trigger “ or progesterone administration enhances uterine blood flow and estrogen delivery to the uterine lining and so improves endometrial thickening. Then In October 2002, I reported 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 and 45% of these women achieved live IVF- births following a single cycle of treatment with Viagra. Nine percent (9%) miscarried. None of the women who had failed to achieve an improvement in endometrial thickness following Viagra therapy, subsequently and who underwent embryo transfers achieved viable pregnancies.
2.Uterine Pathology:
It has long been suspected that anatomical defects of the uterus might result in infertility.
While myomas (fibroids) embedded deep in the uterine wall, are unlikely to cause infertility, an association between their presence and infertility has been observed in cases where they distort the uterine cavity, or protrude as submucous polyps through the endometrial lining. It would appear that even small submucous myomas have the potential to prejudice implantation.
Far too many infertile women found to have a partial or complete septum in the uterus are subjected to surgical excision of the septum with a promise that this will enhance subsequent implantation. This is an erroneous belief. Contrary to popular belief, the presence of a septum that partially or completely partitions the uterine cavity, while being responsible (in some cases) for late miscarriages and premature onset of labor, does NOT cause failed implantation.
It is likely that most surface lesions in the uterine cavity, whether due to an endometrial, placental or fibroid polyp (no matter how small), or intrauterine adhesions, have the potential to interfere with implantation by producing a local “inflammatory”- type response, not too dissimilar in nature from that which is caused by a foreign body such as a intrauterine contraceptive device. Unfortunately, a dye X-Ray test (hysterosalpingogram/HSG) will often miss many smaller such lesions. The only reliable methods for diagnosing even the smallest of such lesions, is through the performance of a hysterosongram (HSN),a hysteroscopy or an MRI.
Hysterosonogram (syn. Saline ultrasound): This procedure involves the trans-cervical injection of a physiological saline solution via a catheter, into the uterine cavity. The fluid distended cavity is then examined by vaginal ultrasound for any irregularities that might point to surface lesions such as polyps, fibroid tumors, scarring, or a uterine septum. If performed correctly, the HSN is highly effective in recognizing even the smallest surface lesions that protrude into the uterine cavity. It is less expensive, less traumatic, and diagnostically, equally reliable as hysteroscopy. The only disadvantage lies in the fact that if a lesion is detected, it may require the subsequent performance of hysteroscopic surgical approach to treating the problem..
Hysteroscopy: Diagnostic hysteroscopy is an office procedure that is performed under intravenous sedation, general or local anesthesia, with minimal discomfort to the patient. The procedure involves the insertion of a thin, lighted, telescope like instrument known as a hysteroscope through the vagina and cervix into the uterus in order to fully examine the uterine cavity. The uterus is first distended with carbon dioxide gas, which is passed through a sleeve adjacent to the hysteroscope. As is the case with FUS, diagnostic hysteroscopy facilitates examination of the inside of the uterus under direct vision for defects that might interfere with implantation.
We have observed that approximately 8% of candidates for IVF have intrauterine lesions that require attention prior to undergoing IVF in order to optimize the chances of a successful outcome. We strongly recommend that all patients who have such lesions undergo surgery (D&C and/or hysteroscopic resection) to correct the pathology prior to undergoing IVF. Depending on the severity and nature of the pathology, therapeutic hysteroscopy may require general anesthesia. If so, it should be performed in an outpatient surgical facility or in a conventional operating room.
3. Immunologic factors
The implantation process begins six or seven days after fertilization of the egg. At this time, specialized embryonic cells (i.e., the trophoblast), which later becomes the placenta; begin growing into the uterine lining. When the trophoblast and the uterine lining meet, they, along with Immune cells in the lining, become involved in a “cross talk” through mutual exchange of hormone-like substances called cytokines. Because of this complex immunologic interplay, the uterus is able to foster the embryo’s successful growth. Thus, from the very earliest stage of implantation the trophoblast establishes a foundation for the future nutritional, hormonal and respiratory interchange between mother and baby. In this manner, the interactive process of implantation is not only central to survival in early pregnancy but also to the quality of life after birth.
Considering its importance, it is not surprising that failure of proper function of this immunologic interaction during implantation has been implicated as a cause of recurrent miscarriage, late pregnancy fetal loss, IVF failure, and infertility. A partial list of immunologic factors that may be involved in these situations includes anti-phospholipid antibodies (APA), antithyroid antibodies (ATA), and most importantly activation of uterine natural killer cells (NKa). Presently, these immunologic markers in the blood can be only adequately measured by a handful of highly specialized reproductive immunology laboratories in the United States. I personally use Reproductive Immunology Associates in Van Nuys, CA or Reprosource in Boston, MA.
The Central role of Natural Killer cells: After ovulation and during early pregnancy, NK cells comprise more than 70% of the immune cell population of the uterine lining. NK cells produce a variety of local hormones known cytokines. Uncontrolled, excessive release of certain cytokines (i.e. TH-1 cytokines) is highly toxic to the trophoblast (“root system”) of the embryo” leading to their programmed death (apoptosis) and, subsequently to failed or compromised/dysfunctional implantation. In the following situations NK cells become activated, and start to produce an excess of TH-1 cytokines:
•Autoimmune Implantation Dysfunction: This is most commonly seen in association with a personal or family history of autoimmune diseases such as ith conditions such as Rheumatoid arthritis, hypothyroidism endometriosis and Lupus Erythematosus, Scleroderma, Dermatomyositis etc. It is also encountered in one third of women who have endometriosis (regardless of its severity), and in cases of “unexplained infertility” as well as with recurrent pregnancy loss (RPL).
•Alloimmune implantation dysfunction where the male and female partners share specific genetic (DQ-alpha and/or HLA) similarities This is commonly seen in cases of RPL and in cases of secondary infertility
Activated NK cells (NKa) can be detected through the K-562 target cell blood test and (more recently) through uterine biopsy for TH-1 cytokine activity. Treatment involves selective use of Intralipid (IL) or immunoglobulin (IVIG) therapy combined with oral steroids, initiated more 10-14 days prior to embryo transfer and in most cases of alloimmune implantation dysfunction, the transfer of a single blastocyst at a time.
Geoff Sher
Hi Dr. Scher and thank you!
I am 39, with an AMH of 0.6, last FSH 12. My last IVF cycle got cancelled due to a cyst/follicle (I was on BCP for 4 weeks, I actually think the BCP contributed to this because the BCP prevented ovulation). I wanted to do a E-prime microdose lupron flare protocol next (I’ve done this before and it worked) but my RE suggests a microdose lupron overlap E and P prime? Starting on day 3 of the month before, begin estrace and progesterone, and then start microdose lupron on day 24… I ‘m confused as to what benefits this will have. I feel I will still likely have a lead follicle that I will not be able to ovulate and also I think it might suppress me too much? last month after a few weeks of BCP we really couldn’t see any follicles on one of my ovaries…
Much appreciate any thoughts on that protocol.
So I am tired of waiting for my period to show.. So we can do our next FET.. Can I call and ask my dr for provera will that cause any harm to the outcome of an FET?
You can…and it probably wont do harm.
Geoff Sher
Hello Dr. Sher,
I am 43 years old, have one healthy son born in 2006 conceived naturally, I was on Menopur 300mg for the last 10 months up to June 16 when we were using Timed sexual intercourse to try and conceive some months i produced 2 eggs, one month 3 and in June there was only 1 when I had a transvaginal scan and everything was perfect.
My questions are: I was due to start my first cycle of IVF last Friday and when I was scanned unfortunately my left ovary showed a complex mass in POD 3.1 x 2.1cm Bloods were taken and I am due for an MRI of my pelvis this wednesday.
1. The likely prognosis is either a cyst or a tumour? Will both of these require surgical removal
2. Will this impact my chances of IVF
3. How long will this delay me
4. I read your article about the disadvantages of using Menopur in ladies of my age so should i get my protocol adjusted for going forward
5. I have no history of anything in my reproductive areas and i believe that this growth has been caused my using the drugs for 10 months.
6. would i be better off using egg donor as my uterus is perfect with ideal linings each month etc.?
thanks a million i am in ireland otherwise i would come see you.
1. The likely prognosis is either a cyst or a tumour? Will both of these require surgical removal
2. Will this impact my chances of IVF.
A: That would depend on the type of surgery, how much ovarian tissue is removed, and most important…how long before you can do IVF (given your age and the effect this will have on ovarian reserve)
3. How long will this delay me
A: Probably 2-3 months.
4. I read your article about the disadvantages of using Menopur in ladies of my age so should i get my protocol adjusted for going forward
A: That is something you would need to discuss with your RE.
5. I have no history of anything in my reproductive areas and i believe that this growth has been caused my using the drugs for 10 months.
A: Probably independent of prior treatment.’
6. would i be better off using egg donor as my uterus is perfect with ideal linings each month etc.?
A: No doubt you would be far better off using an egg donor
Good luck!
Geoff Sher