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Our Medical Directors are outstanding physicians that you will find to be very personable and compassionate, who take care to ensure that you have the most cutting-edge fertility treatments at your disposal. This is your outlet to ask your questions to the doctors.

  • Dear Patients,

    I created this forum to welcome any questions you have on the topic of infertility, IVF, conception, testing, evaluation, or any related topics. I do my best to answer all questions in less than 24 hours. I know your question is important and, in many cases, I will answer within just a few hours. Thank you for taking the time to trust me with your concern.

    – Geoffrey Sher, MD

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Morphology

Name: Lisa M

Hello Dr. Sher,

My husband’s semen analysis came back as 250 million motile sperm but only 4% morphology. Is such low morphology an issue in your professional experience? Does this mean that its basically 10 million sperm that are ok – that seems very low. Can this change/be improved?

Author

Answer:

This quite acceptable. I do not see it as a significant issue at all.when it comes to IVF/ICSI,

 

Geoff Sher

Infertility for 14 years

Name: Shama S

Hi, we have been facing recurring losses, dq alpha complete match, nk cells causing allergic reactions at the time of implantation. Is there anything you can suggest for us to be pregnant. I’m 40 and my husband 39, we don’t have family and in this situation looks like our chances are fading.
Please advise

Author

Answer:

When it comes to reproduction, humans are the poorest performers of all mammals. In fact we are so inefficient that up to 75% of fertilized eggs do not produce live births, and up to 30% of pregnancies end up being lost within 10 weeks of conception (in the first trimester). RPL is defined as two (2) or more failed pregnancies. Less than 5% of women will experience two (2) consecutive miscarriages, and only 1% experience three or more.

Pregnancy loss can be classified by the stage of pregnancy when the loss occurs:

  • Early pregnancy loss (first trimester)
  • Late pregnancy loss (after the first trimester)
  • Occult “hidden” and not clinically recognized, (chemical) pregnancy loss (occurs prior to ultrasound confirmation of pregnancy)
  • Early pregnancy losses usually occur sporadically (are not repetitive).

 

In more than 70% of cases the loss is due to embryo aneuploidy (where there are more or less than the normal quota of 46 chromosomes). Conversely, repeated losses (RPL), with isolated exceptions where the cause is structural (e.g., unbalanced translocations), are seldom attributable to numerical chromosomal abnormalities (aneuploidy). In fact, the vast majority of cases of RPL are attributable to non-chromosomal causes such as anatomical uterine abnormalities or Immunologic Implantation Dysfunction (IID).

Since most sporadic early pregnancy losses are induced by chromosomal factors and thus are non-repetitive, having had a single miscarriage the likelihood of a second one occurring is no greater than average. However, once having had two losses the chance of a third one occurring is double (35-40%) and after having had three losses the chance of a fourth miscarriage increases to about 60%. The reason for this is that the more miscarriages a woman has, the greater is the likelihood of this being due to a non-chromosomal (repetitive) cause such as IID. It follows that if numerical chromosomal analysis (karyotyping) of embryonic/fetal products derived from a miscarriage tests karyotypically normal, then by a process of elimination, there would be a strong likelihood of a miscarriage repeating in subsequent pregnancies and one would not have to wait for the disaster to recur before taking action. This is precisely why we strongly advocate that all miscarriage specimens be karyotyped.

There is however one caveat to be taken into consideration. That is that the laboratory performing the karyotyping might unwittingly be testing the mother’s cells rather than that of the conceptus. That is why it is not possible to confidently exclude aneuploidy in cases where karyotyping of products suggests a “chromosomally normal” (euploid) female.

Late pregnancy losses (occurring after completion of the 1st trimester/12th week) occur far less frequently (1%) than early pregnancy losses. They are most commonly due to anatomical abnormalities of the uterus and/or cervix. Weakness of the neck of the cervix rendering it able to act as an effective valve that retains the pregnancy (i.e., cervical incompetence) is in fact one of the commonest causes of late pregnancy loss. So also are developmental (congenital) abnormalities of the uterus (e.g., a uterine septum) and uterine fibroid tumors. In some cases intrauterine growth retardation, premature separation of the placenta (placental abruption), premature rupture of the membranes and premature labor can also causes of late pregnancy loss.

Much progress has been made in understanding the mechanisms involved in RPL. There are two broad categories:

  1. Problems involving the uterine environment in which a normal embryo is prohibited from properly implanting and developing. Possible causes include:
  • Inadequate thickening of the uterine lining
  • Irregularity in the contour of the uterine cavity (polyps, fibroid tumors in the uterine wall, intra-uterine scarring and adenomyosis)
  • Hormonal imbalances (progesterone deficiency or luteal phase defects). This most commonly results in occult RPL.
  • Deficient blood flow to the uterine lining (thin uterine lining).
  • Immunologic implantation dysfunction (IID). A major cause of RPL. Plays a role in 75% of cases where chromosomally normal preimplantation embryos fail to implan
  • Interference of blood supply to the developing conceptus can occur due to a hereditary clotting disorder known as Thrombophili

 

  1. Genetic and/or numerical chromosomal abnormalities(aneuploidy) of the embryo are far away the commonest overall causes of miscarriages. But this only applies to sporadic pregnancy losses (which comprises the majority of all miscarriages. However, recurrent, (consecutive) pregnancy losses are much more likely due to implantation dysfunction than to embryo-related issues, where implantation dysfunction (usually anatomical or immunologic) factors usually underly the problem.
  2. Genetic or Structural chromosomal abnormalities (which only occur in about 1% of cases) can also cause RPL. This is referred to as an unbalanced translocation and they result from part of one chromosome detaching and then fusing with another chromosome. Additionally, genetic defects (unrelated to chromosomal abnormalities) can also affect embryo quality and pregnancy outcome. Damaged sperm DNA can sometimes be diagnosed using the SCSA (see before) which primarily measures the sperm DNA fragmentation index (DFI).

 

IMMUNOLOGIC IMPLANTATION DYSFUNCTIO-IID (see before)

Autoimmune IID: Here an immunologic reaction is produced by the individual to his/her body’s own cellular components. The most common antibodies that form in such situations are APA and antithyroid antibodies

Alloimmune IID, i.e., where there is an immunologic reaction to antigens derived from another member of the same species (i.e. the woman’s immune system reacts to the paternal antigens in the sperm (see above) .

*It is important to recognize that alloimmune (rather than autoimmune) IID is more commonly associated with RPL.

Autoimmune IID is often genetically transmitted. Thus, it should not be surprising to learn that it is more likely to exist in women who have a family (or personal) history of primary autoimmune diseases such as lupus erythematosus (LE), scleroderma or autoimmune hypothyroidism (Hashimoto’s disease), autoimmune hyperthyroidism (Grave’s disease), rheumatoid arthritis, etc. Reactionary (secondary) autoimmunity can occur in conjunction with any medical condition associated with widespread tissue damage. One such gynecologic condition is endometriosis. Since autoimmune IID is usually associated with activated NK and T-cells from the outset, it usually results in such very early destruction of the embryo’s root system that the patient does not even recognize that she is pregnant. Accordingly, the condition usually presents as “unexplained infertility” or “unexplained IVF failure” rather than as a miscarriage.

Alloimmune IID, on the other hand, usually starts off presenting as unexplained miscarriages (often manifesting as RPL). Over time as NK/T cell activation builds and eventually becomes permanently established the patient often goes from RPL to “infertility” due to failed implantation. RPL is more commonly the consequence of alloimmune rather than autoimmune implantation dysfunction.

However, regardless, of whether miscarriage is due to autoimmune or alloimmune implantation dysfunction the final blow to the pregnancy is the result of activated NK cells and CTL in the uterine lining that damage the developing embryo’s “root system” (trophoblast) so that it can no longer sustain the growing conceptus. This having been said, it is important to note that autoimmune IID is readily amenable to reversal through timely, appropriately administered, selective immunotherapy, and alloimmune IID is not. It is much more difficult to treat successfully, even with the use of immunotherapy. In fact, in some cases the only solution will be to revert to selective immunotherapy plus using donor sperm (provided there is no “match” between the donor’s DQ alpha/HLA profile and that of the female recipient) or alternatively to resort to gestational surrogacy.

DIAGNOSING THE CAUSE OF RPL

In the past, women who miscarried were not evaluated thoroughly until they had lost several pregnancies in a row. This was because sporadic miscarriages are most commonly the result of embryo numerical chromosomal irregularities (aneuploidy) and thus not treatable. However, a consecutive series of miscarriages points to a repetitive cause that is non-chromosomal and is potentially remediable. Since RPL is most commonly due to a uterine pathology or immunologic causes that are potentially treatable, it follows that early chromosomal evaluation of products of conception could point to a potentially treatable situation. Thus, we strongly recommend that such testing be done in most cases of miscarriage. Doing so will avoid a great deal of unnecessary heartache for many patients.

Establishing the correct diagnosis is the first step toward determining effective treatment for couples with RPL. It results from a problem within the pregnancy itself or within the uterine environment where the pregnancy implants and grows. Diagnostic tests useful in identifying individuals at greater risk for a problem within the pregnancy itself include:

  • Karyotyping (chromosome analysis) both prospective parents
  • Assessment of the karyotype of products of conception derived from previous miscarriage specimens
  • Ultrasound examination of the uterine cavity after sterile water is injected or sonohysterogram, fluid ultrasound, etc.
  • Hysterosalpingogram (dye X-ray test)
  • Hysteroscopic evaluation of the uterine cavity
  • Full hormonal evaluation (estrogen, progesterone, adrenal steroid hormones, thyroid hormones, FSH/LH, )
  • Immunologic testing to include:
    • Antiphospholipid antibody (APA) panel
    • Antinuclear antibody (ANA) panel
    • Antithyroid antibody panel (i.e., antithyroglobulin and antimicrosomal antibodies)
    • Reproductive immunophenotype
    • Natural killer cell activity (NKa) assay (i.e., K562 target cell test)
    • Alloimmune (DQ alpha/HLA) testing of both the male and female partners

 

TREATMENT OF RPL

Treatment for Anatomic Abnormalities of the Uterus: This involves restoration through removal of local lesions such as fibroids, scar tissue, and endometrial polyps or timely insertion of a cervical cerclage (a stitch placed around the neck of the weakened cervix) or the excision of a uterine septum when indicated.

Treatment of Thin Uterine Lining: A thin uterine lining has been shown to correlate with compromised pregnancy outcome. Often this will be associated with reduced blood flow to the endometrium.  Such decreased blood flow to the uterus can be improved through treatment with sildenafil and possibly aspirin.

Sildenafil (Viagra) Therapy (see above). Viagra has been used successfully to increase uterine blood flow. To date, we have seen significant improvement of the thickness of the uterine lining in about 70% of women treated. Successful pregnancy resulted in almost half of those women who responded to the Viagra. It should be borne in mind that most of these women had previously experienced repeated IVF failures.

Use of Aspirin: This is an anti-prostaglandin that improves blood flow to the endometrium. It is administered at a dosage of 81 mg orally, daily from the beginning of the cycle until ovulation.

Treating Immunologic Implantation Dysfunction with Selective Immunotherapy: Modalities such as IL/IVIg, heparinoids (Lovenox/Clexane), and corticosteroids can be used in select cases depending on autoimmune or alloimmune dysfunction.

The Use of IVF in the Treatment of RPL. In the following circumstances, IVF is the preferred option:

  • When in addition to a history of RPL, another standard indication for IVF (e.g., tubal factor, endometriosis, and male factor infertility) is superimposed.
  • In cases where selective immunotherapy is needed to treat an immunologic implantation dysfunction.

The reason for IVF being a preferred approach in such cases is that in order to be effective, the immunotherapy needs to be initiated well before spontaneous or induced ovulation. Given the fact that in the absence of IVF the anticipated birthrate per cycle of COS with or without IUI is at best about 15%, it follows that short of IVF, to have even a reasonable chance of a live birth, most women with immunologic causes of RPL would need to undergo immunotherapy repeatedly, over consecutive cycles. Conversely, with IVF, the chance of a successful outcome in a single cycle of treatment is several times greater and, because of the attenuated and concentrated time period required for treatment, IVF is far safer and thus represents a more practicable alternative

Since embryo aneuploidy is a common cause of miscarriage, the use of PGS/PGT-A can provide a valuable diagnostic and therapeutic advantage in cases of RPL. PGD requires IVF to provide access to embryos for testing.

There are a few cases of intractable alloimmune dysfunction due to “complete DQ alpha matching where Gestational Surrogacy or use of Donor  Sperm could represent the only viable recourse, other than abandoning treatment altogether and/or resorting to adoption. Other non-immunologic factors such as an intractably thin uterine lining or severe uterine pathology might also warrant that last resort consideration be given to gestational surrogacy.

The good news is that if a couple with RPL is open to all of the diagnostic and treatment options referred to above, a live birthrate of 70%–80% is ultimately achievable.

I strongly recommend that you visit www.SherIVF.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
  • Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
  • Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
  • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
  • 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
  • IVF: How Many Attempts should be considered before Stopping?
  • “Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
  • 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
  • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
  • 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

 

 

______________________________________________________

ADDENDUM: PLEASE READ!!

INTRODUCING SHER FERTILITY SOLUTIONS (SFS)

Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.

 

If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or,  enroll online on then home-page of my website (www.SherIVF.com). 

 

PLEASE SPREAD THE WORD ABOUT SFS!

 

Geoff Sher

Test

Name: Medjine E

What test would you consider if someone had 4 miscarriages before 6 weeks
I have done all the basic test
Immune conditions
Chromosome
Ovarian reserve
My husband sperm
Protein
Std
Everything is normal
No polyps
I do have fibroids not in the endo cavity
Biggest is size of a lemon.
No sure what else to test for
Do you have a recurrent pregnancy testing panel
No the usual test but deeper ones .
Thank you

Author

Answer:

When it comes to reproduction, humans are the poorest performers of all mammals. In fact we are so inefficient that up to 75% of fertilized eggs do not produce live births, and up to 30% of pregnancies end up being lost within 10 weeks of conception (in the first trimester). RPL is defined as two (2) or more failed pregnancies. Less than 5% of women will experience two (2) consecutive miscarriages, and only 1% experience three or more.

Pregnancy loss can be classified by the stage of pregnancy when the loss occurs:

  • Early pregnancy loss (first trimester)
  • Late pregnancy loss (after the first trimester)
  • Occult “hidden” and not clinically recognized, (chemical) pregnancy loss (occurs prior to ultrasound confirmation of pregnancy)
  • Early pregnancy losses usually occur sporadically (are not repetitive).

In more than 70% of cases the loss is due to embryo aneuploidy (where there are more or less than the normal quota of 46 chromosomes). Conversely, repeated losses (RPL), with isolated exceptions where the cause is structural (e.g., unbalanced translocations), are seldom attributable to numerical chromosomal abnormalities (aneuploidy). In fact, the vast majority of cases of RPL are attributable to non-chromosomal causes such as anatomical uterine abnormalities or Immunologic Implantation Dysfunction (IID).

Since most sporadic early pregnancy losses are induced by chromosomal factors and thus are non-repetitive, having had a single miscarriage the likelihood of a second one occurring is no greater than average. However, once having had two losses the chance of a third one occurring is double (35-40%) and after having had three losses the chance of a fourth miscarriage increases to about 60%. The reason for this is that the more miscarriages a woman has, the greater is the likelihood of this being due to a non-chromosomal (repetitive) cause such as IID. It follows that if numerical chromosomal analysis (karyotyping) of embryonic/fetal products derived from a miscarriage tests karyotypically normal, then by a process of elimination, there would be a strong likelihood of a miscarriage repeating in subsequent pregnancies and one would not have to wait for the disaster to recur before taking action. This is precisely why we strongly advocate that all miscarriage specimens be karyotyped.

There is however one caveat to be taken into consideration. That is that the laboratory performing the karyotyping might unwittingly be testing the mother’s cells rather than that of the conceptus. That is why it is not possible to confidently exclude aneuploidy in cases where karyotyping of products suggests a “chromosomally normal” (euploid) female.

Late pregnancy losses (occurring after completion of the 1st trimester/12th week) occur far less frequently (1%) than early pregnancy losses. They are most commonly due to anatomical abnormalities of the uterus and/or cervix. Weakness of the neck of the cervix rendering it able to act as an effective valve that retains the pregnancy (i.e., cervical incompetence) is in fact one of the commonest causes of late pregnancy loss. So also are developmental (congenital) abnormalities of the uterus (e.g., a uterine septum) and uterine fibroid tumors. In some cases intrauterine growth retardation, premature separation of the placenta (placental abruption), premature rupture of the membranes and premature labor can also causes of late pregnancy loss.

Much progress has been made in understanding the mechanisms involved in RPL. There are two broad categories:

  1. Problems involving the uterine environment in which a normal embryo is prohibited from properly implanting and developing. Possible causes include:
  • Inadequate thickening of the uterine lining
  • Irregularity in the contour of the uterine cavity (polyps, fibroid tumors in the uterine wall, intra-uterine scarring and adenomyosis)
  • Hormonal imbalances (progesterone deficiency or luteal phase defects). This most commonly results in occult RPL.
  • Deficient blood flow to the uterine lining (thin uterine lining).
  • Immunologic implantation dysfunction (IID). A major cause of RPL. Plays a role in 75% of cases where chromosomally normal preimplantation embryos fail to implan
  • Interference of blood supply to the developing conceptus can occur due to a hereditary clotting disorder known as Thrombophili
  1. Genetic and/or structural chromosomal abnormality of the embryo.Genetic abnormalities are rare causes of Structural chromosomal abnormalities are slightly more common but are also occur infrequently (1%). These are referred to as unbalanced translocation and they result from part of one chromosome detaching and then fusing with another chromosome. Additionally, a number of studies suggest the existence of paternal (sperm derived) effect on human embryo quality and pregnancy outcome that are not reflected as a chromosomal abnormality. Damaged sperm DNA can have a negative impact on fetal development and present clinically as occult or early clinical miscarriage. The Sperm Chromatin Structure Assay (SCSA) which measures the same endpoints are newer and possibly improved methods for evaluating.

 

IMMUNOLOGIC IMPLANTATION DYSFUNCTION

Autoimmune IID: Here an immunologic reaction is produced by the individual to his/her body’s own cellular components. The most common antibodies that form in such situations are APA and antithyroid antibodies (ATA).

But it is only when specialized immune cells in the uterine lining, known as cytotoxic lymphocytes (CTL) and natural killer (NK) cells, become activated and start to release an excessive/disproportionate amount of TH-1 cytokines that attack the root system of the embryo, that implantation potential is jeopardized. Diagnosis of such activation requires highly specialized blood test for cytokine activity that can only be performed by a handful of reproductive immunology reference laboratories in the United States.

Alloimmune IID, i.e., where antibodies are formed against antigens derived from another member of the same species, is believed to be a relatively common immunologic cause of recurrent pregnancy loss.

Autoimmune IID is often genetically transmitted. Thus it should not be surprising to learn that it is more likely to exist in women who have a family (or personal) history of primary autoimmune diseases such as lupus erythematosus (LE), scleroderma or autoimmune hypothyroidism (Hashimoto’s disease), autoimmune hyperthyroidism (Grave’s disease), rheumatoid arthritis, etc. Reactionary (secondary) autoimmunity can occur in conjunction with any medical condition associated with widespread tissue damage. One such gynecologic condition is endometriosis. Since autoimmune IID is usually associated with activated NK and T-cells from the outset, it usually results in such very early destruction of the embryo’s root system that the patient does not even recognize that she is pregnant. Accordingly the condition usually presents as “unexplained infertility” or “unexplained IVF failure” rather than as a miscarriage.


Alloimmune IID,
on the other hand, usually starts off presenting as unexplained miscarriages (often manifesting as RPL). Over time as NK/T cell activation builds and eventually becomes permanently established the patient often goes from RPL to “infertility” due to failed implantation. RPL is more commonly the consequence of alloimmune rather than autoimmune implantation dysfunction.

However, regardless, of whether miscarriage is due to autoimmune or alloimmune implantation dysfunction the final blow to the pregnancy is the result of activated NK cells and CTL in the uterine lining that damage the developing embryo’s “root system” (trophoblast) so that it can no longer sustain the growing conceptus. This having been said, it is important to note that autoimmune IID is readily amenable to reversal through timely, appropriately administered, selective immunotherapy, and alloimmune IID is not. It is much more difficult to treat successfully, even with the use of immunotherapy. In fact, in some cases the only solution will be to revert to selective immunotherapy plus using donor sperm (provided there is no “match” between the donor’s DQa profile and that of the female recipient) or alternatively to resort to gestational surrogacy.

DIAGNOSING THE CAUSE OF RPL

In the past, women who miscarried were not evaluated thoroughly until they had lost several pregnancies in a row. This was because sporadic miscarriages are most commonly the result of embryo numerical chromosomal irregularities (aneuploidy) and thus not treatable. However, a consecutive series of miscarriages points to a repetitive cause that is non-chromosomal and is potentially remediable. Since RPL is most commonly due to a uterine pathology or immunologic causes that are potentially treatable, it follows that early chromosomal evaluation of products of conception could point to a potentially treatable situation. Thus I strongly recommend that such testing be done in most cases of miscarriage. Doing so will avoid a great deal of unnecessary heartache for many patients.

Establishing the correct diagnosis is the first step toward determining effective treatment for couples with RPL. It results from a problem within the pregnancy itself or within the uterine environment where the pregnancy implants and grows. Diagnostic tests useful in identifying individuals at greater risk for a problem within the pregnancy itself include:

  • Karyotyping (chromosome analysis) both prospective parents
  • Assessment of the karyotype of products of conception derived from previous miscarriage specimens
  • Ultrasound examination of the uterine cavity after sterile water is injected or sonohysterogram, fluid ultrasound, etc.)
  • Hysterosalpingogram (dye X-ray test)
  • Hysteroscopic evaluation of the uterine cavity
  • Full hormonal evaluation (estrogen, progesterone, adrenal steroid hormones, thyroid hormones, FSH/LH, )
  • Immunologic testing to include:
    1. Antiphospholipid antibody (APA) panel
    2. Antinuclear antibody (ANA) panel
    3. Antithyroid antibody panel (i.e., antithyroglobulin and antimicrosomal antibodies)
    4. Reproductive immunophenotype
    5. Natural killer cell activity (NKa) assay (i.e., K562 target cell test)
    6. Alloimmune testing of both the male and female partners

TREATMENT OF RPL

Treatment for Anatomic Abnormalities of the Uterus: This involves restoration through removal of local lesions such as fibroids, scar tissue, and endometrial polyps or timely insertion of a cervical cerclage (a stitch placed around the neck of the weakened cervix) or the excision of a uterine septum when indicated.

Treatment of Thin Uterine Lining: A thin uterine lining has been shown to correlate with compromised pregnancy outcome. Often this will be associated with reduced blood flow to the endometrium.  Such decreased blood flow to the uterus can be improved through treatment with sildenafil and possibly aspirin.

Sildenafil (Viagra) Therapy. Viagra has been used successfully to increase uterine blood flow. However, to be effective it must be administered starting as soon as the period stops up until the day of ovulation  and  it must  be administered  vaginally (not  orally). Viagra in the form of vaginal suppositories given in the dosage of 25 mg four times a day has been shown to increase uterine blood flow as well as thickness of the uterine lining. To date, we have seen significant improvement of the thickness of the uterine lining in about 70% of women treated. Successful pregnancy resulted in 42% of women who responded to the Viagra. It should be remembered that most of these women had previously experienced repeated IVF failures.


Use of Aspirin: This is an anti-prostaglandin that improves blood flow to the endometrium. It is administered at a dosage of 81 mg orally, daily from the beginning of the cycle until ovulation.

Treating Immunologic Implantation Dysfunction with Selective Immunotherapy: Modalities such as IL/IVIg, heparinoids (Lovenox/Clexane), and corticosteroids (dexamethasone, prednisone, prednisolone) can be used in select cases depending on autoimmune or alloimmune dysfunction.

The Use of IVF in the Treatment of RPL

In the following circumstances, IVF is the preferred option:

  1. When in addition to a history of RPL, another standard indication for IVF (e.g., tubal factor, endometriosis, and male factor infertility) is superimposed.
  2. In cases where selective immunotherapy is needed to treat an immunologic implantation dysfunction.

The reason for IVF being a preferred approach in such cases is that in order to be effective, the immunotherapy needs to be initiated well before spontaneous or induced ovulation. Given the fact that the anticipated birthrate per cycle of COS with or without IUI is at best about 15%, it follows that short of IVF, to have even a reasonable chance of a live birth, most women with immunologic causes of RPL would need to undergo immunotherapy repeatedly, over consecutive cycles. Conversely, with IVF, the chance of a successful outcome in a single cycle of treatment is several times greater and, because of the attenuated and concentrated time period required for treatment, IVF is far safer and thus represents a more practicable alternative

Since embryo aneuploidy is a common cause of miscarriage, the use of preimplantation genetic diagnosis (PGD), with tests such as CGH, can provide a valuable diagnostic and therapeutic advantage in cases of RPL. PGD requires IVF to provide access to embryos for testing.

There are a few cases of intractable alloimmune dysfunction due to absolute DQ alpha matching where Gestational Surrogacy or use of donor  sperm could represent the only viable recourse, other than abandoning treatment altogether and/or resorting to adoption. Other non-immunologic factors such as an intractably thin uterine lining or severe uterine pathology might also warrant that last resort consideration be given to gestational surrogacy.

The good news is that if a couple with RPL is open to all of the diagnostic and treatment options referred to above, a live birthrate of 70%–80% is ultimately achievable.

 

I strongly recommend that you visit www.SherIVF.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.

 

  • A Fresh Look at the Indications for IVF
  • 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.
  • Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
  • IVF and the use of Supplementary Human Growth Hormone (HGH) : Is it Worth Trying and who needs it?
  • 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
  • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
  • IVF: Approach to Selecting the Best Embryos for Transfer to the Uterus.
  • Fresh versus Frozen Embryo Transfers (FET) Enhance IVF Outcome
  • Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
  • Genetically Testing Embryos for IVF
  • Staggered IVF
  • Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
  • 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
  • Endometrial Receptivity Array (ERA): Is There an actual “There, There”?
  • IVF Failure and Implantation Dysfunction:
  • Diagnosing and Treating Immunologic Implantation Dysfunction (IID)
  • 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?
  • The Role of Nutritional Supplements in Preparing for IVF
  • Defining and Addressing an Abnormal Luteal Phase

ADDENDUM: PLEASE READ!!

INTRODUCING SHER FERTILITY SOLUTIONS (SFS)

Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.

 

If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or,  enroll online on then home-page of my website (www.SherIVF.com). 

 

PLEASE SPREAD THE WORD ABOUT SFS!

 

Geoff Sher

 

 

Estrogen levels

Name: Indo I

Hello doctor Sher,

Thanks for taking the time to answer our questions!!
Is it true that vaginal estrogen route result in higher serum estradiol unlike transdermal and intramuscular? Does the estradiol level a day to pio matter ? Can it be too high? What is your cut off?
Thank you doctor!

Author

Answer:

My preference is subcutaneous estradiol twice weekly injections.. My second preference is trans dermal. Vaginal estradiol is not evenly absorbed and oral estradiol is in my opinion the poorest choice because absorption through the GIT passes via the liver to the systemic circulation and this can alter the estradiol. Ideal blood levels of E2 is 500-1000pg/ml.

 

Good luck!

 

 

Sperm retrieval

Name: Kristen S

Hi,

My partner and I have had a friend that was successful at your clinic (Michelle and Steve Christie) and we are exploring a child together but do not have the funds to have it not be successful going back and forth with Canadian clinics like the Christies did.

My partner has two previous children from a marriage that are 10 and 13 (girls) and has had a vasectomy. We would like to have a child together but he is very concerned about the pain and healing of a vasectomy reversal as well as the success of it.

He has a sex preference of a boy (which my friends had selected at your clinic) I dont, but he does. I have a little concern about my fertility ( I am 37 and he is 39) and I am not on birth control and have not used oral contraceptives for years as there was not need. I was told I may have a but of andrometreosis (as I sometimes have pain after intense orgasms) but other than that I am of normal health.

What are our best options, costs etc. ?

Thank you.

Kristen

Author

Answer:

Here is some information on : Previous vasectomy and IVF; Gender selection and Endometriosis and infertility.

 

We should talk,. call Patti Converse (702-533-2691) and set up an online consultation with me.

 

1. GENDER SELECTION

 

Couples have for centuries sought to influence the gender of their offspring. More than seven centuries ago the ancient Chinese developed a birth calendar said to be able to predict gender on the basis of when conception occurred. Later, the ancient Greeks suggested that by lying on her right side during intercourse, a woman could improve the likelihood of having a male child. And 300 years ago, the French suggested that placing a ligature around the right testicle would improve the chance of having a male child.

More recently in the U.S., methods such as timing intercourse, assuming different positions during sex, and (relatively recently) employing rapid sperm centrifugation in an attempt to separate male chromosome-bearing sperm from female sperm prior to artificial insemination were proposed. The fact is that none of these (as well as many other) such anecdotal assertions have been shown to have any real validity.

Currently, in spite of several well described medical approaches, the indisputable fact has emerged that it is only by way of IVF that reliable sex selection can be achieved. This allows for embryos to be screened for gender through preimplantation genetic diagnosis prior to transferring the embryo(s) of the desired gender to the uterus.

Nevertheless, it is an inescapable reality that the very idea of medical sex selection challenges moral and ethical beliefs at their very foundation. Many hold that the growing popularity of gender selection solely for the convenience of altering a family’s gender balance represents an unwanted example of how assisted reproductive technology is subject to abuse…and thus it should be outlawed. They also see it as an example of a disturbing trend towards “designer babies” where genetic engineering could be used to manipulate the intellect, body configuration, build, height, and the talents of future offspring. This assertion is commonly followed by the tantalizing question as to where all this would end and whether we as a society “would really want to live in such a world.”

 There is, however, one clear exception to the apparent across-the-board opposition to sex selection that is well worthy of mention. This applies in cases where sex selection is used to avoid the occurrence of a serious medical disorder that selectively affects one gender or the other (e.g., Hemophilia, a life threatening bleeding disorder that selectively affects male offspring).

 EVALUATING CURRENTLY USED METHODS FOR SEX SELECTION

 

A. SPERM GRADIENT METHODOLOGY (discredited because of a lack of reliability)

This is one of the simplest methods that still (unfortunately) remains in widespread use. Here sperm is rapidly spun down (centrifuged) in the hope of separating the male sperm (those with Y-chromosomes) from the female sperm (those with X-chromosomes). It relies on the assumption that the X chromosome makes sperm heavier, allowing for separation of male from female chromosome-bearing sperm. Though this method is often touted as a low cost method for sex selection, the truth is that it simply does not work!

 B. FLOW CYTOMETRIC TESTING BY THE MICROSORT METHOD (discredited because of a lack of reliability)

This method which is now somewhat discredited by the FDA  employedthe use of a fluorescent dye that adheres to genetic material within the sperm. It was based on the premise that because X-bearing sperm contain more genetic material, these sperm were supposed to pick up more dye than Y-bearing sperm. Thereupon, X and Y bearing sperm are then separated into two groups and used for intrauterine insemination (IUI) or IVF. This method was touted as yielding a 60% to 70% accuracy rate with IUI. This has not been adequately confirmed and in my personal experience its reliability in the IVF setting has been questionable to say the least. The Microsort technique is to my knowledge not presently being offered in the United States.

C. IVF

Preimplantation Genetic Diagnosis (PGD) involves the removal of one or more cells from an embryo, for chromosomal or genetic analysis.  The most widely used and he most reliable PGD method for gender selection is fluorescence in-situ-hybridization (FISH). However, this technique does not identify all 23 pairs of chromosomes in the embryo’s cells. At best it can well identify 12. Thus, while FISH provides an excellent method for gender selection and for identification of structural chromosomal aberrations, it is not a reliable method for diagnosing embryo aneuploidy (“competency”).  Conversely, another PGD method, next generation gene sequencing (NGS) which does assess all the embryo’s chromosomes can be used for both detecting all the embryo’s chromosomes and thus can determine embryo “competency” reliably. It also reliably identifies gender. However, while NGS is very bit as reliable as FISH for gender selection, FISH can be done in fresh cycles (i.e. the ET is done in the same cycle as that in which the ER is done), while NGS requires time for testing that requires Staggered IVF (St-IVF) in which the embryos are biopsied on day 3 or day 5-6 (post-fertilization) and  the blastocysts are ultrarapidly frozen (vitrified) and allowed to proceed in culture to blastocysts whereupon they are ultra-rapidly frozen (vitrified) and are then held for transfer in a subsequent cycle. 

Upon completion of FISH, which takes about 24-36 hours, the couple can select which embryo(s) they will transfer to the uterus. If pregnancy results, there is almost a 100% chance it will result in the desired gender. If NGS is used, the degree of accuracy in diagnosing gender, is as reliable as is FISH but in addition, NGS provides information on the entire karyotype (all 23 pairs of chromosomes) which is extremely beneficial because it assesses embryo “competency, while FISH does not.

PERSONAL OPINION:

Sex selection done purely for  family balancing is somewhat  controversial, raising concern that if  widely accessible and freely available, such practice could distort the natural sex ratio, leading to a population gender imbalance. However, for this to happen, there would have to be a significant population preference for sex selection. In reality, the contrary seems to apply, since studies conducted in western societies discount these concerns. In fact, the relatively high cost of IVF with the added cost of gender selection in the United States makes it unlikely that the demand would ever become large enough to impact overall population gender balance. In addition, several studies done in Western countries have shown that the majority of people do not seem to be concerned about the gender of their offspring, and that with a few notable exceptions, gender preference does not appear to be slanted in the direction of either male or female. Thus, from a practical standpoint, such concerns are overstated.

Given that in the United States most couples do not care about the gender of their offspring, and only a minority are interested in selecting the sex of their children there is currently  no risk that IVF sex-selection will impact the population gender balance. Thus, in  my opinion by and large,  freedom of choice should prevail and a service for sex selection should be freely available

 So, in my personal practice, I absolutely do offer gender selection in the following circumstances.

  • Medical Indications for Gender Selection:
    • For cases associated with
      • sex-linked genetic disorders or,
      • serious genetic disorders that are more likely to occur in one gender or the other.
    • Non-Medical Family balancing
      • For couples who have at least one child of the opposite gender to that which they choose for their IVF embryo transfer and,
      • For those women who do not have any children at all but prefer to have a child of one or the other gender.

 

2.PRIOR VASECTOMY

Men with no sperm in their ejaculates (azoospermia) whether due to non-obstructive or obstructive (usually post-vasectomy) causes, can have their sperm accessed surgically and still propagate pregnancies. There are 2 methods by which this can be achieved. : 1) TESE (testicular sperm extraction), where a biopsy of the testis is done or, 2) TESA (testicular sperm aspiration), which involves introducing a needle into  the testis and aspirating fluid and tissue. Both methods can be conducted under local anesthesia and both will provide sperm-containing tissue and fluid for immediate processing and fertilization (using ICSI) or cryostorage for future use. However, the question is: Which method yields better results. An Israeli study performed on men with non-obstructive azoospermia, conducted about a decade ago, compared the results of TESE with those from TESA in the same patients and found TESE to be the preferred approach.

TSE/TESA is the preferred method for accessing sperm in men with azoospermia. By far the commonest indication for using this approach is post-vasectomy obstructive azoospermia where the use of TESE/TESA is far more successful and uncomplicated than is the alternative of having the man undergo surgical reversal. In fact, TESE/TESA yields a comparable IVF birth rate as for controls where normal sperm derived through masturbation is used. The approach is simple, relatively low-cost, and safe. In most cases, it is relatively painless and has a low complication rate. Moreover, in post-vasectomy men, it avoids the need for riskier and painful surgery designed to reconnect sperm ducts (vasa deferentia) while enabling the man to retain his chosen method of contraception after having propagated another pregnancy. In addition surgical vasectomy often fails to successfully reestablished duct patency and even when successful it often results in the subsequent reocclusion of the sperm ducts due to scar tissue formation. Moreover, in a large percentage of cases where vasectomy reversal was performed > 5 years after the vasectomy antisperm antibodies develop and this will almost always preclude subsequent natural conception even in cases where surgery had reestablished duct patency.

 While in some cases of non-obstructive azoospermia, TESA/TESE will yield sperm capable of achieving fertilization through ICSI and also subsequent viable pregnancies, success rates are low. However, in such cases, this approach yields the only possibility of the male partner participating genetically in propagating pregnancy.

 

3. ENDOMETRIOSIS AND INFERTILITY

When women with infertility due to endometriosis seek treatment, they are all too often advised to first try ovarian stimulation (ovulation Induction) with intrauterine insemination (IUI) ………as if to say that this would be just as likely to result in a baby as would in vitro fertilization (IVF). Nothing could be further from reality It is time to set the record straight. And hence this communication!

Bear in mind that the cost of treatment comprises both financial and emotional components and that it is the cost of having a baby rather than cost of a procedure. Then consider the fact that regardless of her age or the severity of the condition, women with infertility due to endometriosis are several fold more likely to have a baby per treatment cycle of IVF than with IUI. It follows that there is a distinct advantage in doing IVF first, rather than as a last resort.

So then, why is it that ovulation induction with or without IUI is routinely offered proposed preferentially to women with mild to moderately severe endometriosis? Could it in part be due to the fact that most practicing doctors do not provide IVF services but are indeed remunerated for ovarian stimulation and IUI services and are thus economically incentivized to offer IUI as a first line approach? Or is because of the often erroneous belief that the use of fertility drugs will in all cases induce the release (ovulation) of multiple eggs at a time and thereby increase the chance of a pregnancy. The truth however is that while normally ovulating women (the majority of women who have mild to moderately severe endometriosis) respond to ovarian stimulation with fertility drugs by forming multiple follicles, they rarely ovulate > 1 (or at most 2) egg at a time. This is because such women usually only develop a single dominant follicle which upon ovulating leaves the others intact. This is the reason why normally ovulating women who undergo ovulation induction usually will not experience improved pregnancy potential, nor will they have a marked increase in multiple pregnancies. Conversely, non-ovulating women (as well as those with dysfunctional ovulation) who undergo ovulation induction, almost always develop multiple large follicles that tend to ovulate in unison. This increases the potential to conceive al    let me take a stab at explaining why IVF is more successful than IUI or surgical correction in the treatment of endometriosis-related infertility:

  1. The toxic pelvic factor: Endometriosis is a condition where the lining of the uterus (the endometrium) grows outside the uterus. While this process begins early in the reproductive life of a woman, with notable exceptions, it only becomes manifest in the 2ndhalf of her reproductive life. After some time, these deposits bleed and when the blood absorbs it leaves a visible pigment that can be identified upon surgical exposure of the pelvis. Such endometriotic deposits invariably produce and release toxins” into the pelvic secretions that coat the surface of the membrane (the peritoneum) that envelops all abdominal and pelvic organs, including the uterus, tubes and ovaries. These toxins are referred to as “the peritoneal factor”. Following ovulation, the egg(s) must pass from the ovary (ies), through these toxic secretions to reach the sperm lying in wait in the outer part the fallopian tube (s) tube(s) where, the sperm lie in waiting. In the process of going from the ovary(ies) to the Fallopian tube(s) these eggs become exposed to the “peritoneal toxins” which alter s the envelopment of the egg (i.e. zona pellucida) making it much less receptive to being fertilized by sperm. As a consequence, if they are chromosomally normal such eggs are rendered much less likely to be successfully fertilized. Since almost all women with endometriosis have this problem, it is not difficult to understand why they are far less likely to conceive following ovulation (whether natural or induced through ovulation induction). This “toxic peritoneal factor impacts on eggs that are ovulated whether spontaneously (as in natural cycles) or following the use of fertility drugs and serves to explain why the chance of pregnancy is so significantly reduced in normally ovulating women with endometriosis.
  2. The Immunologic Factor: About one third of women who have endometriosis will also have an immunologic implantation dysfunction (IID) linked to activation of uterine natural killer cells (NKa).  This will require selective immunotherapy with Intralipid infusions, and/or heparinoids (e.g. Clexane/Lovenox) that is much more effectively implemented in combination with IVF.
  3. Surgical treatment of mild to moderate endometriosis does not usually improve pregnancy potential:. The reason is that endometriosis can be considered to be a “work in progress”. New lesions are constantly developing. So it is that for every endometriotic seen there are usually many non-pigmented deposits that are in the process of evolving but are not yet visible to the naked eye and such evolving (non-visible) lesions can also release the same “toxins that compromise fertilization. Accordingly, even after surgical removal of all visible lesions the invisible ones continue to release “toxins” and retain the ability to compromise natural fertilization. It also explains why surgery to remove endometriotic deposits in women with mild to moderate endometriosis usually will fail to significantly improve pregnancy generating potential. In contrast, IVF, by removing eggs from the ovaries prior to ovulation, fertilizing these outside of the body and then transferring the resulting embryo(s) to the uterus, bypasses the toxic pelvic environment and is therefore is the treatment of choice in cases of endometriosis-related infertility.
  4. Ovarian Endometriomas: Women, who have advanced endometriosis, often have endometriotic ovarian cysts, known as endometriomas. These cysts contain decomposed menstrual blood that looks like melted chocolate…hence the name “chocolate cysts”. These space occupying lesions can activate ovarian connective tissue (stroma or theca) resulting in an overproduction of male hormones (especially testosterone). An excess of ovarian testosterone can severely compromise follicle and egg development in the affected ovary. Thus there are two reasons for treating endometriomas. The first is to alleviate symptoms and the second is to optimize egg and embryo quality. Conventional treatment of endometriomas involves surgical drainage of the cyst contents with subsequent removal of the cyst wall (usually by laparoscopy), increasing the risk of surgical complications. We recently reported on a new, effective and safe outpatient approach to treating endometriomas in women planning to undergo IVF. We termed the treatment ovarian Sclerotherapy.  The process involves; needle aspiration of the “chocolate colored liquid content of the endometriotic cyst, followed by the injection of 5% tetracycline hydrochloride into the cyst cavity. Such treatment will, more than 75% of the time result in disappearance of the lesion within 6-8 weeks. Ovarian sclerotherapy can be performed under local anesthesia or under conscious sedation. It is a safe and effective alternative to surgery for definitive treatment of recurrent ovarian endometriomas in a select group of patients planning to undergo IVF

  I am not suggesting that all women with infertility-related endometriosis should automatically resort to IVF. Quite to the contrary…. In spite of having reduced fertility potential, many women with mild to moderate endometriosis can and do go on to conceive on their own (without treatment). It is just that the chance of this happening is so is much lower than normal.

 

IN SUMMARY: For young ovulating women (< 35 years of age ) with endometriosis, who have normal reproductive anatomy and have fertile male partners, expectant treatment is often preferable to IUI or IVF. However, for older women, women who (regardless of their age) have any additional factor (e.g. pelvic adhesions, ovarian endometriomas, male infertility, IID or diminished ovarian reserve-DOR) IVF should be the primary treatment of choice.

I strongly recommend that you visit 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 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
  • How Many Embryos should be transferred: A Critical Decision in IVF?
  • 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.
  • Deciding Between Intrauterine Insemination (IUI) and In Vitro Fertilization (IVF).
  • Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s &
  • Induction of Ovulation with Clomiphene Citrate: Mode of Action, Indications, Benefits, Limitations and Contraindications for its use
  • Clomiphene Induction of Ovulation: Its Use and Misuse!

 

 

 

______________________________________________________

ADDENDUM: PLEASE READ!!

INTRODUCING SHER FERTILITY SOLUTIONS (SFS)

Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.

 

If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or,  enroll online on then home-page of my website (www.SherIVF.com). 

 

PLEASE SPREAD THE WORD ABOUT SFS!

 

Geoff Sher

 

 

Ovarian sclerotherapy

Name: sophia G

Hi, I came across your page because I have been dealing with a 5 cm endometrioma and have been looking at different options. I found your article about ovarian sclerotherapy and was wondering if you know where this procedure can be done? I have been trying to look for a place but I’m having trouble!

Author

Answer:

I really do not know who offers this or where you could find out!  You will have to inquire around.

Geoff Sher

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