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.
Dear Dr Sher,
I have finally after 5 failed ivf managed to get pregnant on my 6th attempt. My right ovary was painful with a dull ache on cd29-30 then the pain suddenly stopped. On cd 31 i had light bleeding. On cd 32 small brown clots. This now all stopped and whats left is a bit of brown spotting. My bhcg on 16dpo ( 13 days post a 3 day transfer or cd30) was just 68. Two days later it was 198 which means it nearly tripled. 1), is it possible to rule our a twin pregnancy with auch low numbers? 2) can the ovary pain and spotting mean ectopic pregnancy even though the pain is totally gone? 3) I go back for a repeat hcg test on cd34 (4 days after my last one). I will be 5w1d then. Is it possible to do an ultrasound that day/ so early to rule out ectopic pregnancy? 4) I read your blog about doubling times and molar pregnancy and it really scares me. Could these figures mean molar pregnancy and can this be ruled out 5w1d with a scan? 6) could this be a start of a miscarriage referrig to the bleeding spotting even though my hcg tripled? I just so wish to enjoy this pregnancy now but with the bleeding/spotting all I now do is worry!
Hi Kat,
I really hope this works out for you. Yes, a gestational sav in the uterus, seen at 5-6 weks can virtually rule out an ectopic pregnancy. As far as twins are concerned, while not impossible, these slowly rrising hCG levels make it most unlikely.
Good luck and G-d bless!
Geoff Sher
Dr. Sher,
Today is day 10 of stims (225 gonal f, 75 menopur) 8 days of 250 Cetrotide. My estrogen today was 4700 and i had 24 follicles between 14 and 22 mm. My dr wants me to trigger on half a dose of novarel tonight and do the retrieval on Sunday. In your opinion, does this sound like the right approach or will this increase my odds for OHSS and compromise the egg quality? Would you do a transfer?
Sincerely,
Jen
Traditionally egg retrievals are timed for about 36 hours after a 10,000U hCG “trigger”. The hCG hormone thereupon remains in the system for up to a week. When patients who overstimulate following ovarian stimulation experience prolonged exposure to hCG the risk of developing severe ovarian hyperstimulation syndrome with its incumbent life-endangering complications escalates. Attempts to mitigate this risk have included:
a)withholding the hCG trigger altogether thereby preventing luteinization of follicle granulosa cells and preventing the production of vasoactive substances (e.g. VEGF) which when overproduced escalate the risk/severity of OHSS,
b)prematurely administering the hCG trigger to arrest further follicular growth and escalation in blood estradiol levels,
c)reducing the dosage of hCG by half, to 5,000U in the hope of limiting/restricting the luteinization process and,
d) supplanting the “hCG trigger’ by an “Agonist (e.g. Lupron) trigger” that causes promotes meiotic egg maturation buy causing a surge in the release of pituitary LH.
All of the options above do indeed reduce the risk of developing OHSS. “a)” completely prevents egg maturation from occurring and thus virtually precludes the harvesting of “competent” eggs, while “b), c), and d)”all adversely affect egg “competency” to a lesser or greater degree, thereby compromising both embryo quality and IVF outcome.
Use of the “Lupron trigger” bears further mention: Since its recent introduction, this approach has really gained popularity and caught on in a big way. In truth, there can be little argument that it markedly reduces the incidence, severity and risk of complications associated with severe ovarian hyperstimulation. However use of the “Lupron trigger” often comes at the expense of egg/embryo quality as well as IVF outcome. Thus, the question arises as to whether this approach is advisable, and if not, what the best alternative to its use would be. The reason why the “Lupron trigger” is in my opinion ill-advised, is that in cases of ovarian hyperstimulation, where there are numerous follicles with eggs that need to undergo meiosis following the “trigger”, the magnitude of the LH surge, induced by a “Lupron GnRHa trigger” is often insufficient. This can result in suboptimal egg maturation (meiosis), leading to the generation of an inordinate number of immature/dysmature eggs as well as in an increase in the number of large follicles that fail to yield eggs at all (“so called “empty follicles). This is why I do not employ the “Lupron trigger” approach in my practice, preferring instead to use the long pituitary down-regulation, along with “prolonged coasting” in women who are deemed to be at risk for developing OHSS. My position is further supported by a recent publication showing that for this very reason, the use of a GnRHa-induced “trigger is not helpful.
Prolonged Coasting, my preferred choice!: My approach is consistently to have my patients who are at risk of developing OHSS, launch their ovarian stimulation, coming off a monophasic birth control pill (BCP). The last few days on the BCP is accompanied by the addition of Lupron. Thereupon the BCP is stopped and Lupron therapy is continued. After 3-7 days menstruation usually ensues, at which point the dosage of Lupron is reduced and low dosage FSHr (Follistim/Gonal-F/Puregon) -dominant ovarian stimulation is commenced. Lupron and gonadotropins are then continued together. This approach is referred to as the “Long Pituitary Down-regulation protocol” Use of the BCP is intended to lower LH and thereby reduce stromal activation (hyperthecosis) in the hope of controlling ovarian androgen (mainly testosterone) release (too much ovarian testosterone is harmful to egg development). Seventy five (75) units of LH/hCG (Luveris/Menopur) is added from the 3rd day of gonadotropin stimulation. Starting on the 7th day of ovarian stimulation with gonadotropins, I start watching daily for the # and size of follicles developing and for the rise in blood [E2]. If there are > 25 follicles, the patient becomes a candidate for “prolonged coasting” I keep stimulating with gonadotropins (regardless of the [E2]) until: a) 50% of all follicles reach 14mm and b) the [E2] reaches 2500pg/ml. At that point, gonadotropin stimulation is discontinued abruptly while daily Lupron injections continue. Thereupon I follow the daily blood [E2] without doing further US examinations. The [E2] will almost invariably continue to rise. I carefully plot the rise in [E2] (regardless of how high it goes). Usually, within 1-3 days it will plateau and then start to decline. As soon as the [E2] drops below 2500pg/ml (and not before then), I administer the 10,000U hCGu (Novarel/Pregnyl/Profasi) “trigger” or 500mcg of hCGr (Ovidrel) and then schedule an egg retrieval for 36h later. ICSI is a MUST because “coasted” eggs usually have few or no surrounding cumulus cells and eggs without a cumulus layer will not readily fertilize on their own. All fertilized eggs are cultured to the blastocyst (up to 6 days) whereupon I transfer up to two into the uterus, or vitrify all expanded blastocysts for subsequent dispensation at the directive of the patient. In some cases the embryos are biopsied for PGS testing prior to being cryostored. Subsequent frozen embryo transfers are conducted as per the wishes of the patients.
It is important to point out that the success of this “prolonged coasting” approach depends on precise timing of the initiation and the conclusion of “prolonged coasting”. If you start too early, follicle growth will stop and the cycle will be lost. If you start too late, you will encounter too many post-mature/cystic follicles (>22mm) that usually harbor abnormally developed eggs.
Use of the above approach avoids unnecessary cycle cancellation, severe OHSS, and optimizes egg/embryo quality. The worst you will encounter is mild to moderate OHSS and this too is uncommon.
The use of an agonist or GNRH trigger while reducing the risk of severe OHSS developing comes at the expense of egg/embryo quality and could compromise IVF outcome.
Hope this helps!
Geoff Sher
Dear DR,
Is a DNA test on sperm useful even when doing ICSI. I presume if high DNA problems the only option is ICSI anyway or would donor sperm be needed if high DNA problems with sperm? iS there a connection with abnormal shape and high DNA problems with sperm?
Thanks
Yes, the test would be helpful from a prognostic point of view. Frankly, even if the DFI is very elevated, this alone is rarely an indication for using donor sperm. It is advisable to be checked for a varicocele though.
Geoff sher
Dear Dr. Sher,
A few years back I was diagnosed with subclinical hypothyroidism and have been on synthroid ever since. I had my thyroid tested exactly one month ago and my TSH was 1.3 and Free T4 was 1.23. I am just about to start my second IVF cycle (1st was a failure) and I had my TSH tested and it had jumped to 3.11 in one month! I am already on day 2 of Lupron. Should I cancel my cycle? I am worried about my low thyroid impacting the quality of my eggs. I suspect the jump might have something to do with the coq10 I’ve been taking. I do wait at least 3-4 hours after my synthroid to take it though. Please let me know if you think this could jeopardize egg quality.
With gratitude,
Jennifer
Hypothyroidism in women is commonly due to autoimmune factors. Between 2% and 5% of women of the childbearing age have reduced thyroid hormone activity (hypothyroidism). Women with hypothyroidism often manifest with reproductive failure i.e. infertility, unexplained (often repeated) IVF failure, or recurrent pregnancy loss (RPL). The condition is 5-10 times more common in women than in men. In most cases hypothyroidism is caused by damage to the thyroid gland resulting from of thyroid autoimmunity (Hashimoto’s disease) caused by damage done to the thyroid gland by antithyroglobulin and antimicrosomal auto-antibodies.
The increased prevalence of hypothyroidism and thyroid autoimmunity (TAI) in women is likely the result of a combination of genetic factors, estrogen-related effects and chromosome X abnormalities. This having been said, there is significantly increased incidence of thyroid antibodies in non-pregnant women with a history of infertility and recurrent pregnancy loss and thyroid antibodies can be present asymptomatically in women without them manifesting with overt clinical or endocrinologic evidence of thyroid disease. In addition, these antibodies may persist in women who have suffered from hyper- or hypothyroidism even after normalization of their thyroid function by appropriate pharmacological treatment. The manifestations of reproductive dysfunction thus seem to be linked more to the presence of thyroid autoimmunity (TAI) than to clinical existence of hypothyroidism and treatment of the latter does not routinely result in a subsequent improvement in reproductive performance.
It follows, that if antithyroid autoantibodies are associated with reproductive dysfunction they may serve as useful markers for predicting poor outcome in patients undergoing assisted reproductive technologies.
Some years back, I reported on the fact that 47% of women who harbor thyroid autoantibodies, regardless of the absence or presence of clinical hypothyroidism, have activated uterine natural killer cells (NKa) cells and cytotoxic lymphocytes (CTL) and that such women often present with reproductive dysfunction. We demonstrated that appropriate immunotherapy with IVIG or intralipid (IL) and steroids, subsequently often results in a significant improvement in reproductive performance in such cases.
The fact that almost 50% of women who harbor antithyroid antibodies do not have activated CTL/NK cells suggests that it is NOT the antithyroid antibodies themselves that cause reproductive dysfunction. The activation of CTL and NK cells that occurs in half of the cases with TAI is probably an epiphenomenon with the associated reproductive dysfunction being due to CTL/NK cell activation that damages the early “root system” (trophoblast) of the implanting embryo. We have shown that treatment of those women who have thyroid antibodies + NKa/CTL using IL/steroids, improves subsequent reproductive performance while women with thyroid antibodies who do not harbor NKa/CTL do not require or benefit from such treatment.
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 promptl
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•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?
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
•Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
•Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•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
•Measuring and Interpreting Blood hCG to Assess Pregnancy Viability Following ART Treatments.
I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.
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.
Geoff Sher
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Hi Dr Sher,
I have repeatedly tested negative for Thyroid antibodies but I am doing a freeze all cycle so I can investigate IVIG before transfer. But do you think my high TSH/low T4 could have an effect on the quality of eggs/embryos and would be reason enough to postpone my ivf cycle? Or is it just the implantation dysfunction you are concerned with?
Age 28… Severe endometriosis… Found multiceated cysts +0. 8 mm fibroid.. + partial blockage in one tube. To resolve laproscopy was done.. Result – cyst drained + adhesions removed. 3 months zoladex treatment done. Now 7 th week from last injection of zoladex. What can I do best to conceive sooner naturally… Thanx
You would need IVF but first, see the following:
Endometriosis is a condition that occurs when the uterine lining (endometrium) grows not only in the interior of the uterus but in other areas, such as the fallopian tubes, ovaries and the bowel. Endometriosis is a complex condition where, the lack or relative absence of an overt anatomical barrier to fertility often belies the true extent of reproductive problem(s).
All too often the view is expounded that the severity of endometriosis-related infertility is inevitably directly proportionate to the anatomical severity of the disease itself, thereby implying that endometriosis causes infertility primarily by virtue of creating anatomical barriers to fertilization. This over-simplistic and erroneous view is often used to support the performance of many unnecessary surgeries for the removal of small innocuous endometriotic lesions, on the basis of such “treatment” evoking an improvement in subsequent fertility.
It is indisputable that even the mildest form of endometriosis can compromise fertility. It is equally true that, mild to moderate endometriosis is by no means a cause of absolute “sterility”.
Rather, when compared with normally ovulating women of a similar age who do not have endometriosis, women with mild to moderate endometriosis are about four to six times less likely to have a successful pregnancy.
Endometriosis often goes unnoticed for many years. Such patients are frequently, erroneously labeled as having “unexplained infertility”, until the diagnosis is finally clinched through direct visualization of the lesions at the time of laparoscopy or laparoscopy. Not surprisingly, many patients with so called “unexplained” infertility, if followed for a number of years, will ultimately reveal endometriosis.
Women who have endometriosis are much more likely to be infertile. There are several reasons for this:
•First-Ovulation Dysfunction: In about 25 – 30% of cases, endometriosis is associated with ovulation dysfunction. Treatment requires controlled ovarian stimulation (COS). The problem is that the toxic pelvic environment markedly reduces the likelihood that anything other than IVF will enhance pregnancy potential.
•Second- Toxic Pelvic environment that compromises Fertilization Endometriosis is associated with the presence of toxins in peritoneal secretions while it is tempting to assert that normally ovulating women with mild to moderate endometriosis would have no difficulty in conceiving if their anatomical disease is addressed surgically or that endometriosis-related infertility is confined to cases with more severe anatomical disease…nothing could be further from the truth. The natural conception rate for healthy ovulating women in their early 30’s (who are free of endometriosis) is about 15% per month of trying and 70% per year of actively attempting to conceive. Conversely, the conception rate for women of a comparable age who have mild or moderate pelvic endometriosis (absent or limited anatomical disease) is about 5-6% per month and 40% after 3 years of trying. As sperm and egg(s) travel towards the fallopian tubes they are exposed to these toxins which compromise the fertilization process. In fact it has been estimated that there is a 5-6 fold reduction in fertilization potential because of these toxins which cannot be eradicated. Frankly, it really does not matter whether an attempt is made to remove endometriosis deposits surgically as this will not improve pregnancy potential. The reason is that for every deposit observed, there are numerous others that are in the process of developing and are not visible to the naked eye and whether visible or not, such translucent deposits still produce toxins. This also explains why surgery to remove visible endometriosis deposits, controlled ovarian stimulation with or without intrauterine insemination will usually not improve pregnancy potential. Only IVF, through removing eggs before they are exposed to the toxic pelvic environment, fertilizing them in-vitro and then transferring the embryos to the uterus represents the only way to enhance pregnancy potential.
•Third-Pelvic adhesions and Scarring: In its most severe form, endometriosis is associated with scarring and adhesions in the pelvis, resulting in damage to, obstruction or fixation of the fallopian tubes to surrounding structures, thereby preventing the union of sperm and eggs.
•Fourth-Ovarian Endometriomas, Advanced endometriosis is often associated with ovarian cysts (endometriomas/chocolate cysts) that are filled with altered blood and can be large and multiple. When these are sizable (>1cm) they can activate surrounding ovarian connective tissue causing production of excessive male hormones (androgens) such as testosterone and androstenedione. Excessive ovarian androgens can compromise egg development in the affected ovary (ies) resulting in an increased likelihood of numerical chromosomal abnormalities (aneuploidy) and reduced egg/embryo competency”. In my opinion large ovarian endometriomas need to be removed surgically or rough sclerotherapy before embarking on IVF.
•Fifth- Immunologic Implantation Dysfunction (IID). Endometriosis, regardless of its severity is associated with immunologic implantation dysfunction linked to activation of uterine natural killer cells (NKa) and cytotoxic uterine lymphocytes (CTL) in about 30 of cases. This is diagnosed by testing the woman’s blood for NKa using the K-562 target cell test or by endometrial biopsy for cytokine analysis, and, for CTL by doing a blood immunophenotype. These NKa attack the invading trophoblast cells (developing “root system” of the embryo/early conceptus) as soon as it tries to gain attachment to the uterine wall. In most cases, this results in death of the embryo even before the pregnancy is diagnosed and sometimes, in a chemical pregnancy or even an early miscarriage. . As such, many women with endometriosis, rather than being infertile, in the strict sense of the word, often actually experience repeated undetected “mini-miscarriages”.
Advanced Endometriosis: In its most advanced stage, anatomical disfiguration is causally linked to the infertility. In such cases, inspection at laparoscopy or laparoscopy will usually reveal severe pelvic adhesions, scarring and “chocolate cysts”. However, the quality of life of patients with advanced endometriosis is usually so severely compromised by pain and discomfort, that having a baby is often low on the priority list. Accordingly, such patients are usually often more interested in relatively radical medical and surgical treatment options (might preclude a subsequent pregnancy), such as removal of ovaries, fallopian pubis and even the uterus, as a means of alleviating suffering.
Moderately Severe Endometriosis. These patients have a modest amount of scarring/ adhesions and endometriotic deposits which are usually detected on the ovaries, fallopian tubes, bladder surface and low in the pelvis, behind the uterus. In such cases, the fallopian tubes are usually opened and functional.
Mild Endometriosis: These patients who at laparoscopy or laparotomy are found to have no significant distortion of pelvic anatomy are often erroneously labeled as having “unexplained” infertility. To hold that the there can only infertility can only be attributed to endometriosis if significant anatomical disease can be identified, is to ignore the fact that, biochemical, hormonal and immunological factors profoundly impact fertility. Failure to recognize this salient fact continues to play havoc with the hopes and dreams of many infertile endometriosis patients.
TREATMENT:
The following basic concepts apply to management of endometriosis-related infertility:
1.Controlled Ovulation stimulation (COS) with/without intrauterine insemination (IUI): Toxins in the peritoneal secretions of women with endometriosis exert a negative effect on fertilization potential regardless of how sperm reaches the fallopian tubes. This helps explain why COS with or without IUI will usually not improve the chances of pregnancy (over no treatment at all) in women with endometriosis. IVF is the only way by which to bypass this problem.
2.Laparoscopy orLaparotomy Surgery aimed at restoring the anatomical integrity of the fallopian tubes does not counter the negative influence of toxic peritoneal factors that inherently reduce the chances of conception in women with endometriosis four to six fold. Nor does it address the immunologic implantation dysfunction (IID) commonly associated with this condition. Pelvic surgery is relatively contraindicated for the treatment of infertility associated with endometriosis, when the woman is more than 35 years of age. With the pre-menopause approaching, such women do not have the time to waste on such less efficacious alternatives. In contrast, younger women who have time on their side might consider surgery as a viable option. Approximately 30 -40 percent of women under 35 years of age with endometriosis will conceive with in two to three years following corrective pelvic surgery.
3.Sclerotherapy for ovarian endometriomas.: About 10 years ago I introduced “sclerotherapy”, a relatively non-invasive, safe and effective outpatient method to permanently eliminate endometriomas without surgery being required. Sclerotherapy for ovarian endometriomas involves needle aspiration of the liquid content of the endometriotic cyst, followed by the injection of 5% tetracycline into the cyst cavity. Treatment results in disappearance of the lesion within 6-8 weeks, in more than 75% of cases so treated. Ovarian sclerotherapy can be performed under local anesthesia or under general anesthesia. It has the advantage of being an ambulatory office- based procedure, at low cost, with a low incidence of significant post-procedural pain or complications and the avoidance of the need for laparoscopy or laparotomy
4.The role of selective immunotherapy Women with antiphospholipid antibodies (APA’s) experience improved IVF birth rates when heparinoids (Clexane/Lovenox) is administered from the onset of ovarian stimulation with gonadotropins until the 10th week of pregnancy.
a.About Intralipid (IL) and steroid therapy: Intralipid (IL) is a solution of small lipid droplets suspended in water. When administered intravenously, IL provides essential fatty acids, linoleic acid (LA), an omega-6 fatty acid, alpha-linolenic acid (ALA), an omega-3 fatty acid.IL is made up of 20% soybean oil/fatty acids (comprising linoleic acid, oleic acid, palmitic acid, linolenic acid and stearic acid) , 1.2% egg yolk phospholipids (1.2%), glycerin (2.25%) and water (76.5%).IL exerts a modulating effect on certain immune cellular mechanisms largely by down-regulating activated natural killer cells (NKa). This effect is enhanced through the concomitant administration of corticosteroids such as dexamethasone, prednisone, and prednisolone which enhance the therapeutic effect by suppressing cytotoxic/activated T-lymphocytes (CTL). This effect of IL might is likely due to its ability to
5. In vitro fertilization is the treatment of choice for women with endometriosis. This is especially true for women more than 35 years of age or where surgery and treatment with fertility agents has proven to be unsuccessful. We anticipate that approximately 75 percent of such women will achieve the birth of one or more babies within three IVF attempts performed at SIRM.
6.
?suppresses pro-inflammatory cellular (Type-1) cytokines such as interferon gamma and TNF-alpha. In-vitro testing has shown that IL successfully and completely down-regulates activated natural killer cells (NKa) within 2-3 weeks in 78% of women experiencing immunologic implantation dysfunction. In this regard it is just as effective as Intravenous Gamma globulin (IVIg) but at a fraction of the cost and with a far lower incidence of side-effects. Its effect lasts for 4-9 weeks when administered in early 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
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•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.
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•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?
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
•Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
•Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
•Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•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
I invite you to call 702-699-7437 or 800-780-7437 or go online on this site and set up a one hour Skype consultation with me to discuss your case in detail.
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.
Geoff Sher