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Hello Dr Sher, I read your article on high levels of LH and their deleterious effects on egg quality. I have DOR, but when I stimmed last year on 600 IU puregon, I found my LH was completely expunged to the point where even with Luveris 75 IU supplementation, my LH level the following day was below the normal range.. it was very low, so the fertility specialist recommended doubling the dose of Luveris so it was 2 lots of 75 IU a day.. What is the impact of very low levels of LH even with Luveris supplementation? You say that LH rises and falls in waves, but when ever my LH levels were tested, they were always low and I’m 42 years of age. There was a study to suggest that supplementation with Luveris helped improve egg quality in those whose LH dropped below the recommended level.
Some LH-induced testosterone is necessary to cause follicle growth and estrogen development as well as orderly egg development. It is only excessive LH that is harmful. So if the LH was very low then in yur case, all amount of supplementation in the form of Luveris or Menopur, might have been appropriate.
Good luck!
Geoff Sher
I got IUI done yesterday….During the process the doctor said it was difficult to pass in the catheter due to obstruction. But eventually succeeded in passing it and injecting the sperm. should I worry?
As long as the catheter was intruded into the uterus it should be fine.
Geoff Sher
Hi Dr, Sher,
Have you had patients (or know of any other cases) who’s initial beta numbers did not double in 48-72 hours and yet had a healthy pregnancy? Is this a possibility?
Thanks!
Yes! I do! But it is not common!
For about 10% of all infertile couples, the cause of the infertility cannot be readily determined using conventional diagnostic methods. Such cases are often referred to as “unexplained infertility.” The truth however is that in most such cases, the diagnosis of “unexplained infertility is in fact “presumptive because a more in-depth evaluation would have revealed a cause. This having been said, people diagnosed with so called “unexplained infertility” fall into two broad groups: a)those couples who don’t have any biological problems interfering with pregnancy and, b) those who do but the reason cannot be found due to insufficient medical information or technology. It is in this latter group that improved testing techniques have made infertility easier to diagnose and treat.
In order to make even a presumptive diagnosis of “unexplained infertility” the answers to the following questions must be in the affirmative.
?Is the woman ovulating normally?
?Is the couple having intercourse regularly in the periovulatory phase of the cycle?
?Are the fallopian tubes normal and open?
?Can endometriosis be excluded?
?Does the male partner have normal semen parameters (most specifically with regard to sperm count and motility?
?Is the post coital (Huhner) test (periovulatory examination of cervical mucous, done 6-18 hours after intercourse) normal?
The definitive diagnosis of “unexplained infertility” has a lot to do with the thoroughness of the health care provider in excluding all possible causes. The fewer tests performed, the more likely a presumptive diagnosis
For Example:
?Abnormalities of the fallopian tubes (adhesions or developmental defects) of the finger-like “petals” at their outer ends of the tubes that help sweep eggs inside (i.e. fimbriae). can prevent eggs from being collected and transported to the awaiting sperm
?Chromosomal abnormalities of eggs or embryos: Eggs must be euploid (contain the right number of chromosomes) to be successfully fertilized and embryos must also be euploid in order to implant successfully in the uterine lining. Until recently there was no reliable method for determining whether eggs and embryos were euploid. The recent introduction of genetic tests such as comparative genomic hybridization (CGH) now allows for identification of all chromosomes in the egg and embryo. As such CGH represents an important addition to the “infertility” diagnostic armamentarium.
?Luteinized Unruptured Follicle (LUF)Syndrome: Here, the eggs can become trapped in the follicle and not be released (trapped ovulation) In such cases routine tests done to detect ovulation ((temperature charting, Urine LH testing, Blood progesterone levels) may be normal resulting in false interpretation that ovulation is actually occurring.
?Ovulation (hormonal) Dysfunction: Abnormalities in ovarian hormone production in the preovulatory phase of the cycle (follicular phase defect) and/or in the postovulatory phase (luteal phase defect) can negatively affect preparation of the uterine lining (endometrium), thus thwarting normal implantation.
?Immunologic implantation dysfunction (IID): Sometimes, the woman’s or the man’s own immune system can attack sperm cells, killing them or causing them to become immobilized. Also, immunologic dysfunction involving the uterine lining can cause the implanting embryo to be rejected so early that the woman does not even recognize that she in fact had conceived.
?Cervical infection; Ureaplasma urealyticum infection of the cervical glands can prevent sperm from migrating through the cervix and uterus to reach the egg(s) in the fallopian tube(s). Such infection will usually not be detectable through routine examination and/or cervical culturing methods.
?Mild or Moderate Endometriosis: Endometriosis is in 100% of cases associated with the production of “pelvic toxins” that reduce the fertilization potential of otherwise normal eggs by a factor of 3-5. In addition, about 1/3 of woman with endometriosis (regardless of its severity) have immunologic implantation dysfunction (IID). Furthermore mild and often even moderately severe endometriosis can only be accurately diagnosed by direct visualization of the lesions through laparoscopy or laparotomy and, the detection of IID requires highly sophisticated tests that can only be adequately performed by a handful of Reproductive Immunology Reference Laboratories in the United States. Finally, a condition called nonpigmented endometriosis, in which the endometrium may be growing inside the pelvic cavity with many of the same deleterious effects as overt endometriosis, cannot be detected even by direct vision (at laparoscopy/laparotomy). The fertility of these patients may be every bit as compromised as if they had detectable endometriosis.
?Psychological Factors: The entire reproductive process is governed by the brain. Thus it should come as no surprise that stress and negativity can interfere with hormonal balance and decrease the ability to conceive.
?Mild Male Factor
?Antisperm antibodies in the man or woman.
Management:
Successful management of “Unexplained Infertility” requires that a very individualized approach be taken. Wherever possible the underlying cause should first be identified. Problems that involve ovulation dysfunction (hormonal imbalance) require ovulation induction with oral or injectible fertility drugs. Cervical mucous hostility due to infection with ureaplasma (which is transferred back and forth sexually to both partners) requires specific and concurrent antibiotic therapy. In other cases involving younger women (under 39 years) where there is a problem with sperm migration via the cervix and uterus to the fallopian tube(s) intrauterine insemination (IUI) with or without ovulation induction, is indicated. When these treatments fail, in cases, women over the age of 39 years, in women with IID, in men or women who harbor antisperm antibodies in significant concentrations and in cases associated with tubal abnormalities, in vitro fertilization (IVF) is needed. All cases of intractable, moderate or severe male infertility call for injecting sperm directly into the egg to achieve forced fertilization (intracytoplasmic sperm injection-ICSI).
It is an indisputable fact that most causes of infertility can be diagnosed and it is a great pity that the diagnosis of “unexplained infertility” is often used as an excuse for not having performed a full and detailed evaluation of the problem. Couples should not simply accept a diagnosis of “unexplained infertility” at face value since treatment is most likely to be successful when the specific cause of the problem can be fully identified
Geoff Sher
Hi Dr. Sher,
I am 34 yo and currently prepping for my first IVF cycle. I have never been pregnant and my husband has never fathered a child. We failed 3 rounds of IUI with Clomid. I ovulate regularly, HSG normal, FSH 7, AMH 2.47, Estrogen 39, TSH 1.67 (on Synthroid for subclinical hypothyroid).
My husband had bilateral varicocelectomy (sub-inguinal microscopic) surgery for severe bilateral varicoceles 2 weeks ago. His sperm analysis pre-surgery ranged from 1.2-12 million count, morph 2%, and motility always >65%.
My planned protocol is long Lupron with Lupron (10 units then 5), Follistim (225) and HCG trigger (10,000). Does this seem reasonable? I feel like everyone I hear about also has Menopur in their protocol.
Secondly, should I request a DNA fragment test for my husband? Should we do PGS testing and a frozen ET? Or should those be reserved for after a failed cycle?
Our IVF cycle will be done only 60 days after his surgery because of insurance coverage, work travel schedules, and the understanding that the surgery might not be successful in turning around count and morphology.
Thank you!
Sarah
In addition – we are planning on IVF with ICSI and my husband has been on Vitamin C, E, L-Carnitine, and Acetyl-L-Carnitine
I would suggest you first get a repeat semen-analysis done 3-6 months before doing IVF. If it has not improved after 6 months there is probably little you scan do except ICSI. My prediction is that the surgery is not very likely to significantly improve sperm parameters. It rarely does so when there is a low sperm count. You will need ICSI of course, but he chance of success with this approach is good.
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.
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•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
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•The Fundamental Requirements For Achieving Optimal IVF Success
•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.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
•Male Factor Infertility
•Routine Fertilization by Intracytoplasmic Sperm Injection (ICSI): An Argument in Favor
•Hormonal Treatment of Male Infertility
•Hormonal Treatment of Male Infertility
•Antisperm Antibodies, Infertility and the Role of IVF with Intracytoplasmic Sperm Injection (ICSI)
•Testicular Sperm Extraction (TESE) and Testicular Sperm Aspiration (TESA): Surgical Approaches for Accessing Sperm from men who have no sperm in their ejaculates (Azoospermia)
•The Sperm Chromatin Structure Assay (SCSA): A Measure of the Potential of Sperm to Help Propagate a Viable Pregnancy
patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Dear Dr. Sher
I hope this message finds you well. Please I would like to know if it’s possible to do fetal reduction and cervical cerclage in the same setting or not?
Thanks for your positive response which is highly appreciated
I would advise against it. The reason is that if something goes wrong, you would not know which was the cause.
Geoff Sher