Varicocele and Male Infertility

What is a varicocele? The testicles are housed in the scrotum, a skin-covered sac that houses the two testicles as well as blood vessels that deliver blood to these glands, nerves, and lymphatics. An abnormality of the plexus of veins (the pampiniform plexus) that carry blood away from the testicles can result in their distention, proliferation and enlargement within the scrotum. We refer to this as the development of varicosities similar to varicose veins that can occur in the leg.

How does a varicocele cause male infertility? The increased scrotal blood flow often raises the temperature in the scrotum by 1-2 degrees. This in turn sometimes results in decreased sperm production and functionality as well as testicular shrinkage (atrophy), leading to male infertility. However, the existence of a varicocele by no means inevitably compromises sperm production and functionality.

Who develops a varicocele and how common is the condition? About 15 percent of men have varicoceles. These generally form during puberty and are more commonly found on the left side than on the right side of the scrotum. Rarely are both sides of the scrotum affected. Most males are diagnosed between the ages of 15 and 25 years of age. There are no established risk factors for developing a varicocele, and the exact cause is unclear.

How does a varicocele present and how can it be diagnosed? The presence of a varicocele does not invariably mean that it is the cause of male infertility. In fact many males who have varicoceles do not have any fertility problem at all. Also, in many cases the detection of a varicocele is an “incidental finding and is not the cause of coexisting male infertility. You see, contrary to popular belief, varicoceles seldom reduce sperm count. In fact, in many cases of low-sperm count, treatment of the varicocele rarely results an improvement in sperm production. It is important to recognize that the majority of men who have varicoceles, do not have evidence of sperm dysfunction.

Most varicoceles are not even symptomatic. In fact, most are never detected. Those that are symptomatic present with scrotal enlargement, scrotal and/or lower abdominal pain, and infertility. The condition is often diagnosed by physical examination where, to the touch, a varicocele feels like a “bag of worms”. However ultrasound examination of the scrotum offers a more definitive diagnostic capability.

When a varicocele causes sperm dysfunction, this most commonly manifests with a normal or even raised sperm count. However, there is usually markedly reduced motility and sperm progression, but a high percentage of sperm are found to be “immature” Collectively this is referred to as a “stress pattern”. In many such cases the Sperm Chromatin Structure Assay (SCSA) will show an increase in the DNA Fragmentation Index (DFI). These are the cases where treatment of the varicocele will often improve sperm function, along with improving the likelihood of a viable pregnancy occurring naturally or following IVF with intracytoplasmic sperm injection (ICSI).

Treatment: There are two approaches to treating varicoceles:

  • Traditional treatment of a varicocele is through ligation (under general anesthesia) of one or both spermatic veins that carry blood from the pampiniform venous plexus (“varicocelectomy”). While surgery is in most cases curative, post-surgical recurrence is not uncommon.
  • Another approach is interventional radiological obliteration of one or both the spermatic veins. This approach involves passing a balloon catheter via a groin blood vessel, under radiological view, into the spermatic vein and inflating the balloon in that position. This causes the spermatic vein to permanently occlude. Sometime later, the catheter is withdrawn and the vein remains occluded causing the varicocele to collapse and the pampiniform plexus to shrink or disappear. This radiological approach is often more effective, far less costly, less traumatic and less likely to, result in a recurrence than is spermatic vein, surgical ligation. It is also conducted under local anesthesia and as an out-patient procedure. In my opinion this approach has become the preferred method for treating varicoceles.  

Regardless of whether surgical or interventional radiological treatment is contemplated, it is in my opinion, advisable for the patient to take a male fertility blend that is rich in antioxidants (I recommend a product called Proceptin, which requires online purchase). This will sometimes result in an improvement in the DFI within 3-6 months.. It should be taken for at least 12 weeks whereupon the SCSA should be repeated.

It is important to bear in mind that both surgical and radiological treatment will only improve sperm function in about 35% of men who have varicocele. Understandably, it is tempting to attribute a cause and effect relationship to fertility problem and a varicocele. However, the existence of a varicocele is often coincidental (unrelated) to the underlying cause of the infertility.

Under what circumstances will treatment be unlikely to succeed? The following, in my opinion, represent situations where treatment of a varicocele (whether surgical or radiologic) is unlikely to resolve the male infertility issue.

  • When the man has an elevated blood FSH level (greater than 12MIU/ml)
  • In cases where there is a persistently low sperm count (<20million/ml).
  • When the DFI is below 30%. In such cases ICSI is the best approach.

6 Comments

Dr. Geoffrey Sher

Indeed it can.

What is a varicocele? The testicles are housed in the scrotum, a skin-covered sac that houses the two testicles as well as blood vessels that deliver blood to these glands, nerves, and lymphatics. An abnormality of the plexus of veins (the pampiniform plexus) that carry blood away from the testicles can result in their distention, proliferation and enlargement within the scrotum. We refer to this as the development of varicosities similar to varicose veins that can occur in the leg.
How does a varicocele cause male infertility? The increased scrotal blood flow often raises the temperature in the scrotum by 1-2 degrees. This in turn sometimes results in decreased sperm production and functionality as well as testicular shrinkage (atrophy), leading to male infertility. However, by no means does the existence of a varicocele inevitably compromise sperm production and functionality.
Who develops a varicocele and how common is the condition? About 15 percent of men have varicoceles. These generally form during puberty and are more commonly found on the left side than on the right side of the scrotum. Rarely are both sides of the scrotum affected. . Most males are diagnosed between the ages of 15 and 25 years of age. There are no established risk factors for developing a varicocele, and the exact cause is unclear.
How does a varicocele present and how can it be diagnosed? The presence of a varicocele does not invariable mean that it is the cause of male infertility. In fact many males who have varicoceles do not have any fertility problem at all. Also, in many cases the detection of a varicocele is an “incidental finding and is not the cause of coexisting male infertility. You see, contrary to popular belief, varicoceles seldom reduce sperm count. In fact in many cases of low-sperm count, treatment of the varicocele, rarely results an improvement in sperm production. It is important to recognize that the majority of men who have varicoceles, do not have evidence of sperm dysfunction.
Most varicoceles are not even symptomatic. In fact most are not ever detected. Those that are symptomatic present with scrotal enlargement, scrotal and/or lower abdominal pain, and infertility. The condition is often diagnosed by physical examination where, to the touch, a varicocele feels like a “bag of worms”. However ultrasound examination of the scrotum offers a more definitive diagnostic capability.

When a varicocele causes sperm dysfunction, this most commonly manifests with a normal or even raised sperm count. However, there is usually markedly reduced motility and sperm progression, but a high percentage of sperm are found to be “immature” Collectively this is referred to as a “stress pattern”. In many such cases the Sperm Chromatin Structure Assay (SCSA) will show an increase in the DNA Fragmentation Index (DFI). These are the cases where treatment of the varicocele will often improve sperm function, along with improving the likelihood of a viable pregnancy occurring naturally or following IVF with intracytoplasmic sperm injection- (ICSI)

Treatment: There are two approaches to treating varicoceles:
• Traditional treatment of a varicocele is through ligation (under general anesthesia) of one or both spermatic veins that carry blood from the pampiniform venous plexus (“varicocelectomy”). While surgery is in most cases curative, post-surgical recurrence is not uncommon.
• Another approach is interventional radiological obliteration of one or both the spermatic veins. This approach involves passing a balloon catheter via a groin blood vessel, under radiological view, into the spermatic vein and inflating the balloon in that position. This causes the spermatic vein to permanently occlude. Sometime later, the catheter is withdrawn and the vein remains occluded causing the varicocele to collapse and the pampiniform plexus to shrink. Disappear. This radiological approach is often more effective, far less costly, less traumatic and less likely to, result in a recurrence than is spermatic vein, surgical ligation. It is also conducted under local anesthesia and as an out-patient procedure. In my opinion this approach has become the preferred method for treating varicoceles.

Regardless of whether surgical or interventional radiological treatment is contemplated, it is in my opinion, advisable for the patient to take a male fertility blend that is rich in antioxidants (I recommend a product called “Proceptin) which is not currently sold at Drug Stores and requires online purchase). This will sometimes result in an improvement in the DFI within 3-6 months.. It should be taken for at least 12 weeks whereupon the SCSA should be repeated..

It is important to bear in mind that both surgical and radiological treatment will only improve sperm function in about 35% of men who have varicocele.. Understandably, it is tempting to attribute a cause and effect relationship to fertility problem and a varicocele. But, the truth is that the existence of a varicocele is often coincidental (unrelated) to the underlying cause of the infertility

Under what circumstances will treatment be unlikely to succeed? The following, in my opinion, represent situations where treatment of a varicocele (whether surgical or radiologic) is unlikely to resolve the male infertility issue.
.
• When the man has an elevated blood FSH level (greater than 12MIU/ml)
• In cases where there is a persistently low sperm count (<20million/ml).
• When the DFI is below 30%. In such cases ICSI is the best approach.

Hope this helps.

If you wish to discuss, call 800-780-7437 and ask Julie to set you up with a Skype consultation with me.

Geoff Sher

reply
simone

Hi Dr Sher, My husband has bilateral varicoceles – albeit apparently small, and a hydrocele and a small cyst. The specialist he saw thought it was unlikely he would need treatment. He had a DNA fragmentation test about a year ago and it was excellent. I am worried that the varicoceles are affecting his sperm morphology as it is very low. He has had varying results of between 6 and 9% normal morphology which is above the minimum range, but it still very low. We have recurrent miscarriages, not sure whether this is relevant… Do you think its still worth operating to remove the varicoceles and is this likely to improve his sperm morphology? All other parameters are normal…

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Dr. Geoffrey Sher

I agree with the medical advice you received. I do not believe his varicocele likely explains your Recurrent Pregnancy Loss (RPL).

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 implant.
• Interference of blood supply to the developing conceptus can occur due to a hereditary clotting disorder known as Thrombophilia.
2. Genetic and/or structural chromosomal abnormality of the embryo.Genetic abnormalities are rare causes of RPL. 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, etc.)
• Immunologic testing to include:
a) Antiphospholipid antibody (APA) panel
b) Antinuclear antibody (ANA) panel
c) Antithyroid antibody panel (i.e., antithyroglobulin and antimicrosomal antibodies)
d) Reproductive immunophenotype
e) Natural killer cell activity (NKa) assay (i.e., K562 target cell test)
f) 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.

Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
• The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
• Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
• The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
• IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
• Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 1-Background
• Immunologic Implantation Dysfunction (IID) & Infertility (IID):PART 2- Making a Diagnosis
• Immunologic Dysfunction (IID) & Infertility (IID):PART 3-Treatment
• Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
• Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report
• Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
• Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• The Role of Nutritional Supplements in Preparing for IVF

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

Geoff Sher

reply
Richard

Dr, my doctor suspected I had a varicole. However a hydrocele was actually diagnosed. Possible impact on my fertility due to abnormal semen test? Cause for concern?

Thank you

reply
Dr. Geoffrey Sher

Not if your sperm parameters are normal.

Please visit my new Blog on this very site, http://www.DrGeoffreySherIVF.com, find the “search bar” and type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly
• Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
• Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
• IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
• Traveling for IVF from Out of State/Country–
• A personalized, stepwise approach to IVF
• How Many Embryos should be transferred: A Critical Decision in IVF.
• The Role of Nutritional Supplements in Preparing for IVF
• Male Factror Infertility

Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
• Email: Julied@sherivf.com
• Phone: 702-533-2691

I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

Geoff Sher

reply

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