Before I started this last cycle, I had been on a three-month dose of lupron. I began stimming exactly three months to the day of my lupron injection, even though I still had hot flashes and only had six follicles to start.
Follicles grew from 6 to 8 to 12 the day of the trigger. Normally my number of follicles are in the teens at the beginning of the cycle. I even mentioned this to the doctor and told him that I was still having hot flashes as well. Is it possible that my ovaries were over-suppressed, which resulted in just two immature eggs out of 15?
Usually the stimulation, if given in adequate dosage, is enough to overcome the Lupton suppression, but I think that your thinking may be right, and that your ovaries may have been suppressed enough so as to not perform as well in the last cycle and the stimulation was not enough to overcome that suppression.
Though there are many reasons you might consider reducing or eliminating your ability to get pregnant, if you later decide to start a family, you have options available. Read on to learn more. Protecting your health is protecting your fertility. Choosing to get regular check-ups can protect you from issues later down the line, or prepare you for any possible issues. Read on to learn more about the importance of wellness exams.
Is there even a difference? In this blog, we explain the difference between perimenopause and menopause and how you can get relief from your less-than-pleasant symptoms. Learn more about how your fertility changes with age. Schedule a virtual visit. It describes a circumstance usually encountered in poor prognosis patients who produce small numbers of eggs and embryos and where, therefore, every egg and embryo really counts [ Lee et al.
What it means is that, if immature eggs are obtained at egg retrieval, a maximal attempt is made to mature those eggs in vitro i. In practical terms this meant that embryologists after retrieval, as is routinely done in all IVF laboratories, strip eggs of attached cumulus cells because, as long as those cells remain attached to eggs the maturity grade of eggs cannot be accurately determined. When we strip them off, eggs continue their in vitro maturation while starving. Many embryologists, therefore, do not even try to mature immature eggs in vitro because, especially with very premature eggs, so-called GV-stage eggs , maturation only relatively rarely succeeds in leading to pregnancy.
These eggs, therefore, then can be cultured overnight with their cumulus cells still attached. Though this new approach has only been in used at CHR for ca. And since egg quality translates into embryo quality, and embryo quality into pregnancy rates, we are confident that this change in embryology practice at CHR will also improve IVF pregnancy rates. Mini-IVF is a procedure that involves ovarian stimulation with oral fertility drugs such as clomiphene or letrozole to promote the development of follicles, for egg extraction.
This is on the pretext that Mini-IVF, involves the administration of oral low-dosage medication, cuts down on cost, reduces the need for intensive monitoring and is highly successful. The process involves the use of very low dosage gonadotropin stimulation administered every other day , thereby virtually eliminating the risk of complications. The process also requires minimal monitoring. It does all this at virtually the same low cost as Mini-IVF while offering a much higher potential for success and a greater likelihood that there will be left-over embryos for cryopreservation with a view to later use.
Use of fewer drugs translates into lower cost. This would be true, were it not for the fact that success rates with mini-IVF across the board are much lower than with conventional ovarian stimulation.
Absent or milder stimulation using oral agents such as clomiphene, letrozole reduces stress on the ovaries and overall risk associated with IVF. This argument, while perhaps having some merit when applied to mini-IVF conducted in younger women who usually have normal ovarian reserve, does not hold water when it comes to older women and those with diminished ovarian reserve DOR.. Furthermore, there is good body of evidence to show that both clomiphene and letrozole increase the release of LH-by the pituitary gland which so increases ovarian testosterone as to potentially further compromise egg development and maturation.
This assertion is totally flawed. That is simply not how FSH stimulates follicle development. Mini-IVF is less technology driven, less stressful and easier to execute. There is some merit to this assertion although all IVF cycles require careful monitoring and the same involvement of the embryology laboratory.
There is no single stimulation protocol that is suitable for all IVF patients. It must be individualized…. So, what about younger women with normal or increased ovarian reserve? If mini-IVF has any role at all, it could be in such cases. In fact, such an approach is neither safe nor acceptable. My AMH is 19pMol maybe 2. My AFC appears to be reasonable with around 28 follicles in total. I had my day 9 scan on thursday day 8 of stimulation , and i was disappointed to learn i only have 3 follicles above 10mm but alot of smaller ones.
I have another scan on monday as my dosage of stimulation has been upped. I started on bemfola and now am If i have a poor response does thag mean my outlook is not great longer term? Respectfully Daniella, I am not a big Bemfola fan.
It is too difficult to regulate and adjust dosages. I can say that with your AMH being normal, this is a surprising response. It suggests to me that the protocol used for ovarian stimulation could possibly have been suboptimal and will likely need to be thoroughly reviewed and substantively revised.
This having been said, without access to much more information, I cannot comment authoritatively. We would need to talk! Consider calling my assistant, Patti Converse and setting up an online consultation with me. FSH targets cells that line the inner wall of the follicle granulosa cells and also form the cumulus cells that bind the egg to the inner surface of the follicle.
Granulosa cells are responsible for estrogen production. Ovarian androgens can also reach the uterine lining where they sometimes will compromise estrogen receptor -induced endometrial growth and development. A significant percentage of older women and those who have diminished ovarian reserve DOR have increased LH activity is increased.
Thus they too often manifest with increased ovarian androgen production. Similarly, drugs such as clomiphene or Letrozole that cause the pituitary gland to release excessive amounts of LH, are also potentially harmful to egg development and in my opinion, are best omitted from IVF COS protocols.
This is especially the case when it comes to older women and those with DOR, who in my opinion should preferably be stimulated using FSH-dominant products such as Follistim, Puregon, Fostimon and Gonal-F. They act by causing an initial outpouring followed by a depletion of pituitary gonadotropins. In contrast, when the GnRHa administration commences along with the initiation of gonadotropin therapy, there will be a resultant immediate surge in the release of pituitary LH with the potential to increase ovarian testosterone to egg-compromising levels , from the outset of COS.
This, in my opinion could be particularly harmful when undertaken in older women and those who have DOR. GnRH-antagonists such as Ganirelix, Cetrotide and Orgalutron, on the other hand, act very rapidly within hours to block pituitary LH release. GnRH antagonists are traditionally given, starting after 5th -7th day of gonadotropin stimulation.
However, when this is done in older women and those regardless of age who have DOR, LH-suppression might be reached too late to prevent the deleterious effect of excessive ovarian androgen production on egg development in the early stage of ovarian stimulation. This is why, it is my preference to administer GnRH-antagonists, starting at the initiation of gonadotropin administration. Here, GnRHa is given, starting a week or so prior to menstruation. This results in an initial rise in FSH and LH , which is rapidly followed by a precipitous fall to near zero.
In many such cases I often supplement with human growth hormone HGH in such cases in an attempt to enhance egg mitochondrial activity and so enhance egg development. This approach is often augmented with preimplantation genetic screening PGS of all embryos that reach the expanded blastocyst stage of development by day post-fertilization.
I also commonly recommend blastocyst banking to many such patients. This involves initiating gonadotropin therapy commensurate with initiation of gonadotropin administration. Accordingly, I do not prescribe such protocols to my IVF patients. We start with estrogen skin patches applied every 2nd day or with the BCP for 10 days or longer, overlap it for 3 days with a GnRHa whereupon the estrogen priming is stopped.
Th GnRHa is continued until the onset of menstruation usually days later to cause pituitary LH, down-regulation. Estrogen Priming has succeeded in significantly enhancing ovarian response to gonadotropins in many of otherwise very poor responders. Any lesser dosage often will reduce the efficiency of meiosis and increase the risk of the eggs being aneuploid.
This may be true, but it comes at the expense of egg quality because the extent of the induced LH surge varies and if too little LH is released, meiosis can be compromised, thereby increasing the likelihood of aneuploid and immature MI eggs. And there are other better approaches to preventing OHSS e. In natural unstimulated as well as in cycles stimulated with fertility drugs, the ability of follicles to properly respond to FSH stimulation is dependent on their having developed FSH-responsive receptors.
This suppression needs to be countered by artificially causing blood FSH levels to rise in order to cause PAF to AF conversion prior to COS commencing, otherwise pre-antral-to —antral follicle conversion will not take place in an orderly fashion, the duration of ovarian stimulation will be prolonged and both follicle and egg development may be compromised.
By overlapping the BCP with an agonist for a few days prior to menstruation the early recruited follicles are able to complete their developmental drive to the AF stage and as such, be ready to respond appropriately to optimal ovarian stimulation.
Using this approach, the timing of the initiation of the IVF treatment cycle can readily and safely be regulated and controlled by varying the length of time that the woman is on the BCP. Initiating ovarian stimulation in women taking a BCP, without doing this is suboptimal. I strongly recommend that you visit www. Good evening Dr.
I am a 41 year old woman. AMH : 1. Of these 3 eggs degraded and 2 were immature. We froze 3 embryos on day 3 1 good quality 8 cell , 1 fair quality 6 cell and 1 poor quality 5 cell. I started cycle day 4 and already had a 13mm lead follicle.
Should I start earlier? I took Gonal F for 7 days and Cetrotide starting day 4 and triggered with units of Pregnyl. Thank you! That is why, the likelihood of failure to conceive, miscarrying and of giving birth to a chromosomally defective child e.
In addition, as women age beyond 35Y there is commonly a progressive diminution in the number of eggs left in the ovaries, i. Menopur can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited. Hi Dr. Sher, I am 31, with an AMH that 2 years ago was detected at 4, which 4 months later jumped back up to 7 and is now 2. We started TTC in October By January , I had an early 5 weeks miscarriage followed by a sub-pregnancy in May to 16 weeks, baby affected with CF.
My husband has low sperm count, specifically relating to morphology. Our cycle resulted in 9 eggs retrieved but only 3 mature and 1 fertilised via ICSI. However, I am not convinced this could be the only issue, given I have fallen pregnant twice within a 12 month period.
Whilst I find your responses to these questions so helpful thank you! My protocol started with a mcg Decapeptyl on day 2 evening and mcg day 3 morning along with Bemfola IU from day 3 — day 9. A one off dose of Elonva IU was administered on day 3.
Luveris 75IU was given from day 3 — day Orgalutran mcg started on day 7 — day I was also on Clexane 40mg due to Factor V Leiden. I administered mcg Decapeptyl trigger on day 16 at 7pm. Egg pick up was at 7am on day Is there anything you would change to this protocol to yield more mature eggs? I read in one of your responses about the testosterone and too much of it potentially causing issues. Do you think this could be likely if I had an LH surge too early without adding in the antagonist until day 7?
Thanks so much for your help. This forum is so appreciated. I do not use long-acting gonadotropins at all. It is in my opinion, hard to regulate. I agree with you, endometriosis does not adequately explain your situation and unless you have ovarian endometriomas that require correction prior to IVF, I would not do a laparoscopy. When women with infertility due to endometriosis seek treatment, they are all too often advised to first try ovarian stimulation ovulation Induction with intrauterine insemination IUI ………as if to say that this would be just as likely to result in a baby as would in vitro fertilization IVF.
Nothing could be further from reality It is time to set the record straight. And hence this communication! Bear in mind that the cost of treatment comprises both financial and emotional components and that it is the cost of having a baby rather than cost of a procedure.
Then consider the fact that regardless of her age or the severity of the condition, women with infertility due to endometriosis are several fold more likely to have a baby per treatment cycle of IVF than with IUI.
It follows that there is a distinct advantage in doing IVF first, rather than as a last resort. So then, why is it that ovulation induction with or without IUI is routinely offered proposed preferentially to women with mild to moderately severe endometriosis?
Could it in part be due to the fact that most practicing doctors do not provide IVF services but are indeed remunerated for ovarian stimulation and IUI services and are thus economically incentivized to offer IUI as a first line approach? Or is because of the often erroneous belief that the use of fertility drugs will in all cases induce the release ovulation of multiple eggs at a time and thereby increase the chance of a pregnancy.
This is because such women usually only develop a single dominant follicle which upon ovulating leaves the others intact. This is the reason why normally ovulating women who undergo ovulation induction usually will not experience improved pregnancy potential, nor will they have a marked increase in multiple pregnancies.
Conversely, non-ovulating women as well as those with dysfunctional ovulation who undergo ovulation induction, almost always develop multiple large follicles that tend to ovulate in unison. This increases the potential to conceive along with an increased risk multiple pregnancies.
So let me take a stab at explaining why IVF is more successful than IUI or surgical correction in the treatment of endometriosis-related infertility: 1.
The toxic pelvic factor: Endometriosis is a condition where the lining of the uterus the endometrium grows outside the uterus. While this process begins early in the reproductive life of a woman, with notable exceptions, it only becomes manifest in the 2ndhalf of her reproductive life.
After some time, these deposits bleed and when the blood absorbs it leaves a visible pigment that can be identified upon surgical exposure of the pelvis. Following ovulation, the egg s must pass from the ovary ies , through these toxic secretions to reach the sperm lying in wait in the outer part the fallopian tube s tube s where, the sperm lie in waiting.
As a consequence, if they are chromosomally normal such eggs are rendered much less likely to be successfully fertilized. Since almost all women with endometriosis have this problem, it is not difficult to understand why they are far less likely to conceive following ovulation whether natural or induced through ovulation induction.
The Immunologic Factor: About one third of women who have endometriosis will also have an immunologic implantation dysfunction IID linked to activation of uterine natural killer cells NKa. Surgical treatment of mild to moderate endometriosis does not usually improve pregnancy potential:.
New lesions are constantly developing. It also explains why surgery to remove endometriotic deposits in women with mild to moderate endometriosis usually will fail to significantly improve pregnancy generating potential. In contrast, IVF, by removing eggs from the ovaries prior to ovulation, fertilizing these outside of the body and then transferring the resulting embryo s to the uterus, bypasses the toxic pelvic environment and is therefore is the treatment of choice in cases of endometriosis-related infertility.
Ovarian Endometriomas: Women, who have advanced endometriosis, often have endometriotic ovarian cysts, known as endometriomas.
These space occupying lesions can activate ovarian connective tissue stroma or theca resulting in an overproduction of male hormones especially testosterone.
An excess of ovarian testosterone can severely compromise follicle and egg development in the affected ovary. Thus there are two reasons for treating endometriomas. The first is to alleviate symptoms and the second is to optimize egg and embryo quality.
Conventional treatment of endometriomas involves surgical drainage of the cyst contents with subsequent removal of the cyst wall usually by laparoscopy , increasing the risk of surgical complications. We recently reported on a new, effective and safe outpatient approach to treating endometriomas in women planning to undergo IVF. We termed the treatment ovarian Sclerotherapy.
Ovarian sclerotherapy can be performed under local anesthesia or under conscious sedation.
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