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.
I just finished my first IVF cycle. I am 22 and have no issue conceiving but am doing IVF for my husbands chromosome issue. We did a banking cycle so not transfer planned. I stimmed starting on 03/12 for 9 days and on my last ultrasound before ER I had 43 follicles. With my largest 5 being 20mm+ and all others being 17 or less. I had bloodwork on 3/20 showing LH of .38 and progesterone of 0.375. We triggered with Lupron 80 units at 8:40pm on 03/20, I had blood work on 3/21 after 12 hrs past trigger showing LH of 39.22 and progesterone 6.48. I then had retrieval at 7:40 on 03/22/17. Out of my 43 follicles we only retrieved 15 eggs, 5 were mature and 4 fertilized. My highest E2 that was seen was on 3/20 at 2161 and was not tested again. We are possibly pursuing another round but looking for reasons as to why this happened. I have no fertility issues besides miscarriage due to the chromsome issue. I have conceieved 6 times total with 1 live birth and 5 miscarriages after. I would greatly appreciate your input. Thank you.
Hi Kaitlyn,
With so many follicles there clearly was a risk of OHSS….hence the Lupron trigger. The Lupron trigger reduces the risk to the woman but in my opinion is detrimental to egg quality.
Ovarian hyperstimulation syndrome (OHSS) is a life-endangering condition that occurs following ovarian stimulation for the treatment of infertility. It occurs due to overstimulation of the ovaries with the development of numerous follicles in susceptible women. Systemic effects can be very serious and can lead to life-endangering complications. Thus every effort must be made to avoid the condition and when it does threaten, to take the necessary steps to mitigate its effects, and at the same time attempt to protect egg quality which often is adversely affected as well. Prevention starts with recognizing those women who are at the greatest risk of developing OHSS. They include:
•Those with a history of having hyperstimulated on fertility drugs in the past.
•Younger women (<25y)
•Women who have biochemical indicators that suggest they are so at risk of developing OHSS (e.g. An AMH of >5ng/ml; basal FSH of <5MIU/ml; basal LH level being significantly higher than LH; Antral follicle count of >25)
•Women who have dysfunctional or absent ovulation.
•Women diagnosed with polycystic Ovarian Syndrome (PCOS)
In such cases, it is prudent to minimize the dosage of gonadotropins administered, but alas, this often will not eliminate risk of OHSS developing anyway. Aside from the risk that OHSS places the woman at, it can also have a devastating effect on egg quality/competency. Thus, all too often, the measures taken (see below) to reduce maternal risk come at a price.
PRESENTATION AND MANAGEMENT OF OHSS:
The onset of OHSS, heralded by the presence of large numbers (>25) of developing ovarian follicles and rapidly rising plasma estradiol levels, often exceeding 3000pg/ml within 7 or 9 days of stimulation, and rapidly peaking above 6,000 pg/ml prior to hCG administration. When this happens, the risk of OHSS developing is above 80%. The fear of this escalating often leads physicians to prematurely administer hCG in an attempt to abruptly arrest the process and prevent escalation of risk to the patient. However, the premature administration of the “trigger” shot arrests egg development and adds to the problem of poor egg/embryo quality in such cases.
Symptoms and signs of OHSS include: abdominal distention due to fluid collection (ascites), fluid in the chest cavity (hydrothorax), rapid weight gain (of a pound or more per day) due to tissue fluid retention, abdominal pain, lower back ache, nausea, diarrhea, vomiting, visual disturbances such as blurred vision and spots in front of the eyes (scotomata), a rapidly declining urine output, cardiovascular collapse and failure of blood to clot which sometimes results in severe bruising (ecchymosis) and frank bleeding. These symptoms and signs may appear before pregnancy can be diagnosed. If pregnancy occurs, the condition is likely to worsen progressively over a period of 3-5 weeks whereupon it rapidly resolves spontaneously over a few days. If no pregnancy occurs, the symptoms and signs all disappear spontaneously within 10-12 days of the hCG injection.
When increasing fluid collection in the abdominal cavity (ascites) starts to compromise breathing raising the head of the bed rose slightly by placing a 4-6 inch block at the base of each head post and using a few additional pillows, will sometimes help ameliorate the problem. In cases where this does not help or symptoms become severe, all or most of the fluid can readily and safely be drained through t transvaginal sterile needle aspiration (vaginal paracentesis-performed once or sometimes twice a week) can be performed once or twice weekly . The problem will usually self corrects within 10-12 days of the hCG shot if pregnancy does not occur or, by the 8th week of pregnancy.
Urine output should be monitored daily to see if it drops below about 500ml a day (about two cups and a half). A chest X-ray, to evaluate for fluid collection in the chest and around the heart should be done weekly along with blood tests for hematocrit, BUN, electrolytes, creatinine, platelet count and fibrin split products (FSP). If indicated on the basis of a deteriorating clinical situation, hospitalization might be needed for close observation and if necessary, to provide intensive care.
In all case of OHSS, the ovaries and contain numerous theca-lutein cysts and will invariably be considerably enlarged. This is irrelevant to the final outcome, unless ovarian torsion (twisting of the ovary on its axis), an extremely rare complication occurs. The latter would usually require surgical emergency surgical intervention.
Human chorionic gonadotropin (hCG) “Fans the flames “ of OHSS. That is why the occurrence of pregnancy worsens the condition. In women who do not conceive, the clinical severity of OHSS will usually peak 7-10 days after the hCG “trigger”, plateaus for another 3-4 days and thereupon rapidly improves within the ensuing week. Thus in the absence of hCG the condition is “self-limited”. Sometimes severe symptoms due ascites make it imperative to drain the fluid transvaginally (often repeatedly). This brings immediate relief but it can be short-lived requiring repeated drainage a few days later until the condition resolves. If the woman conceives following a fresh embryo transfer, the rising hCG blood levels can exacerbate the OHSS for several weeks, but either way, it usually disappears spontaneously by the 8th to 9th harrowing week of pregnancy. This is why there is a growing tendency to avoid fresh embryo transfers, preferring to do FET’s later once the woman is out of risk. It is also the reason for a move to avoid using 10,000U of hCG for the “trigger shot” or to avoid to supplant hCG with an “agonist” trigger. But this comes at a price…see below.
OHSS ANF POOR EGG/EMBRYO QUALITY/COMPETENCY:
OHSS is also associated with e poor egg/embryo quality. This is especially so in women with high ovarian LH-induced testosterone (e.g. those with PCOS). The often present with poorly developed (“dysmorphic”) eggs, with reduced fertilization potential and yielding “poor quality embryos”. However, in the author’s opinion (which admittedly runs contrary to popular opinion), this is unlikely to be due to an intrinsic deficit in egg quality. Rather, it more likely relates to intra-ovarian hormonal changes brought about by hyperstimulation and which compromise egg development. This effect, in my opinion, can often be significantly reduced through implementation of an individualized or customized ovarian stimulation protocols that minimize exposure of the developing follicles and eggs to excessive LH-induced ovarian androgens. This can be best achieved by limiting the use of LH-containing gonadotropins such as Menopur through selective institution of “prolonged coasting” (see below). Approaches to preventing OHSS include:
1.PROLONGED COASTING (My preferred approach) : My approach is to use a long pituitary DR protocol coming off up to 2 months on the BCP, overlapped in the last 3 days with the agonist, Lupron. The BCP is intended to lower LH and thereby reduce stromal activation (hyperthecosis) in the hope of controlling ovarian androgen (predominantly, testosterone) production and release. I then stimulate with low dosage FSHr (Follistim/Gonal-F/Puregon) to which I add a smidgeon of LH/hCG (Luveris/Menopur) from the 3rd day. Then, starting on day 7 of ovarian stimulation, I perform serial blood estradiol (E2) and ultrasound follicle assessments, watching for the # of follicles and [E2]. If there are > 25 follicles, 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 (without continuing US, follicle measurements) ) daily. The [E2] will almost invariably increase for a few days. I watch the E2 rise (regardless of how high a blood concentration it reaches) and then track it coming down again. As soon as the [E2] drops below 2500pg/ml (and not before then), I administer a “trigger” shot of 10,000U hCGu (Profasi/ Novarel/Pregnyl) or hCGr (Ovidrel/Ovitrel-500mcg) and perform an egg retrieval 36 hours later. ICSI is a MUST because “coasted” eggs usually have no cumulus oophoris envelopment 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 blastocyst (up to 6 days) and are then either vitrified and preserved for subsequent transfer in later hormone replacement cycles or up to two (2) fresh blastocysts are transferred transvaginal under US guidance.. The success of this approach depends on precise timing of the initiation and 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 “Coasting” 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 obvious remedy for these adverse effects on egg and endometrial development is to employ stimulation protocols that limit ovarian over-exposure to LH and allowing the time necessary for the follicles/eggs to develop optimally, prior to administering hCG through the judicious implementation of “Prolonged coasting” (PC).
2.MULTIPLE FOLLICLE ASPIRATION: In some cases, where because of mean follicle size exceeding 16mm or when “coasting” fails to effectively lower the [E2} below 2,500pg/ml within 3 days, the number of developing follicles can effectively and drastically reduced through target transvaginal aspiration, 1-3 PRIOR to planned the hCG trigger. This will almost invariably be accompanied by a rapid and significant drop in the plasma [E2] and in the process will drastically reduce reduce the risk of OHSS occurring without significantly compromising egg/embryo quality. The drawback of this effective approach is the fact that it interjects an additional surgical intervention into an already complex and stressful situation. i
3.TRIGGERING WITH LOW DOISAGE hCG; Because of the fact that hCG augments the development of OHSS (unless preceded by “coasting”), may RE’s prefer to use a lower dosage of hCG for the “trigger. This is either done by administering 5,000U (half the traditional dosage) or by administering, a 250mcg (rather than 500mcg) of DNA recombinant form of hCGr (Ovidrel/Ovitrel. Some clinicians, when faced with a risk of OHSS developing will deliberately elect to reduce the “trigger” dosage of hCG administered (from 10,000U to 5,000U or 250mcg of recombinant hCG-Ovidrel) in the hope that by doing so the risk of critical OHSS developing will be lowered. While this might indeed be true, it is my opinion, that such a reduced dosage is usually insufficient to optimize the efficiency of egg meiosis, e3specially when there are so many follicles present. While the use of a reduced “trigger” dosage of hCG does indeed reduce the risk and occurrence of OHSS-related life-endangering complications, the price to be paid is reduced egg quality/”competency”.
4.“TRIGGERING” WITH A GnRH AGONIST (E.G. “LUPRON/BUSERELIN): More recently, an increasing number of RE’s prefer to trigger meiosis by way of an agonist (Lupron/Buserelin/Superfact () “trigger” rather than through the use of hCG. The idea is to mimic what happens in natural cycles to promote egg maturation (meiosis) and ovulation, namely to have the agonist cause a “surge” in the release of body’s own pituitary LH to trigger egg meiosis (maturation) .But the amount of LH released in by the pituitary gland is often insufficient to optimize meiotic egg maturation and thus, while this approach also lowers the risk of OHSS it again comes at the expense of egg quality/competency.
A word of caution: I do not use long term administration of antagonists (Ganirelix/Cetrotide/Orgalutron), such as with the agonist/antagonist conversion protocol (A/ACP) in high responders whom are at risk of developing OHSS prolonged in-cycle administration of because it can interferes with the E2 assay (often causing the value to be understated), and serial measurement of E2 is a vital part of monitoring patients undergoing “coasting”
Geoff Sher
PH: 800-780-7437
My husband got his semen analysis results back and our doctor told us there is basically no chance we will conceive without IVF. He also said that Clomid, supplements (like Fertilaid) and lifestyle changes would not be able to make a dent in the motility numbers, which from what I understand, are the main issues. I’m not sure what to make of the viscosity result. Looking at his results, do you agree? I thought we may be able to bring his motility number up, which would put us in a better place for conception, either naturally or via IUI. I’m just wondering if our chances are basically hopeless, or if we have a chance of bringing his numbers up.
Here are his results:
Liquefaction: 60
Viscosity: 3 (1,2) *abnormal*
Color: White
Volume: 1.8mL
pH: 8.3
Count 1: 55
Count 2: 58 M/ml
Concentration: 57
Total Sperm Count (TSC): 103M
Motility: 14.00%
Progression 2(3)
Total Motile Sperm (TMS): 14 M
Agglutination: 0
Round Cells: 0
Leukocytes: 0
Morphology: 4%
Stain Acceptable: YES
Major Defect: bent/coiled tails
GII: 66%
GIII 30%
Thank you for any advice or thoughts you can give.
These sperm parameters virtually mandate IVF ICSI. But that would only be the case if your husband has an elevated blood FSH level.
I would be happy to discuss your case in detail.
In 1 to 2 percent of cases, male infertility is the result of problems in an area of the brain (the hypothalamus) and or in a small gland situated just below the base of the brain known as the pituitary gland. The pituitary gland produces two gonadotropin hormones: The first is FSH that controls production of sperm (spermatogenesis) by Sertoli cells in the testes and the second, luteinizing hormone (LH) that controls male hormone production (predominantly testosterone) by testicular Leydig cells. In the woman, these same gonadotropin hormones control ovarian production of estrogen, progesterone and male hormones such as androstenedione and testosterone. A sustained reduction in FSH production, is capable of resulting in reduced sperm count, motility and morphology while a sustained reduction in LH can result in low blood testosterone levels with associated Low-Testosterone Syndrome which includes but is not limited to mood changes, reduced energy level and libido, redistribution of muscle mass, breast development (gynecomastia) and progressive demasculinization. If judiciously and selectively administered to qualifying patients, the use of oral treatment with clomiphene or the parenteral administration of gonadotropins for 3-6 months (sometimes a longer duration of therapy is needed) will often successfully reverse the male infertility in such cases.
While a woman’s ovulatory cycle usually lasts about 28 days, in the man, there exists a cyclical production of sperm over a period of about100 days. This is why any assessment of the effect of treatment administered to the man to improve sperm production requires waiting for a time period of at least 100 days.
There are two basic approaches to the hormonal enhancement of sperm production:
1.Clomiphene Citrate: Clomiphene citrate is a hormone which, through its central action on the brain, stimulates the pituitary gland to produce natural FSH in large amounts. The FSH, in turn, as mentioned above, stimulates spermatogenesis. The treatment is very simple, and involves the administration of 1/2 tablet (25 mg.) of clomiphene citrate every alternate 1-2 days perform a baseline semen analysis, FSH, LH, and male hormone measurements immediately, and then to serially repeat all of these tests intermittently throughout the treatment with Clomiphene. The final assessment of response can only be made approximately 90 days after initiating therapy. This administration of clomiphene is essentially harmless to the man. He may experience some minor side effects such as spots in front of the eyes, dryness of the mouth, headaches, slight changes in mood, and rarely, hot flashes. These side effects are all reversible upon discontinuation of therapy. This having been said, it is best to confine treatment to a period of 6 months, but certainly not for longer than 12 months. Thus in cases where a significant improvement occurs in sperm parameters, it is often advisable to collect the treated man’s sperm and cryobank it for future use, thereby mitigating the need for prolonged or repeated bouts of treatment. Since clomiphene increases both FSH and LH production by the pituitary, the increase in LH ill reciprocally increase testicular testosterone output and thereby reverse symptoms associated with low testosterone syndrome.
2.Letrozole: Like clomiphene, Letrozole is also an oral agent that causes FSH and LH to be released. The mechanism of action by which it does so is similar to clomiphene. The FSH then promotes Sertoli cell activity and spermatogenesis. Thus Letrozole can supplant clomiphene for promoting spermatogenesis. The duration of treatment is the same as for clomiphene.
3.Gonadotropin Therapy: In cases where clomiphene/letrozole therapy fails or in certain situations where such treatment does not stimulate the pituitary gland, FSH can be administered directly by injection, alone, or combined with hCG. hCG functions similar to LH to further enhance the production of male hormones in cases where demasculinization is associated with reduced sperm production. These hormones must be administered 3 times per week, for a period of about 90 days, whereupon hormonal and sperm assessments are repeated to determine the effect. Such treatment is relatively harmless and side effects are minor and reversible upon discontinuation of therapy.
4.Treatment of Other Endocrine Conditions: Thyroid hormone is given in cases of hypothyroidism. Diabetes is treated with hypoglycemic agents such as Metformin or insulin, and elevated blood prolactin levels can be lowered with bromocriptine (Paroled/Dostinex) which will often effect an improvement in sperm quality.
5.Testosterone Therapy: Some doctors prescribe testosterone preparations to men with compromised sperm production and/or function. Such treatment is to be decried since it will invariably make matters worse. The reason for this is that testosterone suppresses pituitary FSH production and thus reduces sperm production and quality. It is, of course, not practical or safe to administer potent medications such as clomiphene, FSH, LH, or hCG for an indefinite period of time. Thus, in cases where the patient responds favorably to such treatment it is advisable to collect and cryostore a number of masturbation specimens for future use, so that there will always be relatively good quality sperm on hand when the fertility treatment is discontinued
Adjunct treatments:
•Antioxidants and Vitamins: There is evidence (although anecdotal) that for males with unexplained infertility, dietary supplementation with commercially available products such as ProXeed or Proceptin (that contain a combination of non-invasive vitamins and vitamin-like agents, such as L-carnitine, acetyl carnitine, Co-enzyme Q, vitamins C and E, and fructose, citric acid, selenium and zinc), might improve sperm quality.
•Treatment of Varicocele (a collection of dilated veins in the scrotum): There are many men who have varicoceles but do not have a fertility problem. Sometimes however, sperm quality can be compromised and when that happens, occluding dilated blood vessels either by surgically tying off one or both spermatic veins (varicocelectomy), or by interventional radiological obliteration of the spermatic vein(s) can be curative
•Intrauterine insemination (IUI might be of benefit in the treatment of “mild” male infertility, there is no conclusive evidence that it will improve pregnancy potential in cases of moderate or severe male infertility (regardless of whether the woman receives fertility drugs or not).
•Intracytoplasmic Sperm Injection (ICSI):ICSI is a procedure where fertilization is achieved through the direct injection of a single sperm into the substance of each mature egg. Until the introduction ICSI in the mid-90s, IVF was relatively unsuccessful in achieving pregnancies in cases of male infertility. ICSI changed all that. Now, IVF/ICSI is the treatment of choice for refractory, moderate or severe male infertility.
•Testicular Sperm Aspiration (TESA): The TESA process involves the introduction of a thin needle directly into the testicle(s), to aspirate sperm or directly into sperm bearing tissue and then taking hair-thin biopsy specimens for processing. Sperm so obtained is treated in the laboratory whereupon each egg is injected with a single sperm using ICSI. TESA is a procedure performed when there are no sperm in the ejaculate (azoospermia) or when the man is unable to ejaculate at all. In most cases it is done when the sperm ducts are blocked or absent but the testicles are still fully capable of producing sperm. It can also be used in non-obstructive cases of male infertility where the failure to ejaculate live sperm is due to partial testicular failure. In cases of obstructive azoospermia the fertilization rate is about 50-60% and the anticipated birth rate is similar to that achieved in the absence of male factor and no different to that seen in conventional IVF conducted on in women of comparable age. When it comes to non-obstructive azoospermia the results are much poorer. TESA is a simple, relatively low-cost, safe, and virtually pain-free procedure. Most men can literally take off a few hours for the procedure and return to normal activity immediately thereafter. In about 80% of cases, TESA procedures are done in cases of men who had a previous vasectomy. The introduction of TESA has in fact made surgical reconnection of sperm ducts (i.e. vasectomy reversal) obsolete. This is especially so because TESA is far more successful in initiating a pregnancy than is surgical reversal and because it achieves the desired end point result while leaving the vasectomy intact for future contraception.
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
•Male Factor Infertility
•Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in Favor
•Antisperm Antibodies, Infertility and the Role of IVF with Intracytoplasmic Sperm Injection (ICSI)
•Testicular Sperm Extraction (TESE) and Testicular Sperm Aspiration (TESA): Surgical Approaches for Accessing Sperm from men who have no sperm in their ejaculates (Azoospermia)
•Varicocele and Male Infertility: When and how should it be treated?
•The Sperm Chromatin Structure Assay (SCSA): A Measure of the Potential of Sperm to Help Propagate a Viable Pregnancy
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
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.
I have my first FET coming up next month. My doctor strongly suggested that I transfer two embryos since I have stage 1 endometriosis. I am 32 and I have five PGS normal embryos (graded 4BB,3BB,3BA,3B-C,3B-B-) I understand my doctor truly wants to help me to get pregnant. However, the idea of having twins terrifies us. We prefer singleton. So our question is, is it comparable to do five single transfers compared to two transfers with two embryos?
I transfer up to 2 embryos at a time. However, if you are concerned about twins, you can transfer one at a time . The cumulative outcome will be the same, except it might take longer with single embryo transfers.
Geoff sher
I am 44 yrs old. Attempting FET with donated embryo. My lining hasn’t responded and only increases to 4. I feel that my clinic isn’t being aggressive. Currently, 5 units of Lupron and estradiol valrate (.2 ml then moving to .4) aren’t there other treatments to increase lining. My FS said that if my lining doesn’t respond this time I will need to look at a surrogate. This will only be our second cycle. Not been able to get to transfer since lining doesn’t respond. I am running out of time due to my advanced age. I would be happy to pay for a consultation with you if you think there is something different I can do. I started seeing a Chinese medicine Dr for acupuncture and added a baby aspirin. I appreciate your insight.
Hi Nicole!
I suggest we talk. I would need much more information to respond authoritatively.
Geoff Sher
Hello Dr.Sher
I have had one successful donor egg FET, followed by two failed. I have two 5day blasts left and it’s my last shot for a sibling for my daughter. I have severe endometriosis and have followed the same protocol each time. Estrace, medrol and antibiotic 5 days prior to transfer, progesterone, lovenox, and baby asiprin. I have not had immune testing due to the cost. I only have enough savings left to perform the actual last FET.
Any suggestions on changes to protocol I can suggest to my clinic? Any help is much appreciated.
More than half of women who have endometriosis harbor antiphospholipid antibodies (APA) that can compromise development of the embryo’s root system (trophoblast). In addition and far more serious, is the fact that in about one third of cases endometriosis, regardless of its severity is associated with NKa and cytotoxic uterine lymphocytes (CTL) which can seriously jeopardize implantation. This immunologic implantation dysfunction (IID) is diagnosed by testing the woman’s blood for APA, for NKa (using the K-562 target cell test or by endometrial biopsy for cytokine activity) and, for CTL (by a blood immunophenotype). Activated NK cells 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 rejection of the embryo even before the pregnancy is diagnosed and sometimes, in a chemical pregnancy or 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”.
Women who harbor APA’s often experience improved IVF birth rates when heparinoids (Clexane/Lovenox) are administered from the onset of ovarian stimulation with gonadotropins until the 10th week of pregnancy. NKa is treated with a combination of 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 NKa.
The therapeutic effect of IL/steroid therapy is likely due to an ability to suppress pro-inflammatory cellular (Type-1) cytokines such as interferon gamma and TNF-alpha. IL/steroids down-regulates NKa within 2-3 weeks of treatment the vast majority of women experiencing immunologic implantation dysfunction. In this regard IL 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.
The toxic pelvic environment caused by endometriosis, profoundly reduces natural fertilization potential. As a result normally ovulating infertile women with endometriosis and patent Fallopian tubes are much less likely to conceive naturally, or by using fertility agents alone (with or without intrauterine (IUI) insemination. The only effective way to bypass this adverse pelvic environment is through IVF. I am not suggesting here that all women who have endometriosis require IVF! Rather, I am saying that in cases where the condition is further compromised by an IID associated with NKa and/or for older women(over 35y) who have diminished ovarian reserve (DOR) where time is of the essence, it is my opinion that IVF is the treatment of choice.
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 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)
•Intralipid (IL) Administration in IVF: It’s Composition; How it Works; Administration; Side-effects; Reactions and Precautions
•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
•Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year
•A personalized, stepwise approach to IVF
•Endometriosis and Infertily
•Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
•Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
•Treating Ovarian Endometriomas with Sclerotherapy.
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
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.