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.
Hello Dr.Sher
Me and my husband have gone through 4 treatments. 1 IVF and 4 ICSI.
1. Treatment in August 2014. Puregon 175-225 and 300 last 9-10 days. 9 eggs that did not fertilize with IVF and no transfer.
2. Treatment in Oct 2014. Puregon 225 days 1-4 and 300 days 5-12. 7 eggs that did ICSI and we got 4 embryos. Two transferred and we did not get anything in the freezer. These two embryos that were transferred were 2 days old and had the grade 2 (were 2 cells) and 2,5 (4 cells). Negative pregnancy test.
3. Treatment in January 2015. Menopur 300, days 1-10. 9 eggs and 5 embryos. Two transferred and we did not get anything in the freezer. These two embryos that were transferred were 2 days old and have the grade 2,5 (4 cells) and 2,5 (2 cells). Negative pregnancy test.
4. Treatment in March 2015. Menopur 300, days 1-12. 5 eggs just one embryo were transferred and we did not get anything in the freezer. This embryo that was transferred was 2 days old and had the grade 2 and was 4 cells.
They did AHA at that time and I was on Ovitrelle, Lutinus and Decortin. Negative pregnancy test.
5.Treatment in June 2016. Gonal f 400 for 2 days, 375 for 3 days, 300 for 6 days. They got 8 aspirated follicles and 7 aspirated oocytes. 5 fertilized and in the end we got 2 blastocyst 3ab that were transferred. They did AHA and I was on Prolutex, Utrogestan, Clexane, Intralipid (one doze 8 days before transfer day and another doze at the transfer day) and Prednisolone (20mg). This was the first time we were able to grow to blastocyst. We got negative test again.
In August we went to check the nk cells and the result is that I have increasing cd57 cells.
Our question to you do we need to worry that it did not work out for the first time with blastocyst, Intralipid, Prednisolone and Clexane?
Do you recommend to try something else like donor eggs?
Thank you very much
Lilja
Hi Lija,
In my opinion, the moist important determinant of outcome is the protocol used for ovarian stimulation. This is even more relevant when it comes to women who have diminished ovarian reserve (see below) and based upon your blunted response, I suspect that you might have DOR. You might well, in addition , have activation of uterine NK cells but the best way to diagnose this is through a K-562 target cell test. I recommend that your blood be sent to Reproductive Immunology Associates (RIA) in Van Nuys, CA for this test, for antithyroid antibodies, antiphospholoipid antibodies IAPA) and an immunophenotype.
As women age beyond 35Y there is commonly a progressive diminution in the number of eggs left in the ovaries, i.e. diminished ovarian reserve (DOR). So it is that older women as well as those who (regardless of age) have DOR 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 age-related effect on the woman’s “biological clock, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can 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 older women and those 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 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 Aproach
•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
•Optimizing Response to Ovarian Stimulation in Women who Have Compromised Ovarian Response to Ovarian Stimulation in Women who Have Compromised Ovarian Reserve: A Personal Approach.
•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
•Why did my IVF Fail
•Blastocyst Embryo Transfers Done 5-6 Days Following Fertilization are Fast Replacing Earlier day 2-3 Transfers of Cleaved Embryos.
•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
•IVF Failure and Implantation Dysfunction:
•The Role of 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)
•Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
•Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
•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
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.
Geoff Sher
Dear Dr Sher,
1-In IVF what are the situations in which outer cumulus cells of a retrieved egg has to be removed?
2- Is it always done when any egg is retrieved for IVF or done only if doing genetic testing of eggs?
1. When you need to assess egg maturation (i.e. look for the presence of the 1st polar bodoy-PB-1)
2. When a polar body biopsy needs to be done to assess eggg maturation or perform other genetic tests
3. When you do ICSI
It is not done when conventional fertilization ius contemplated because it would hinder spontaneous fertilization if youn did so.
Geoff Sher
Dear Dr Sher,
Is it normal for Progesterone to decrease from CD1 to CD10?
That depends on the protocol of stimulation used…but yes!
Geoff Sher
Hi Dr. Sher,
I just had my 2nd failed FET (1st was last year). I am 38 years old with a history of Thyroid and Ovarian Cancer. I had a complete thyroidectomy in 1997 and have been on full replacement thyroid medication since then (currently levothyroid and cytomel). I have also been on some form of HRT (estrogen/progesterone) since 2011, although I can’t honestly say it has been without its ups and downs as I have struggled to find the right dose to rid all of the symptoms brought on by surgical menopause.
Upon my diagnosis of Ovarian Cancer I had surgery to remove one of my ovaries that was encapsulated by the tumor. My initial pathology came back as borderline ovarian cancer, but my frozen pathology came back as stage 1. Prior to starting chemotherapy I worked with a fertility clinic locally to freeze my eggs. I was able to freeze 10 eggs in 2010. By 2015, I had gotten married and we were ready to try for a child. 4 solid embryos were formed using my husband’s sperm. We transferred 1 embryo right away, but it failed.
My protocol was not very different from others I know who have gone through this process. Below is my most recent protocol (which was slightly different then my protocol last year since my Dr. retired and I was changed to a different doctor).
Day of cycle 1-5: Estrace (1 mg, 1 tab twice daily)
Day of cycle 6-9: Estrace (1 mg, 2 tabs twice daily)
Day of cycle 10: Estrace (1 mg, 2 tabs three times daily)
Day of cycle 11-14: Estrace (2mg, 3 times daily orally, 1 time vaginally)
Day 15-19: Estrace (2mg, 3 times daily orally, 1 time vaginally)
Progesterone Oil 50 mg IM
Doxycycline 100 mg – 1 pill twice daily
Medrol 16mg – 1 pill daily
Day 20 forward: Estrace (2mg, 3 times daily orally, 1 time vaginally)
Progesterone Oil 50 mg IM
On day 11, I went in for E2 testing and a lining check. My lining was only at 5.1 so they asked me to add the 1 tab of Estrace vaginally. A retest of my lining on day 14 showed my lining increased to 7.6 and I started the Progesterone on day 15 as scheduled. The transfer took place on day 20.
On the day of transfer, my labs came back as Estradiol: 1326 and Progesterone: 11.83. My progesterone was low so Crinone was added to my protocol. The day of my Beta (9 days after transfer) my labs were as follows: Estradiol: 316 and Progesterone 18.
During this time, I had extremely severe side effects from the vaginal Estrace and the nurse advised me I could stop the vaginal dose since my levels were high during day of transfer. I was hesitant, but did discontinue the vaginal dose the day prior to my Beta test.
My questions for you are:
-Is this the right protocol for me given I do not have a thyroid or ovaries? I also have hypoparathyroidism and insulin resistance – all of which I take some form of medicine for.
-Should my Estradiol level dropped so dramatically just because I stopped the vaginal Estrace for 1 day?
-Is there any chance because of the menopause and hypothyroidism that I may need to get another beta later then 9 days post transfer?
At this point, we have 2 embryos left and I want to be sure we have all of the information needed. I read your post about immunologic implantation dysfunction as well as the need to prep the uterus during menopause and found that information extremely helpful.
Sorry for the length of this question. Thank you in advance for your help!
Very respectfully,
I do not believe that it is wise transfering embryos to a uterus with a lining of <8mm. The chance of viable implantation is too low to justify this in my opinion. There are many reasons why a lining can be thin. One of these could be prolonged estrogen starvation brought about by menopause. While your having been on full HRT should have prevented this, I would need to have much more information to comment authoritatively on this aspect. Other causes are mentioned below. Frankly, I prescribe parenteral (injected) estradiol valerate twice weekly for FET preparation. Also, in your case I would recommend using vaginal viagra to improve blood flow to the uterine lining.
The considerable emotional, physical and financial burden associated with infertility treatment in general and with IVF in specific, demand that factors known to affect outcome be identified and regulated prior to initiating treatment.
Just as a successful garden needs a ”good” seed properly planted in fertile soil to produce healthy plants, successful embryo implantation requires a good seed (genetically “normal” embryo) and fertile soil (receptive uterine lining) to make a healthy baby. I have long used this “Seed/Soil Relationship” analogy to help clarify the critical nature of the interaction between embryo and endometrium in the successful propagation of pregnancy..
There have in the last decade been numerous reports suggesting that certain drugs/supplements (e.g. GCSF) and endometrial receptivity testing/preparation might dramatically improve implantation. As yet, none of these have been proven to be effective. This article addresses the influence of the most relevant and important factors that are known to affect .endometrial receptivity and discusses approaches to treatment:
1. Endometrial thickness
In 1989, I first demonstrated that in both normal and "hormonally stimulated” cycles, preovulatory endometrial thickness as assessed by ultrasound examination, is partially predictive of embryo implantation (pregnancy) potential following IVF. Ideally the endometrium should measure at least 8.0mm in thickness, (but preferably >9mm).
A “poor” endometrial lining is most commonly due to: 1) inflammation of the uterine lining (endometritis) that usually occurs as a result of endometritis (inflammation of the uterine lining that can follow a septic delivery, partial retention of the placenta following delivery, abortion or miscarriage, 2) severe adenomyosis (gross invasion of the uterine muscle by endometrial glandular tissue), 3) multiple fibroid tumors of the uterine wall) 4) prenatal exposure to the synthetic hormone, diethylstilbestrol (DES) and, 5) following >3, consecutive, back to back cycles of clomiphene citrate ovulation induction.
Treatment with vaginal Sildenafil (Viagra): Hitherto, attempts to augment endometrial growth in women with poor endometrial linings by bolstering circulating estrogen blood levels (through the administration of increased doses of fertility drugs, aspirin administration and with supplementary estrogen therapy) have yielded disappointing results.
In the mid-90’s I first reported on the finding that thee vaginal administration of Viagra for several days prior to the “hCG trigger “ or progesterone administration enhances uterine blood flow and estrogen delivery to the uterine lining and so improves endometrial thickening. Then In October 2002, I reported on the administration of vaginal Viagra to 105 women with repeated IVF failure due to persistently thin endometrial linings. All of the women had experienced at least two (2) prior IVF failures attributed to intractably thin uterine linings. About 70% of these women responded to treatment with Viagra suppositories with a marked improvement in endometrial thickness and 45% of these women achieved live IVF- births following a single cycle of treatment with Viagra. Nine percent (9%) miscarried. None of the women who had failed to achieve an improvement in endometrial thickness following Viagra therapy, subsequently and who underwent embryo transfers achieved viable pregnancies.
2.Uterine Pathology:
It has long been suspected that anatomical defects of the uterus might result in infertility.
While myomas (fibroids) embedded deep in the uterine wall, are unlikely to cause infertility, an association between their presence and infertility has been observed in cases where they distort the uterine cavity, or protrude as submucous polyps through the endometrial lining. It would appear that even small submucous myomas have the potential to prejudice implantation.
Far too many infertile women found to have a partial or complete septum in the uterus are subjected to surgical excision of the septum with a promise that this will enhance subsequent implantation. This is an erroneous belief. Contrary to popular belief, the presence of a septum that partially or completely partitions the uterine cavity, while being responsible (in some cases) for late miscarriages and premature onset of labor, does NOT cause failed implantation.
It is likely that most surface lesions in the uterine cavity, whether due to an endometrial, placental or fibroid polyp (no matter how small), or intrauterine adhesions, have the potential to interfere with implantation by producing a local “inflammatory”- type response, not too dissimilar in nature from that which is caused by a foreign body such as a intrauterine contraceptive device. Unfortunately, a dye X-Ray test (hysterosalpingogram/HSG) will often miss many smaller such lesions. The only reliable methods for diagnosing even the smallest of such lesions, is through the performance of a hysterosongram (HSN),a hysteroscopy or an MRI.
Hysterosonogram (syn. Saline ultrasound): This procedure involves the trans-cervical injection of a physiological saline solution via a catheter, into the uterine cavity. The fluid distended cavity is then examined by vaginal ultrasound for any irregularities that might point to surface lesions such as polyps, fibroid tumors, scarring, or a uterine septum. If performed correctly, the HSN is highly effective in recognizing even the smallest surface lesions that protrude into the uterine cavity. It is less expensive, less traumatic, and diagnostically, equally reliable as hysteroscopy. The only disadvantage lies in the fact that if a lesion is detected, it may require the subsequent performance of hysteroscopic surgical approach to treating the problem..
Hysteroscopy: Diagnostic hysteroscopy is an office procedure that is performed under intravenous sedation, general or local anesthesia, with minimal discomfort to the patient. The procedure involves the insertion of a thin, lighted, telescope like instrument known as a hysteroscope through the vagina and cervix into the uterus in order to fully examine the uterine cavity. The uterus is first distended with carbon dioxide gas, which is passed through a sleeve adjacent to the hysteroscope. As is the case with FUS, diagnostic hysteroscopy facilitates examination of the inside of the uterus under direct vision for defects that might interfere with implantation.
We have observed that approximately 8% of candidates for IVF have intrauterine lesions that require attention prior to undergoing IVF in order to optimize the chances of a successful outcome. We strongly recommend that all patients who have such lesions undergo surgery (D&C and/or hysteroscopic resection) to correct the pathology prior to undergoing IVF. Depending on the severity and nature of the pathology, therapeutic hysteroscopy may require general anesthesia. If so, it should be performed in an outpatient surgical facility or in a conventional operating room.
3. Immunologic factors
The implantation process begins six or seven days after fertilization of the egg. At this time, specialized embryonic cells (i.e., the trophoblast), which later becomes the placenta; begin growing into the uterine lining. When the trophoblast and the uterine lining meet, they, along with Immune cells in the lining, become involved in a “cross talk” through mutual exchange of hormone-like substances called cytokines. Because of this complex immunologic interplay, the uterus is able to foster the embryo’s successful growth. Thus, from the very earliest stage of implantation the trophoblast establishes a foundation for the future nutritional, hormonal and respiratory interchange between mother and baby. In this manner, the interactive process of implantation is not only central to survival in early pregnancy but also to the quality of life after birth.
Considering its importance, it is not surprising that failure of proper function of this immunologic interaction during implantation has been implicated as a cause of recurrent miscarriage, late pregnancy fetal loss, IVF failure, and infertility. A partial list of immunologic factors that may be involved in these situations includes anti-phospholipid antibodies (APA), antithyroid antibodies (ATA), and most importantly activation of uterine natural killer cells (NKa). Presently, these immunologic markers in the blood can be only adequately measured by a handful of highly specialized reproductive immunology laboratories in the United States. I personally use Reproductive Immunology Associates in Van Nuys, CA or Reprosource in Boston, MA.
The Central role of Natural Killer cells: After ovulation and during early pregnancy, NK cells comprise more than 70% of the immune cell population of the uterine lining. NK cells produce a variety of local hormones known cytokines. Uncontrolled, excessive release of certain cytokines (i.e. TH-1 cytokines) is highly toxic to the trophoblast (“root system”) of the embryo” leading to their programmed death (apoptosis) and, subsequently to failed or compromised/dysfunctional implantation. In the following situations NK cells become activated, and start to produce an excess of TH-1 cytokines:
•Autoimmune Implantation Dysfunction: This is most commonly seen in association with a personal or family history of autoimmune diseases such as ith conditions such as Rheumatoid arthritis, hypothyroidism endometriosis and Lupus Erythematosus, Scleroderma, Dermatomyositis etc. It is also encountered in one third of women who have endometriosis (regardless of its severity), and in cases of “unexplained infertility” as well as with recurrent pregnancy loss (RPL).
•Alloimmune implantation dysfunction where the male and female partners share specific genetic (DQ-alpha and/or HLA) similarities This is commonly seen in cases of RPL and in cases of secondary infertility
Activated NK cells (NKa) can be detected through the K-562 target cell blood test and (more recently) through uterine biopsy for TH-1 cytokine activity. Treatment involves selective use of Intralipid (IL) or immunoglobulin (IVIG) therapy combined with oral steroids, initiated more 10-14 days prior to embryo transfer and in most cases of alloimmune implantation dysfunction, the transfer of a single blastocyst at a time.
Hope this helps!
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.
Geoff Sher
Hello Dr Sher, sorry but for some reason the system would not let me reply to your comment .
I’m 31y, initially took 8 months to first get pregant naturally, then mmc @12w, immediately pregnant again naturally, mmc @14w (both POC were karyotyped as normal, both times heart just stopped beating) then waited a few months after the last mc to TTC again and then no pregnancy ever again for 2 years after that despite everything else being normal and TTC actively.
No DQ alpha match but high NK cells @ 14% and low T cells in LAD (T cells where low, at 11.4 and B cells borderline normal at 51.2).
Had a failed IUI and then a failed fresh IVF transfer both w/dex and IL recently, embryos were perfect. Nobody knows why my elevated NK cells, endo is speculated but not for sure- any other autoimmune cause has been ruled out, everything done by reputable USA labs you recommend.
1) Why although my husband and I do not have a DQ alpha match, do I have a low LAD? Does this LAD test mean anything to you? I have read conflicting views. How can we have a low LAD without a DQ alpha match?
2) Should I be doing more HLA testing beyond DQ alpha?
3) Do you think IVF w/ immune protocol didn’t work the first time just because of bad luck? In theory if the only issue found after a plethora of tests was elevated NK cells and low LAD. Should I have a good chance of success w/ IVF w/ immune protocol within 3 tries or should I consider a surrogate if we want biological children?
4) do you believe that a serotonin deficiency could cause infertility? That’s a test I haven’t had done but I do have symptoms of it.
) Why although my husband and I do not have a DQ alpha match, do I have a low LAD? Does this LAD test mean anything to you? I have read conflicting views. How can we have a low LAD without a DQ alpha match?
A:The low LAD does not meen much in my opinion. It does not preclude a non-matching DQa.
2) Should I be doing more HLA testing beyond DQ alpha?
A: Probably so…but we should talk first.
3) Do you think IVF w/ immune protocol didn’t work the first time just because of bad luck? In theory if the only issue found after a plethora of tests was elevated NK cells and low LAD. Should I have a good chance of success w/ IVF w/ immune protocol within 3 tries or should I consider a surrogate if we want biological children?
A: There is so much more to discuss relating to the precise treatment, timing and implementation.
4) do you believe that a serotonin deficiency could cause infertility? That’s a test I haven’t had done but I do have symptoms of it.
A: No!
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
•Recurrent Pregnancy Loss (RPL): Why do I keep losing my Pregnancies
•IVF Failure and Implantation Dysfunction:
•The Role of 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)
•Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
•Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•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
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.
Geoff Sher