Ask Our Doctors – Archive
Our Medical Directors are outstanding physicians that you will find to be very personable and compassionate, who take care to ensure that you have the most cutting-edge fertility treatments at your disposal. This is your outlet to ask your questions to the doctors.
Dear Dr. Sher,
I’m planning to do IVF with my partner who is a current female patient of yours. She has frozen her eggs and they are stored with your Lab. I had a sperm test done the other day and my results were of an approximate 8million count with only 40 of normal form. apparently, my urologist identified that I have a varecocele which would need outpatient procedure to possibly help improve my count and quality. Before I do that, my question to you is:
Based on my 8million count with 40% normal, Would you be able to select sufficient normal form in order to create an number of embryo’s?
If you can email me at jstiena@aol.com or 310.433.8745 with your thoughts. I’m based in LA and would like to come to your office once I have a clarity on the best way forward for myself.
Sincerely,
John Partouche
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.
Geoff Sher
Hey Dr Sher,
I’m 7 days past my transfer of a hatching 6 day blast (AB). I haven’t noticed an increase in cervical mucus during the two week wait like I did on my other pregnancies where I conceived naturally. I feel like my CM has decreased since before the transfer, would this be normal? Im still on .125 cc estradiol valerate injections every tues/fri and 1 ml PIO every day. Do the hormones act differently since they aren’t being produced by my ovaries? I would think with the same amount of hormones I would still be getting CM post transfer. Do you have any insight?
The progesterone produced post-ER and the supplemental progesterone will decrease CM production profoundly. Try to be patient until the pregnancy test!
Geoff Sher
Dear Dr Sher,
I am 36 and I have completed 3 IVF cycles to date over the past year. IVF 1, 17 retrieved, 6 blasts, 3 PGS normal. None implanted. IVF 2, 11 retrieved, 4 blasts, 2 PGS normal. IVF 3, 23 retrieved, 7 blasts, 1 normal. IVF 2 and 3 were done back to back. Only difference was IVF 2 involved EPP, IVF 3 was the same as IVF 1. Our last cycle really did a number on me as we only got 1 normal from 7 blasts. The center has no explanation other than it’s just plan bad luck as they were expecting 50% normals for my age. All my lab work is within normal range so I was given the ‘unexplained IF’ diagnosis. The doctors also don’t know why the 3 normal embryos from my first retrieval did not take. We did a hysteroscopy and ERA test – all good. I now have a 3 frozen normals from the last 2 cycles but I am terrified to transfer any because I am getting older and want 2 kids so I don’t feel 3 normals is sufficient given my IVF 1 results. Should I continue to try and bank more embryos? Is this an uncommon result for someone my age to have an increasing number of abnormals and have no PGS embryos implant?? How many rounds of IVF do I need to be prepared to do to bring home a baby?
Hi Dr Sher: my daughter is now 33 weeks pregnant after FET of a genetically tested normal embryo. At 11 weeks she had a major bleed and was diagnosed with a SCH. No bleeding since. Then, her PAPP-A was 5, indicating a possible growth problem. Subsequent ultrasounds have indicated normal growth. Three weeks ago at a prenatal visit and uktrasound they noticed a few small leaks in the placenta that they state is sometimes seen in IVF parients and want to repeat an ultrasound next week to rule out an accreta. From what I’ve read this is a very dangerous complication. Is this all bad luck or could this all be related to IVF? Does a leaking placenta usually indicate an accreta? Thank you!
Ultrasound is 85% reliable in diagnosing placenta accreta prenatally. But now that the diagnosis is suspected, appropriate action can be taken tom protect both mother and baby.
My bet is that all will be fine!
Please keep me in the loop!
Good luck!
Geoff Sher
Hi Dr. Sher,
I am 37, amh 5.7pmol. Recently I had a failed short protocol. I am going to try the long protocol but worried about it. Is it possible to be oversuppressed and instead of a two week long menopause end up with permanent menopause? I’m worried what if my ovaries just don’t bounce back? Is this a valid concern?
Thank you.
No…highly unlikely.
One often hears the expressed opinion that the BCP suppresses response to ovarian stimulation. This is not the case, provided that the BCP is overlapped with administration of an agonist (e.g. Lupron, Buserelin, Superfact) for several days leading up to the start of menstruation and the initiation of ovarian stimulation cycle with gonadotropin drugs. If the latter precaution is not taken, and the cycle of stimulation is initiated coming directly off the BCP the response will often be blunted and subsequent egg quality could be adversely affected. The explanation for this is that in natural (unstimulated) as well as in cycles stimulated with fertility drugs, the ability of follicles to properly respond to FSH stimulation is dependent on their having developed FSH-responsive receptors . Pre-antral follicles (PAF) do not have such primed FSH receptors and thus cannot respond properly to FSH stimulation with gonadotropins. The acquisition of FSH receptor responsivity requires that the pre-antral follicles be exposed to FSH, for a number of days (5-7) during which time they attain “FSH-responsivity” and are now known as antral follicles (AF). These AF’s are now able to respond properly to stimulation with administered FSH-gonadotropins. In regular menstrual cycles, the rising FSH output from the pituitary gland insures that PAFs convert tor AF’s. The BCP (as well as prolonged administration of estrogen/progesterone) suppresses FSH. This suppression needs to be countered by artificially causing blood FSH levels to rise in order to cause PAF to AF conversion prior to COS commencing, otherwise pre-antral-to –antral follicle conversion will not take place in an orderly fashion, the duration of ovarian stimulation will be prolonged and both follicle and egg development may be compromised. GnRH agonists (e.g. Lupron, Buserelin, Superfact) , cause an immediate surge in release of FSH by the pituitary gland thus causing conversion from PAF to SAF. This is why, women who take a BCP to launch a cycle of COS need to have an overlap of the BCP with an agonist. By overlapping the BCP with an agonist for a few days prior to menstruation the early recruited follicles are able to complete their developmental drive to the AF stage and as such, be ready to respond appropriately to optimal ovarian stimulation. Using this approach, the timing of the initiation of the IVF treatment cycle can readily and safely be regulated and controlled by varying the length of time that the woman is on the BCP.
Since optimizing follicular response to COS requires that prior to stimulation with gonadotropins, FSH-induced conversion from PAF to AF’s first be completed and the BCP suppresses FSH, it follows when it comes to women launching COS coming off a BCP something needs to be done to cause a rise in FSH for 5-7 days prior to menstruation heralding the cycle of CO S.This is where overlapping the BCP with an agonist (e.g. Lupron/Superfact/Buserelin) comes in. The agonist causes FSH to be released by the pituitary gland and if overlapped with the BCP for several days and this will (within 2-5 days) facilitate PAF to AF conversion…. in time to start COS with the onset of menstruation. Initiating ovarian stimulation in women taking a BCP, without doing this is suboptimal
I believe it to be essential regardless of the protocol of COS protocol being contemplated, for women who launching ovarian stimulation coming off a BCP to overlap with an agonist for several days in advance of initiating ovarian stimulation with the onset of menstruation,
Geoff Sher