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.

19,771 Comments

  1. Dr Sher, for my last cycle I took OCP for 6 weeks, overlapping agonist for 2 days and continued on with 10IU Lupron. 9 days later my estrogen blood test was 10 pg/ml! You say estrogen has to be below 70 pg/ml, but mine was 10! Is that too low??

    • It is low, but that probably does not matter!

      Geoff Sher

  2. Hi Dr Sher, I’ve been on OCP for 3 weeks and my RE overlapped Lupron for 5 days before making me stop the OCP. Any idea how long before I get a period?

    • Usually within 5-7 days on Lupron…unless you have an ovarian cyst. Get a blood estradiol measurement and a pelvic ultrasound examination done to see .

      Geoff Sher

  3. Dr Sher, do you provide a service where you review and monitor a patient’s cycle who is located overseas for a fee? If so, how do I go about setting this up?

    • Unfortunately not…both for ethical and personal reasons I do not offer this service. Sorry!

      However, I do treat many patients from afar. In fact, about 70% of my patients are from out out of state and out of country.

      out of state and out of country. I typically schedule my IVF cycles 6 months in advance, for specific dates. The cycles last about two weeks, and I do limit the number of cases in each batch in order to make sure I can personally monitor the cycles, and dedicate special attention to each patient. Given my very busy schedule, it is always advisable for you to schedule possible treatment for the earliest convenient date. Both, the financial and clinical coordinators will help you work out logistic issues, and assist you in finalizing the ideal dates for your treatment. We require that all patients make a modest non-refundable deposit to secure the date. This deposit is deducted from the cost of the cycle of treatment.
      We recognize that regardless of the nature of your reproductive issue both partners have a stake in the process and its outcome. Accordingly, both would usually wish to be present throughout most of the 7-14 days of management. From a practical standpoint however, this might not always be possible (or even necessary). In such cases, we would be able to provide the male partner at least 3 days’ advance notice of when he would be to be present in Las Vegas for one day. In cases where frozen embryo transfers (FETs) are being done, the male partner will not even be required to be present in Las Vegas. Moreover, selectively when sperm is required from a fertile male partner, we can even arrange for frozen semen sample to be shipped timely for the fertilization process.
      There is rarely a need for women undergoing controlled ovarian stimulation (COS) for IVF to begin serial monitoring by ultrasound and/or blood testing prior to the 7th day of stimulation. As such, the female partner is not needed to arrive in Las Vegas prior to the 7th day of fertility drug administration, All preliminary preparatory testing can thus be done at your home setting by your primary GP or OB/GYN, including (if needed) bloodwork and a baseline ultrasound examination with the start of the menstrual period that launches the cycle of ovarian stimulation. After treatment is completed, you can return home. We will follow up with you and/or your partner by phone or Skype communication. We will also interact as needed with your primary care OB/GYN to supervise post-treatment and early-pregnancy management.
      While this process might at first glance seem somewhat complex, in reality with a dedicated Clinical Coordinator assisting you, we have developed over the past 30 years of providing infertility treatment to more than 70,000 patients a very easy, convenient, safe and effective method for treating local patients as well as those traveling to Las Vegas from out of state or from abroad.

      I invite you to 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.
      •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)
      •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) versus “Fresh” ET: How to Make the Decision
      •Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
      •PGS in IVF: Are Some Chromosomally abnormal
      •IVF Failure and Implantation Dysfunction:
      •The Role of Immunologic Implantation Dysfunction
      •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
      •IVF Egg Donation: A Comprehensive Overview
      •IVF-Gestational Surrogacy: An Overview

      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.
      •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)
      •Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
      •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 with Compromised Ovarian Response to Ovarian Stimulation: A Personal Approach.
      •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?
      •Blastocyst Embryo Transfers Should be the Standard of Care in IVF
      •Why did my IVF Fail
      •IVF Should Supplant Tubal Fertility Surgery.
      •IVF: How Many Attempts should be considered before Stopping?
      •“Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
      •Secondary Infertility: Addressing the Root Causes
      •Recurrent Pregnancy Loss (RPL): Why do I keep losing my Pregnancies
      •Multiple Pregnancies Carry Serious Risks: How Many Embryos Should we Transfer at One Time?
      •Cervical Incompetence (CI): A common Cause of Late Miscarriage, Premature Birth and 2nd Trimester Recurrent Pregnancy Loss (RPL)
      •Hereditary Clotting Defects (Thrombophilia)
      •Blastocyst Embryo Transfers done 5-6 Days Following Fertilization are Fast Replacing Earlier day 2-3 Transfers of Cleaved Embryos.
      •Embryo Transfer: The “Holy Grail 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
      •Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of 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.
      •IVF: Selecting the Best Quality Embryos to Transfer
      •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 outcome: How Does Advancing Age and Diminished Ovarian Reserve (DOR) Affect Egg/Embryo “Competency” and How Should the Problem be addressed.
      •IVF: The first Choice for Infertile Women 40 to 43 Years of Age!
      •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)
      •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!
      •Endometrial Thickness, Uterine Pathology and Immunologic Factors
      •Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
      •A Thin Uterine Lining: Vaginal Viagra is Often the Answer (update)
      •Cervical Ureaplasma Urealyticum Infection: How can it Affect IUI/IVF Outcome?
      •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
      •How Many Embryos should be transferred: A Critical Decision in IVF.
      •Avoiding High Order Multiple Pregnancies (Triplets or Greater) with IVF
      •The Role of Nutritional Supplements in Preparing for IVF
      •The Basic Infertility Work-Up
      •Defining and Addressing an Abnormal Luteal Phase
      •FDA Ratings for Prescription Drug Use During Pregnancy
      •Functional” Ovarian Cysts and IVF
      •Progesterone-Estrogen Hormonal supplementation in IVF: How Does it Work and what is its Value?
      •Potential Downsides of DHEA Supplementation in Preparing for IVF: Why take the Risk?
      •Measuring and Interpreting Blood hCG to Assess Pregnancy Viability Following ART Treatments.
      •Male Factor Infertility
      •Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in Favor
      •Hormonal Treatment of Male Infertility
      •Hormonal Treatment of Male Infertility
      •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
      •IVF for Women Who Have Previously Conceived (Secondary Infertility).
      •Uterine Fibroids and Fertility
      •Pelvic Inflammatory Disease (PID), Tubal Damage and Hydrosalpinx: Preparing for IVF
      •The Role of IVF in Cases of Tubal Damage
      •Case Study: Treating Hydrosalpinx by Surgical Removal (Salpingectomy) as a Prelude to IVF
      •Raised Blood Prolactin Levels (Hyperprolactinemia) in Women Undergoing Infertility Treatment
      •The Role of IVF in the Management of Infertility Caused by Pelvic Inflammatory Disease (PID).
      •Endometriosis and Infertily
      •Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF
      •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
      •Early -Endometriosis-related Infertility: Ovulation Induction (with or without Intrauterine Insemination) and Reproductive Surgery Versus IVF
      •Treating Ovarian Endometriomas with Sclerotherapy.
      •Effect of Advanced Endometriosis with Endometriotic cysts (Endometriomas) on IVF Outcome & Treatment Options.
      •Adenomyosis-Related Infertility: A Therapeutic Challenge!
      •Cytomegalovirus (CMV) Infection: What are the Implications when it comes to Pregnancy
      •Implications of “Empty Follicle Syndrome and “Premature Luteinization”
      •Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
      •Fertility Preservation (FP) Through Freezing/Banking Human Eggs
      •Preserving Fertility in Female cancer patients
      •Selective Banking of Genetically Tested Donor Eggs:
      •IVF Egg Donation: A Comprehensive Overview
      •IVF-Gestational Surrogacy: An Overview
      •Taking A Fresh Look at Ovarian Hyperstimulation Syndrome (OHSS), its Presentation, Prevention and Management
      •Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting”
      •IVF Outcome in Patients with Polycystic Ovarian Syndrome (PCOS): Minimizing the Risk of Severe Ovarian Hyperstimulation Syndrome (OHSS) and optimizing Egg/Embryo Quality.
      •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?
      •Deciding Between Intrauterine Insemination (IUI) and In Vitro Fertilization (IVF).
      •Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & Con’s!IUI-Reflecting upon its Use and Misuse: Time for a Serious “Reality Check
      •” Mini-IVF” : Is it a Blessing or Curse?
      •Micro-IVF: Often Preferable to Ovarian Stimulation with or Without IUI
      •The Role of Gender Selection in IVF.
      •Infertility Caused by Pelvic Tuberculosis: An Easily Missed Diagnosis
      •IVF Success Rate expressed as Viable Pregnancy Rate per Embryo Transferred (PRPE): A Proposed New Paradigm for Improved Verifiable Reporting of IVF statistics
      •Evaluation of IVF Outcome does not readily lend itself to “Evidence-Based Scientific Scrutiny”
      •IVF for Same Sex Couples
      •Confronting the Financial and Emotional Costs Associated with Doing IVF
      •Hydatidiform Molar Pregnancy: Recognition, Treatment and How IVF with PGS can Help Prevent it from occurring.
      •Molar Pregnancy: What is it? How should it be treated?
      •Ectopic (Tubal) Pregnancy and IVF
      •IVF Pregnancy with a “Vanishing Twin”
      •First trimester Bleeding: How serious is it?
      •Fragile X Syndrome: Which IVF Candidates Should be tested and How Should Results be interpreted?
      •IVF: There is a Price to pay ….
      •IVF: How do you decide how many embryos to transfer?
      •Having Realistic Expectations Regarding IVF Outcome: When is it Time to Stop or Change Course?
      •The Issue of Left-over Frozen Embryos: A moral/ethical Dilemma!
      •Autism, Infertility and IVF: What is the Relationship?
      •Being Overweight with a high BMI: How Does it Affect Fertility and IVF Outcome?
      •Advancing Age of the Woman and IVF: How Old is too old?
      •Cytomegalovirus (CMV) Infection: What are the Implications when it comes to Pregnancy?
      •IVF pregnancies: Why They Carry a Greater Risk?
      •Is there a link between the use of Fertility Drugs and of Ovarian Cancer?
      •Are Injectable Fertility Drugs Safe?
      •CASE REPORT: A woman in her Early 40’s who has Diminished Ovarian Reserve Requiring IVF with Embryo Banking and PGS.
      •Induction of Ovulation With Clomiphene Citrate: Mode of Action, Indications, Benefits, Limitations and Contraindications for its ue
      •Clomiphene Induction of Ovulation: Its Use and Misuse!
      •My Retirement in the Year Ahead: A letter of Thanks From me to You!

      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.

      Geoff Sher

  4. Hi Dr Sher, thanks for always being available to answer everyone’s questions! You’re a wonderful and caring RE!!

    Can I ask, you talk about introducing some form of LH (luveris or menopur) from day 2 of stims onwards on a long cycle. What would happen if a form of LH wasn’t introduced? Would it stunt follicle growth?

    • Mellie,

      That would depend on the type of protocol being used.

      Thanks for your kind sentiments…I appreciate it.

      Geoff Sher

  5. Hi Dr. Sher,
    I am a 37 year old female now diagnosed with endometriosis. 1 year ago my AMH was 3.5. After laproscopic surgery 1 year ago to remove adhesions from the endometriosis I currently have a 2 x 1.3 x 1.9cm endometrioma on my right ovary and a 1.3 x 1.1 x 1.2 on my left. My AMH is now 0.5. I am very concerned about how much it has dropped. We have a consult with a reproductive endocrinologist soon and before this have been just working with my obgyn. We live in an area where the nearest RE is 4-5 hours away. The endometrioma appeared after 1 round of clomid in March. I then took 2 months off and then did 3 months of femara. The first month with iui and the last two months I ovulated so early, day 9 then 7 that they thought I was wrong. My question is, based on this info do you think I would have any success with IVF with my own eggs?

    Thank you,

    Jessica

    • 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 or Laparotomy 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 (“chocolate” cysts). About 15 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 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.
      5.The role of IVF: 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.

      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.

      Geoff Sher