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.
Thank you so much for answering all of our questions. Will you keep answering these even after your retirement, or does this forum stop then?
I do not know at this time…but thank you. I will be retiring in 2019.
Geoff Sher
Hello Dr Sher, I had CCS performed and an embryo transfer at the end of 2017. The implantation was successful and a heart beat was found at week 6. Unfortunately 2 weeks later the heart beat slowed, and to where no heart beat was found 2 days later. I underwent a D&C and pathology test was done on the fetal tissue and it wasnfound to have Turner’s syndrome, which was diagnosed as the likely cause of the miscarriage.
I have read over the last few weeks about Mosaicism, and our genetic counselor and IVF physician has determined that this would have lead the CCS genetic testing lab to have missed this result.
I have started to question CCS and I am loosing confidence in the remaining “healthy” embryo.
Have you encountered this previously? The genetic testing lab reviewed their procedures and reran the tests, and found no issues with their work.
Kind regards,
Ariel
Hi Ariel,
Respectfully, I question the assertion that the loss was due to a mod]saic Turner’s. It is possible but in my opinion, more likely that the diagnosis was missed.
Geoff Sher
PH: 800-780-7437
Hi Dr. Sher.
I had a 5day blast IVF transfer completed on February 28th. I did my beta blood work this morning at 12 days past transfer. The blood work confirmed my pregnancy with and HCG reading of 115. I haven’t had any spotting whatsoever except for on the day the embryo implanted. But today I noticed quite a bit, and a brighter color, not the brownish tint. It’s not enough to soak a panty liner but enough to make me panic. Is this normal? My nurse said it can sometimes happen but didn’t explain why. Should I be worried? Is my HCG level where it should be for being 12 days past transfer?
Vaginal bleeding occurs in about 25% of all pregnancies. When it happens, it almost invariably raises the concern of pregnancy loss (miscarriage). Bleeding can also be a sign of a tubal (ectopic) pregnancy, and in cases where the distended Fallopian tube ruptures it can precipitate a life-threatening crises. However, a small amount of painless vaginal bleeding can also be the result of normal embryo implantation (i.e. implantation bleeding) or it can result a local erosion of the vagina or cervix and/or trauma during intercourse.
Notwithstanding, in virtually all cases the occurrence of early pregnancy vaginal bleeding congers concerns or even alarm regarding the possibility of miscarriage. And when this happens to women who conceived following infertility treatment, the alarm often turns into panic. However, the truth is that in most such cases the bleeding soon stops and the pregnancy proceeds unabated to the birth of a healthy baby. However, because some do progress and end in miscarriage, and in most cases, only time will tell how things will ultimately turn out, we use the term “threatened miscarriage” to describe such early bleeding. The term “inevitable miscarriage” is used once symptoms and signs confirm a miscarriage is in progress. The term “complete miscarriage” is used if all products of conception are passed, leaving the uterus “empty”. An “incomplete miscarriage” refers to cases where some products remain retained in the uterus.
Good luck!
Geoff Sher
Hey Dr, Sher, how long do you have your patients stay on vaginal viagra leading up to FET? Once stopped, does the uterine lining regress?
It is ideally started soon after the period and stopped on the day progesterone starts. However 48-72 hours of vaginal Viagra is often sufficient to rescue a thin endometrium. Once stopped the lining should not regress.
Good luck!
Geoff Sher
800-780-7437
You recommend the long agonist down-regulation IVF protocol with prolonged coasting for PCOS patients. However, there are some studies suggesting that PCOS patients get as good pregnancy results with antagonist protocol as with agonist protocol, but with a lesser risk of OHSS (don’t know if coasting was part of the studies). Do you think that the agonist protocol in the studies differs from the one you recommend or why would this be?
Actually there seems to be a lot of studies with different results… some say agonist gets better pregnancy results. This is weird.
With the Agonist/Antagonist conversion protocol (A/ACP), GnRH antagonist (Ganirelix, Cetrotide, and Orgalutron) is administered by daily injection from the onset of COS. The A/ACP COS-cycle is launched with the woman coming off a monophasic birth control pill that was administered starting in the 1st 5 days of the preceding cycle and continued for at least 10 days. The BCP is then overlapped with an agonist (e.g. Lupron/buserelin) for three days, whereupon the BCP is stopped and the agonist (Lupron/buserelin) is continued until the onset of menstruation. At or around this point, the agonist (Lupron/Buserelin) is supplanted by an antagonist (Cetrotide/Ganirelix/Orgalutron) and concurrently COS is initiated using an FSH-dominant bias (mainly Follistim/Gonal-F/ Puregon + a small dosage of a menotropins such as Menopur). The combined antagonist/gonadotropin therapy is continued until the hCG trigger. For the reasons cited above, I prescribe some form of the A/ACP for my older IVF patients and those with DOR. ]
There is one draw-back to the use of the A/ACP. This is the fact that prolonged administration of GnRH antagonist throughout the stimulation phase of the COS cycle compromises the predictive use of serial plasma estradiol measurements as an indication of ovarian response to COH. The blood estradiol levels tend to be much lower in comparison with cases where GnRHa alone is used.The reason for the lower blood concentration of estradiol seen with prolonged exposure to GnRH-antagonist might be due to the result of subtle, antagonist-induced alterations in the configuration of the estradiol molecule, such that currently available commercial test used to measure estradiol levels are rendered less sensitive/specific. Accordingly, when the A/ACP protocols are employed, we rely much more heavily on the measurement of follicle growth by ultrasound than on the estradiol levels. Because of this downside, I refrain from using this approach in “high responders” who may be at risk of developing of severe ovarian hyperstimulation syndrome (OHSS) and in whom the accurate measurement of plasma estradiol plays a very important role in the safe management of their COS cycles.
Polycystic ovary syndrome (PCOS) is a common hormonal system disorder among women affecting between 5% and 10% of women of reproductive age worldwide. Women with PCOS may have enlarged ovaries that contain multiple small collections of fluid (subcapsular microcysts) that are arranged like a “string of pearls” immediately below the ovarian surface (capsule).interspersed by an overgrowth of ovarian connective tissue (stroma). The condition is characterized by abnormal ovarian function (irregular or absent periods, abnormal or absent ovulation and infertility, androgenicity (increased body hair or hirsutism, acne) and increased body weight –body mass index or BMI.
Women with PCOS are at increased risk that ovarian stimulation with gonadotropins will result in the, of development of severe ovarian hyperstimulation syndrome (OHSS), a life-endangering condition that is often accompanied by a profound reduction in egg “competency” and on fertilization often yield an inordinately high percentage of “incompetent” embryos which have a reduced potential to propagate viable pregnancies.
Concern and even fear that their PCOS patients will develop of OHSS often leads the treating RE to take measures aimed at reducing the risk of this life-endangering condition. One such measures is to “trigger” egg maturation prematurely in the hope of arresting further follicular growth and the other, is to initiate the “trigger” with a reduced dosage of hCG (i.ed. 5,000U rather than the usual 10,000U of of Pregnyl/Profasi/Novarel, to use or 250mcg rather than 500mcg of Ovidrel or to supplant the hCG “trigger” with a Lupron “trigger” which causes a prompt LH surge from the woman’s pituitary gland to take place. While such measures do indeed reduce the risk of OHSS to the mother, this often comes at the expense of egg quantity and “competency”. Fewer than the anticipated number of eggs are harvested and those that are retrieved are far more likely to be “immature” and chromosomally abnormal (aneuploid”), or “immature” , thereby significantly compromising IVF outcome.
Against this background, It is my considered opinion that when it comes to performing IVF in women with PCOS, the most important consideration must be the selection and proper implementation of an individualized or customized ovarian stimulation protocol. Thereupon, rather than prematurely initiating the “trigger” to arrest further follicle growth, administering a reduced dosage of hCG or “triggering with a GnRH agonist (e.g. Lupron/Buserelin) that can compromise egg “competency”….. use of one of the following techniques will often markedly reduce the risk of OHSS while at the same time protecting egg quality:
1. PROLONGED COASTING…my preferred approach: My preferred approach is to use a long pituitary down-regulation protocol coming off the BCP which during the last 3 days is overlapped with the agonist, Lupron/Buserelin/Superfact. The BCP is intended to lower LH and thereby reduce stromal activation (hyperthecosis) in the hope of controlling LH-induced ovarian androgen (predominantly, testosterone) production and release. I then stimulate my PCOS patients using a low dosage of recombinant FSH-(FSHr) such as Follistim/Gonal-F/Puregon. On the 3rd day of such stimulation a smidgeon of LH/hCG (Luveris/Menopur) is added. Thereupon, starting on day 7 of ovarian stimulation, I perform serial blood estradiol (E2) and ultrasound follicle assessments, watching for the number and size of the follicles and the blood estradiol concentration [E2]. I keep stimulating (regardless of the [E2] until 50% of all follicles reach 14mm. At this point, provided the [E2] reaches at least >2,500pg/ml, I stop the agonist as well as gonadotropin stimulation and track the blood E2 concentration daily. The [E2] will almost invariably increase for a few days. I closely monitor the [E2] as it rises, plateaus and then begins to decline. As soon as the [E2] drops below 2500pg/ml (and not before then), I administer a “trigger” shot of 10,000U Profasi/ Novarel/Pregnyl or 500mcg Ovidrel/Ovitrel. This is followed by an egg retrieval, performed 36 hours later. Fertilization is accomplished using intracytoplasmic sperm injection (ICSI) because “coasted” eggs usually have little or no cumulus oophoris enveloping them and eggs without a cumulus will not readily fertilize naturally. Moreover, they also tend to have a “hardened” envelopment (zona pellucida), making spontaneous fertilization problematic in many cases. All fertilized eggs are cultured to the blastocyst stage (up to day 5- 6 days) and thereupon are either vitrified and preserved for subsequent transfer in later hormone replacement cycles or (up to 2) blastocysts are transferred to the uterus, transvaginally under transabdominal ultrasound guidance. The success of this approach depends on precise timing of the initiation and conclusion of “prolonged coasting”. If started too early, follicle growth will arrest and the cycle will be lost. If commenced too late, too many follicles will be post-mature/cystic (>22mm) and as such will usually harbor abnormal or dysmature eggs. Use of “Coasting” almost always prevents the development of severe OHSS, optimizes egg/embryo quality and avoids unnecessary cycle cancellation. If correctly implemented, the worst you will encounter is moderate OHSS and this too is relatively uncommon.
2. EMBRYO FREEZING AND DEFERMENT OF EMBRYO TRANSFEDR (ET): OHSS is always a self-limiting condition. In the absence of continued exposure to hCG, symptoms and signs as well as the risk of severe complications will ultimately abate. Thus, in the absence of pregnancy, all symptoms, signs and risks associated with OHSS will disappear within about 10-14 days of the hCG trigger. Conversely, since early pregnancy is always accompanied by a rapid and progressive rise in hCG , the severity of OHSS will increase until about the 9th or tenth gestational week whereupon a transition from ovarian to placental hormonal dominance occurs, the severity of OHSS rapidly diminishes and the patient will be out of risk. Accordingly, in cases where in spite of best effort to prevent OHSS, the woman develops symptoms and signs of progressive overstimulation prior to planned ET, all the blastocysts should be vitrified and cryostored for FET in a subsequent hormone replacement cycle. In this way women with OHSS can be spared the risk of the condition spiraling out of control.
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.
·The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
·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
·Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
·Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
·Egg Maturation in IVF: How Egg “Immaturity”, “Post-maturity” and “Dysmaturity” Influence IVF Outcome:
·Commonly Asked Question in IVF: “Why Did so Few of my Eggs Fertilize and, so Many Fail to Reach Blastocyst?”
·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?
·Taking A Fresh Look at Ovarian Hyperstimulation Syndrome (OHSS), its Presentation, Prevention and Management
·Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting”
·Understanding Polycystic Ovarian Syndrome (PCOS) and the Need to Customize Ovarian Stimulation Protocols.
·“Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
·The “Lupron Trigger” to Prevent Severe OHSS: What are the Pro’s and Con’s?
•.Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•Implications of “Empty Follicle Syndrome and “Premature Luteinization”
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
•Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting”
If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .
*FYI
The 4th edition of my newest book ,”In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoff Sher