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.
Hi Dr Sher,
I had a FET yesterday. I also got my prolactin measured yesterday and it came back 863 uiU/ml while the reference range is 72-577. Do you think this level will affect pregnancy?
Prolactin is a protein hormone (closely related to human growth hormone) that is secreted by specialized cells in the anterior part of the pituitary gland. In addition, the hormone is also produced and secreted by a broad range of other cells in the body, most prominently various immune cells, the brain and the lining of the uterus. Most cells respond to prolactin. In fact it is hard to identify any tissue that does not have prolactin receptors.
Although prolactin’s major target organ is the breast where it stimulates development and milk production, the hormone has many other functions. Several hundred different actions have been reported for prolactin and
Immune cells are rich in prolactin receptors and certain types of lymphocytes in fact synthesize and secrete prolactin. These observations suggest that prolactin may to some extent act as a regulator of the body’s immune activity.
In an area in the brain known as the hypothalamus, a chemical called dopamine is released. Dopamine suppresses prolactin synthesis and release by the pituitary gland. As such it acts as a “hypothalamic brake set” causing prolactin only to be secreted when the “brake” is released. Treatment with dopamine agonists such as bromocriptine (Parlodel) and cabergoline (Dostinex) , by enhancing serotonin production lowers prolactin
Several other hypothalamic hormones, including thyroid releasing hormone (TRH) and gonadotropin releasing hormone (GnRH) cause an increase in prolactin secretion Stimulation of the nipples (including but not limited to nursing) leads to hypothalamic activation and prolactin release Estrogens also exerts a positive control over prolactin synthesis and secretion
Even modestly raised prolactin levels (20ng/ml-40ng/ml) can interfere with estrogen-induced endometrial proliferation as well as egg/ ovarian follicle growth and development. Accordingly treatment with dopamine agonists (bromocriptine/ Cabergoline) might be of benefit in such cases.
Increased PRL secretion reduces the pulsatility of GnRH impairing the pituitary production of FSH and LH and may directly impair the endocrine activity of ovarian follicles as well as endometrial response to estrogen. This can lead to dysfunctional or failed ovulation, a defective luteal phase, and a poorly developed endometrial response to estrogen (a thin endometrial lining). About n 5% of unselected, asymptomatic infertile women have hyperprolactinemia. In such cases long-term use of dopaminergic drugs such as bromocryptine and can normalized prolactin levels leading to reestablishment of functional ovulation and improved endometrial development. About half of the pregnancies occurring during dopaminergic therapy start after the first 6 months of this drug therapy. Treatment should continue for at least 1 year.
Common manifestations of significantly increased prolactin secretion (hyperprolactinemia):
•In women:
oOligo/amenorrhea (reduction or absence of menstrual flow) and galactorrhea (excessive or spontaneous breast secretion of milk).
oA modest elevation in blood prolactin can also point to an underlying state of hypothyroidism
oMarkedly elevated prolactin levels (i.e. >60ng/ml) might point to a prolactin producing pituitary macroadenoma or microadenoma as well as other intracranial lesions such as craniopharyngiomas, meningiomas etc.
•In men: Such men rarely have galactorrhea
oHypogonadism,
oBreast enlargement (gynecomastia),
oErectile dysfunction
oDecreased Libido,
oSperm dysfunction resulting in infertility and with impotence..
Causes of hyperprolactinemia:
•Certain drugs: (e.g. tranquilizers, ganglion blocker antihypertensives, antidepressants, thiazides and narcotics) can also lead to significant elevations in prolactin. Drug-induced hyperprolactinemia can be reversed by modifying or withdrawing the causative medication. In cases where this cannot safely be done, bromocryptine derivatives can be used.
•Pituitary adenomas (prolactinomas)
o Some pituitary adenomas are treated by surgical removal but in most case prolonged treatment with bromocryptine or cabergoline will effectively lower blood concentrations and lead to shrinkage/disappearance of the tumor. Such treatment is also safe during pregnancy.
o Intracranial lesions such as craniopharyngiomas, meningioma causing hyperprolactinemia are usually treated by surgical removal.
Hyperprolactinemia and Reproductive Dysfunction:
•Hypothyroidism in women is often caused by an autoimmune process where antithyroid antibodies progressively replace thyroid glandular tissue with functionless connective tissue. In roughly 50% of such cases there will be increased uterine natural killer cell activity (NKa) which may profoundly impair implantation leading to “perceived infertility” or recurrent pregnancy loss. Thus, ATA with NKa can be present prior to the development of clinically overt autoimmune hypothyroidism (Hashimoto’s disease). Since women with NKa are often infertile, or experience recurrent pregnancy loss, it is important that any unexplained hyperprolactinemia associated with reproductive failure or infertility be evaluated for an immunologic implantation dysfunction (IID) through testing for the presence of antithyroid antibodies and if the ATA level is elevated, that an NKa test (K-562 target cell test) be done. What is not often commonly recognized is that even in cases where autoimmune hypothyroidism is clinically overt, treatment with thyroid hormone replacement will usually not solve the reproductive dysfunction which will usually require selective immunotherapy with Intralipid (IL) infusions plus steroid therapy. IL is administered intravenously about 4-7 days prior to ovulation or egg retrieval and then repeated one more time upon biochemical confirmation of early pregnancy. The steroids are continued to the 8th week of pregnancy and then tailed off over 2 weeks.
•Ovarian Hyperstimulation Syndrome (OHS): Prolactin facilitates production by ovarian follicle cells of VEGF (a vasoactive substance that increases vascular permeability of blood vessels) In cases of severe ovarian With severe ovarian hyperstimulation syndrome (OHSS) where there are a large number of follicles present (>25) and the blood estradiol level is markedly elevated (4,000pg/ml), even modestly elevated prolactin release can markedly worsen the situation. There is strong evidence to suggest that women with ovarian Hyperstimulation (>20 follicles and blood estradiol levels that peak above 3,000pg/ml) who receive O.5mg of oral administration Cabergoline daily for 7 days, starting on the day of the hCG trigger, experience a significant reduction in the risk and severity of severe ovarian stimulation syndrome (OHSS). This is thought to be due to Cabergoline suppressing the production of vascular vasoactive substances such as VEGF that are produced by luteinized follicular granulosa cells, that increase the vascular permeability of local pelvic blood vessels.
Geoff Sher
Hello Dr. Sher,
I am glad I found your blog.
I am 31 years old female with primary infertility due to male factor. Otherwise, I am healthy although ?? mild PCOS was raised during the assessment.
I am undergoing 1st IVF. I am on day 5 and E2 was 9800 pg/ml. There were around 20 follicles but I am not sure about the size. I was on Gonal-f 225 IU and Repronex 75 IU for the first 4 days. Today, the 5th day, Repronex 75 IU was stopped and I was given Cetrotide 0.25mg X2 on top of Gonal-f 225 IU.
I am also a doctor (not Obe/Gyn) and I was reading articles about coasting. I would appreciate your opinion on my case?
Thank you in advance,
EA
You must gave had 50 or more follicles. Women like yourself are at 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 that a patient 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 at risk of developing OHSS, 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.
Geoffrey Sher MD
Hi Dr Asher,
I’m 34, AMH 0.6 on my 2nd Ivf. First Ivf was microdose Lupron with 7 eggs retrieved, 5 mature, only one fertilized via icsi. 3 day transfer of 4 cell embryo with 40% fragmentation- unsuccessful. Got pregnant with an IUI a few months after, but only the gestational sac developed, so miscarriage at 8 weeks.
I just had my egg collection from Ivf # 2 yesterday- estrogen priming protocol. The scan on trigger day showed 5 follicles on the right ovary (3 around 14mm and 2 around 18 mm.) The left ovary had 2 around 16 mm and 3 around 20mm.
6 follicles were aspirated at egg pickup and one the doctor (filling in my my normal
Doctor) said that she couldn’t safely access the 7th follicle because my right ovary was high. She aspirated 3 from the left and 3 from the right (I was surprised since my scan on the day of trigger showed the 5 largest on the right). Today I found out that of the 6 eggs, only 3 were mature. 2 fertilized with conventional Ivf- one with 2 PN and 1 was one PN but the embryology lab tech said maybe it was further in development. The other mature egg was unfertilized and I was told it probably was originally immature and matured in the lab so they’re leaving it with the sperm. I feel maybe I was triggered early to avoid a weekend retrieval. The nurse had told me I was on the border of being ready for the trigger. I’m feeling like I may need to change clinics if the trigger was rushed before being ready. What do you think?
Women who (regardless of age) have diminished ovarian reserve (DOR) , as you do, have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production of LH biological activity which can result in excessive LH-induced ovarian male hormone (predominantly testosterone) production which in turn can have a deleterious effect on egg/embryo “competency”.
While it is presently not possible by any means, to reverse the effect of DOR, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can in my opinion, make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.
I try to avoid using such protocols/regimes (especially) in women with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy
Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and 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
•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
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
•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?
•Blastocyst Embryo Transfers Should be the Standard of Care in IVF
•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.
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation.
•Preimplantation Genetic Testing (PGS) in IVF: It Should be Used Selectively and NOT be Routine.
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•PGS in IVF: Are Some Chromosomally Abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
•PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•How Many Embryos should be transferred: A Critical Decision in IVF.
•The Role of Nutritional Supplements in Preparing for IVF
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
•IVF Egg Donation: A Comprehensive Overview
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:
Email: Julied@sherivf.com
OR
Phone: 702-533-2691
800-780-7437
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Hi Dr. Sher,
Thank you for this opportunity. I have a question about my testosterone and DHEA levels and whether I should try to change them. I am trying to get pregnant with own egg. I am 48. Yes, I know. Please, don’t tell me the lecture about the depleting basket of eggs and such. Heard it already dozens of times. I had a female comprehensive panel done at Any Lab Tests now on cycle day 3 while we were on vacation. I could not find an ivf center to do a monitoring so I don’t have an antral follicle count. However, I did get hormone results about testosterone levels and such that ivf clinics have never given me. My FSH level in the last two years has ranged between 8-11. It was an unusually high 12 last month but I think that was because I did not take Cabergoline for 2 months (my primary care doctor is a jerk and won’t let me have it and my RE has been booked solid for months until August). I have a macro prolactinoma. Anyway, last month my prolactine level skyrocketed to 136 and I had only one antral follicle (I usually have between 5 and 10). I got back on the Cabergoline and I think my prolactine level is back to normal since my breasts are not sore anymore and it looks like my hormone levels went back to normal. Here are the results from my latest cycle day 3 this week. FSH 8.1 IU/L. LH 9.7 IU/L (I am not sure I believe this as my LH strips are not matching this. I have no line so far at all on them for this cycle. I always use the same brand strips and when the blood results for LH are around 10, I usually have a medium dark line on the LH strips. My LH levels are usually around 4-7 on cycle day 3.) TSH 2.3 mIU/L. Estradiol 68 pg/mL (usually this is over 100 so again I am kind of wondering about this lab’s results). DHEA sulfate 63 ug/dL. Testosterone 6 ng/dL. SHBG 188 nmol/L. Testosterone free-Calc 0.3 pg/mL.
So the things marked abnormal on my blood test was HIGH SHBG and low testosterone and low testosterone free-Calc. My Anion Gap was also marked as slightly low and my Carbon Dioxide was slightly high. Not sure if those have any relation to fertility at all but they were the only other abnormal results so I threw them in because maybe they will mean something to you. Would you recommend I do anything? I don’t currently supplement except of course with Cabergoline. I just read online about nettle for my testosterone problems but the literature is inconclusive about whether it has any effect. I went and picked some stinging nettle near the woods and can use the leaves and root just in case it would help. (Don’t worry I am sure it is nettle. I am an expert forager. I have a hobby for years of foraging and identifying plants in my area.) I am not too much into woo woo naturopathic type medicine as usually I think it is snake oil but some stuff does work like American Mandrake root for warts. I used it myself once successfully from roots I dug up in my yard and pharmaceutical companies harvest the root for the podophyllin to treat HPV.
Sorry if this is long. In medicine like anything else, the devil is always in the details. I hope that you can help me. If you have any great ideas for me, please let me know. We don’t have money to spend on consultations where doctors just again tell me to give up because women my age have less than a 1-5% chance of getting a good egg. I can read that all day long for free and hear it every time I talk to a new doctor as well as get it repeated on occasion when I talk to my regular doctor. I am not sure why he imagines that I have some limited capacity to remember the “give up” message since the last time he told it to me. It seems to be him who is not remembering our conversations well as I have told him in response every time that we understand our chances are near zero and we intend to keep trying until we are out of money or out of eggs, whichever comes first. For some reason they think they are giving me something of value by giving me that speech again and again and again. I don’t agree. But if you have something you could do for me to improve my fertility situation that nobody else is suggesting for me, that would have great value to me. Thank you for reading. I hope you have some ideas for me.
Dear Pearl,
I truly wish I could offer you encouragement and new information but alas not. There is nothing that is known presently that can enhance egg quality in women of advanced reproductive age. Of course some women of your age and even older do conceive on their own and have babies but they are few and far between and such cases represent flukes!
So sorry that I have nothing to offer you!
Geoff sher
Hi there Dr Sher,
I am 29 years old and have experienced a total of 8 miscarriages with no living children. 1 chemical, 1 ectopic, and 6 early losses. I have never been able to get past 8 weeks but have seen the heart beat for most of them. I have now seen 2 fertility specialist within the past 3 years with still no answers to why I am miscarrying. They are telling me – we have tested you guys for everything and everything is coming back normal – they are out of things to try for me and my husband. I have been diagnosed with endometriosis and PCOS though. With my last miscarriage I was on neupogen, intralipids (had one infusion done a few weeks after I found out I was pregnant), Lovenox, and progesterone vaginally – this was the first time I tried any of these as the doctor said he was just treating for everything he could think of. After the D&C they tested for chromosome abnormalities and everything came back normal. Do you have an suggestions for us as a next step? We desperately want a family.
Thank you!
Tiffany