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.
Hi, I’m 33 years old, live in the UK and my husband and I have had two rounds of ICSI with zero fertilisation. We had a good number of eggs which were all ‘beautiful’, sperm borderline count and quality but not a problem for ICSI. Both clinics we have been to have no answers or suggestions of what to donext and have never seen this before. Have you? Can you offer any thoughts or suggestions please?! Thank you.
It is not common but it can happen. I would need much more information in order to advise authoritatively. Iassues such as age/ovarian reserve/protocol-regime used for ovarian stimulation and its implementation/sperm parameters etc…, all need to be critically evaluated.
The potential for a woman’s eggs to undergo orderly development and maturation, while in large part being genetically determined can be profoundly influenced by the woman’s age, her “ovarian reserve” and proximity to menopause. It is also influenced by the protocol used for controlled ovarian stimulation (COH) which by fashioning the intra-ovarian hormonal environment, profoundly impacts egg development and maturation.
After the menarche (age at which menstruation starts) a monthly process of repeatedly processing eggs continues until the menopause, by which time most eggs will have been used up, and ovulation and menstruation cease. When the number of eggs remaining in the ovaries falls below a certain threshold, ovarian function starts to wane over a 5 to10-years. This time period is referred to as the climacteric. With the onset of the climacteric, blood Follicle Stimulating Hormone (FSH) and later also Luteinizing Hormone (LH) levels begin to rise…. at first slowly and then more rapidly, ultimately culminating in the complete cessation of ovulation and menstruation (i.e. menopause).
One of the early indications that the woman has entered the climacteric and that ovarian reserve is diminishing DOR) , is the detection of a basal blood FSH level above 9.0 MIU/ml and/ or an AMH level og <2.0ng/ml.
Prior to the changes that immediately precede ovulation, virtually all human eggs have 23 pairs (i.e. 46) of chromosomes. Thirty six to forty hours prior to ovulation, a surge occurs in the release of LH by the pituitary gland. One of the main e purposes of this LH surge is to cause the chromosomes in the egg to divide n half (to 23 in number) in order that once fertilized by a mature sperm ends up having 23 chromosomes) the resulting embryo will be back to having 46 chromosomes. A “competent” mature egg is one that has precisely 23 chromosomes, not any more or any less. It is largely the egg, rather than the sperm that determines the chromosomal integrity of the embryo and only an embryo that has a normal component of 46 chromosomes (i.e. euploid) is “competent” to develop into a healthy baby. If for any reason the final number of chromosomes in the egg is less or more than 23 (aneuploid), it will be incapable of propagating a euploid, “competent” embryo. Thus egg/embryo aneuploidy (“incompetence”) is the leading cause of human reproductive dysfunction which can manifest as: arrested embryo development and/or failed implantation (which often presents as infertility), early miscarriage or chromosomal birth defects (e.g. Down’s syndrome). While most aneuploid (“incompetent”) embryos often fail to produce a pregnancy, some do. However, most such pregnancies miscarry early on. On relatively rare occasions, depending on the chromosome pair involved, aneuploid embryos can develop into chromosomally defective babies (e.g. Down’s syndrome).
Up until a woman reaches her mid- thirties, at best, 1:2 of her eggs will likely be chromosomally normal. As she ages beyond her mid-thirties there will be a a progressive decline in egg quality such that by age 40 years only about 15%-20% of eggs are euploid and, by the time the woman reaches her mid-forties, less than 10% of her eggs are likely to be chromosomally normal. While most aneuploid embryos do appear to be microscopically abnormal under the light microscope, this is not invariably so. In fact, many aneuploid embryos a have a perfectly normal appearance under the microscope. This is why it is not possible to reliably differentiate between competent and incompetent embryos on the basis of their microscopic appearance (morphologic grade) alone.
The process of natural selection usually precludes most aneuploid embryos from attaching to the uterine lining. Those that do attach usually do so for such only a brief period of time. In such cases the woman often will not even experience a postponement of menstruation. There will be a transient rise in blood hCG levels but in most cases the woman will be unaware of even having conceived (i.e. a “chemical pregnancy”). Alternatively, an aneuploid embryo might attach for a period of a few weeks before being expelled (i.e. a “miscarriage”). Sometimes (fortunately rarely) an aneuploid embryo will develop into a viable baby that is born with a chromosomal birth defect (e.g. Down’s syndrome).
The fact that the incidence of embryo aneuploidy invariably increases with advancing age serves to explain why reproductive failure (“infertility”, miscarriages and birth defects), also increases as women get older.
It is an over-simplification to represent that diminishing ovarian reserve as evidenced by raised FSH blood levels (and other tests) and reduced response to stimulation with fertility drugs is a direct cause of “poor egg/ embryo quality”. This common misconception stems from the fact that poor embryo quality (“incompetence”) often occurs in women who at the same time, because of the advent of the climacteric also have elevated basal blood FSH/LH levels and reduced AMH. But it is not the elevation in FSH or the low AMH that causes embryo “incompetence”. Rather it is the effect of advancing age (the “biological clock”) resulting a progressive increase in the incidence of egg aneuploidy, which is responsible for declining egg quality. Simply stated, as women get older “wear and tear” on their eggs increases the likelihood of egg and thus embryo aneuploidy. It just so happens that the two precipitating factors often go hand in hand.
The importance of the IVF stimulation protocol on egg/embryo quality cannot be overstated. This factor seems often to be overlooked or discounted by those IVF practitioners who use a “one-size-fits-all” approach to ovarian stimulation. My experience is that the use of individualized/customized COS protocols can greatly improve IVF outcome in patients at risk – particularly those with diminished ovarian reserve (“poor responders”) and those who are “high responders” (women with PCOS , those with dysfunctional or absent ovulation, and young women under 25 years of age).
While no one can influence underlying genetics or turn back the clock on a woman’s age, any competent IVF specialist should be able to tailor the protocol for COS to meet the individual needs of the patient.
During the normal ovulation cycle, ovarian hormonal changes are regulated to avoid irregularities in production and interaction that could adversely influence follicle development and egg quality. As an example, small amounts of androgens (male hormones such as testosterone) that are produced by the ovarian stroma (the tissue surrounding ovarian follicles) during the pre-ovulatory phase of the cycle enhance late follicle development, estrogen production by the granulosa cells (cells that line the inner walls of follicles), and egg maturation.
However, over-production of testosterone can adversely influence the same processes. It follows that protocols for controlled ovarian stimulation (COS should be geared toward optimizing follicle growth and development (without placing the woman at risk from overstimulation), while at the same time avoiding excessive ovarian androgen production. Achievement of such objectives requires a very individualized approach to choosing the protocol for COS with fertility drugs as well as the precise timing of the “trigger shot” of hCG.
It is important to recognize that the pituitary gonadotropins, LH and FSH, while both playing a pivotal role in follicle development, have different primary sites of action in the ovary. The action of FSH is mainly directed towards the cells lining the inside of the follicle that are responsible for estrogen production. LH, on the other hand, acts primarily on the ovarian stroma to produce male hormones/ androgens (e.g. androstenedione and testosterone). A small amount of testosterone is necessary for optimal estrogen production. Over-production of such androgens can have a deleterious effect on granulosa cell activity, follicle growth/development, egg maturation, fertilization potential and subsequent embryo quality. Furthermore, excessive ovarian androgens can also compromise estrogen-induced endometrial growth and development.
In conditions such as polycystic ovarian syndrome (PCOS), which is characterized by increased blood LH levels, there is also increased ovarian androgen production. It is therefore not surprising that “poor egg/embryo quality” is often a feature of this condition. The use of LH-containing preparations such as Menopur further aggravates this effect. Thus we recommend using FSH-dominant products such as Follistim, Puregon, and Gonal-F in such cases. While it would seem prudent to limit LH exposure in all cases of COS, this appears to be more vital in older women, who tend to be more sensitive to LH
It is common practice to administer gonadotropin releasing hormone agonists (GnRHa) agonists such as Lupron, and, GnRH-antagonists such as Ganirelix and Orgalutron to prevent the release of LH during COS. GnRH agonists exert their LH-lowering effect over a number of days. They act by causing an initial outpouring followed by a depletion of pituitary gonadotropins. This results in the LH level falling to low concentrations, within 4-7 days, thereby establishing a relatively “LH-free environment”. GnRH Antagonists, on the other hand, act very rapidly (within a few hours) to block pituitary LH release, so as achieve the same effect.
Long Agonist (Lupron/Buserelin) Protocols: The most commonly prescribed protocol for Lupron/gonadotropin administration is the so-called “long protocol”. Here, Lupron is given, starting a week or so prior to menstruation. This results in an initial rise in FSH and LH level, which is rapidly followed by a precipitous fall to near zero. It is followed by uterine withdrawal bleeding (menstruation), whereupon gonadotropin treatment is initiated while daily Lupron injections continue, to ensure a “low LH” environment. A modification to the long protocol which I prefer using in cases of DOR, is the Agonist/Antagonist Conversion Protocol (A/ACP) where, upon the onset of a Lupron-induced bleed , this agonist is supplanted by an antagonist (Ganirelix/Cetrotide/Orgalutron) and this is continued until the hCG trigger. In many such cases I supplement with human growth hormone (HGH) to try and further enhance response and egg development.
Lupron Flare/Micro-Flare Protocol: Another approach to COS is by way of so-called “(micro) flare protocols”. This involves initiating gonadotropin therapy simultaneous with the administration of GnRH agonist (e.g. Lupron/Buserelin). The intent here is to deliberately allow Lupron to elicit an initial surge (“flare”) in pituitary FSH release in order to augment FSH administration by increased FSH production. Unfortunately, this “spring board effect” represents “a double edged sword” because while it indeed increases the release of FSH, it at the same time causes a surge in LH release. The latter can evoke excessive ovarian stromal androgen production which could potentially compromise egg quality, especially in older women and women with PCOS, whose ovaries have increased sensitivity to LH. I am of the opinion that by evoking an exaggerated ovarian androgen response, such “(micro) flare protocols” can harm egg/embryo quality and reduce IVF success rates, especially in older women, and in women with diminished ovarian reserve. Accordingly, I do not prescribe them at all.
Estrogen Priming – My approach for “Poor Responders” Our patients who have demonstrated reduced ovarian response to COS as well as those who by way of significantly raised FSH blood levels are likely to be “poor responders”, are treated using a “modified” long protocol. The approach involves the initial administration of GnRH agonist for a number of days to cause pituitary down-regulation. Upon menstruation and confirmation by ultrasound and measurement of blood estradiol levels that adequate ovarian suppression has been achieved, the dosage of GnRH agonist is drastically lowered and the woman is given twice-weekly injections of estradiol for a period of 8. COS is thereupon initiated using a relatively high dosage of FSH-(Follistim, Bravelle, Puregon or Gonal F) which is continued along with daily administration of GnRH agonist until the “hCG trigger.” By this approach we have been able to significantly improve ovarian response to gonadotropins in many of hitherto “resistant patients”.
The “Trigger”: hCG (Profasi/Pregnyl/Novarel) versus Lupron: With ovulation induction using fertility drugs, the administration of 10,000U hCGu (the hCG “trigger”) mimics the LH surge, sending the eggs (which up to that point are immature (M1) and have 46 chromosomes) into maturational division (meiosis) This process is designed to halve the chromosome number , resulting in mature eggs (M2) that will have 23 chromosomes rather that the 46 chromosomes it had prior to the “trigger”. Such a chromosomally normal, M2 egg, upon being fertilized by mature sperm (that following maturational division also has 23 chromosomes) will hopefully propagate embryos that have 46 chromosomes and will be “:competent” to propagate viable pregnancies. The key is to trigger with no less than 10,000U of hCGu (Profasi/Novarel/Pregnyl) and if hCGr (Ovidrel) is used, to make sure that 500mcg (rather than 250mcg) is administered. In my opinion, any lesser dosage will reduce the efficiency of meiosis, and increase the risk of the eggs being chromosomally abnormal. . I also do not use the agonist (Lupron) “trigger”. This approach which is often recommended for women at risk of overstimulation, is intended to reduce the risk of OHSS. The reason for using the Lupron trigger is that by inducing a surge in the release of LH by the pituitary gland it reduces the risk of OHSS. This is true, but this comes at the expense of egg quality because the extent of the induced LH surge varies and if too little LH is released, meiosis can be compromised, thereby increasing the percentage of chromosomally abnormal and of immature (M1) eggs. The use of “coasting” in such cases) can obviate this effect
.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
•The Fundamental Requirements For Achieving Optimal IVF Success
•Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
• A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
•Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
•Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
•Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
•Optimizing Response to Ovarian Stimulation in Women with Compromised Ovarian Response to Ovarian Stimulation: A Personal Approach.
•Egg Maturation in IVF: How Egg “Immaturity”, “Post-maturity” and “Dysmaturity” Influence IVF Outcome:
•Commonly Asked Question in IVF: “Why Did so Few of my Eggs Fertilize and, so Many Fail to Reach Blastocyst?”
•Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Staggered IVF
•Staggered IVF with PGS- Selection of “Competent” Embryos Greatly Enhances the Utility & Efficiency of IVF.
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•Embryo Banking/Stockpiling: Slows the “Biological Clock” and offers a Selective Alternative to IVF-Egg Donation
•Preimplantation Genetic Testing (PGS) in IVF: It should be Used Selectively and NOT be Routine.
•IVF: Selecting the Best Quality Embryos to Transfer
•Preimplantation Genetic Sampling (PGS) Using: Next Generation Gene Sequencing (NGS): Method of Choice.
•PGS in IVF: Are Some Chromosomally abnormal Embryos Capable of Resulting in Normal Babies and Being Wrongly Discarded?
•PGS and Assessment of Egg/Embryo “competency”: How Method, Timing and Methodology Could Affect Reliability
•IVF outcome: How Does Advancing Age and Diminished Ovarian Reserve (DOR) Affect Egg/Embryo “Competency” and How Should the Problem be addressed.
If you are interested in my advice or medical services, I urge you to contact my patient concierge, ASAP to set up a Skype or an in-person consultation with me. You can also set this up by emailing concierge@sherivf.com or by calling 702-533-2691 and/or 800-780-743. You can also enroll for a consultation with me, online at http://www.SherIVF.com.
Also, my book, “In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com .
Geoffrey Sher MD
Is DHEA useful in increasing IVF success rate?
Hi doctor. I am Eesha gupta 29yrs old. Earlier also I contacted you regarding possible mosaic blastocyst. That has helped me to decide. Now I have a query about Fet cycle. Last month my first FET cycle was cancelled due to fluid in endometrium cavity. I was on progynova 4 mg thrice a day from day 3 and viagra 100mg every night my lining was good 8 mm and no fluid but as soon as I started progesterone pessary 400mg twice a day fluid appeard and lining went down to 5.9 mm so my fet got cancelled. Now this month he planned a natural cycle. Today on day 10ie 13th dec 2018 my lining is 3.2 mm and again I have fluid in cavity measuring 1.3 mm. I am not able to understand the cause of this. What steps I should take so that I can get rid of this fluid and if this cycle also get cancelled what steps I should take to make sure that fluid doesn’t comes back in future cycle. Looking forward for your sincere advice. Thank you so much.
There are several causes of this. The most significant is reflux of estrogen-induced cervical mucous back into the cavity. This is treated by reviewing the lining just prior to ET because the progesterone effect will stop mucous production and it will often (not always0 totally absorb. If it absorbs by the day ET is scheduled, I would proceed with the ET,…otherwise not. The second cause is the presence of surface lesions (e.g., polyps, scarring, submucous fibroids etc..) in the uterine cavity. I would suggest doing a hysteroscopy to diagnose and address this, if found.
Good luck!
Geoff sher
hi dr sher
i am devistated
I had FET an got pregnant. when we looked at the baby by ultrasound we saw very good shape of the sac and good heart beat. i didnt want to listen the heart beat because ultrasound vibrations may harm to the baby this early just looked at..there was no clot area or bleeding area or someting ..it was end of the 7th week but the doctor said the baby 6 weeks old and it is normal because of FET and he said to me not to take estrofem (3*1) any more but countinue the progestrone and prednisolone and intralipid.. after that day my cramps strated immediatly a little bit and later my boobs were not swollen or not sensetive and 5days after ultrasound i start bleeding and i had a shot of proluton(progestrone) intramuscular right away ,it didnt work. i was bleeding like a mensturiation my doctor was far away i choose to take a rest in bed i tought may be i can rescue my baby
a few day laters ultrasound confirmed that the heartbeat stoped.. i wonder if the reason of this lost is estrogen withdrawal bleeding. because i cut the estrofem too early and suddenly.. after abortion at the begining my bleeding was not as much as mensturation but continuous.. i dont know it is because off cut off the progestron suppozituar (3*1) or not but after two weeks it not only didn’t stop but also as much as mensturation. the doctor said uterine lining is too thin gave transamine (2*1) and said “the reason of bleeding is hormonal changes” after 2days of transamine i change the medicine : cut transamine ans started cylo-progynova ..and i think ESTROGEN worked and my lining getting thick, my bledding stoped in a few days immediatly.. that is why i cant help thinking of that the reason of the lost this baby is the lack of estrogen, suddenly and too early.. what do you think? my next FET i think to take estrofem for 12 weeks would it cause too much thickness and another problem for the fetus??
my PAI serpine mutasyon homozigot 4G/4G
mthfr A1298C homozigot 1298CC
Factor XIII V34L heterozigot 34VL
the other factors are normal.. some doctors says i need corasprine and clexane; some says only use clexane; some says i need to start clexane at the beginning of the transfer month but some says these factors not important ones and i dont need to use clexane..
what i did i start corasprin right beginning of the transfer month and i start clexane on the day of transfer.. when 8days later a little bit brown black red clot came 3 times (i dont know if it’s implantation blood or not) we cut off the asprine that day and never bleeding again until end of the 7th week .. do you think i should use clexane or plus corasprine or not ..is this clexane the reason of my heavy bleeding at 7 week or estrogen or what dou you think
First, please accept my sympathy for you loss. Frankly, in my opinion, 6 weeks is a little early to discontinue estrogen supplementation. I am not saying this (or this, alone) was the cause of the loss…only that in my opinion, in embryo recipient cycles (e.g., FET)hormone replacement therapy (E+P) should continue until ovarian-placental conversion has been effected..i.e, around 10 weeks.
With few exceptions, I do not recommend aspirin therapy in IVF and then use of heparinoids (e.g.,clexane) have specific indications (e.g., antiphospholipid antibodies and a homozygous MTHFR mutation). For additional information, please read on….
In about 80% of cases, early pregnancy loss (whether due to miscarriage or chemical pregnancy) is due to embryo abnormalities which are usually (but not invariably) related to chromosomal irregularities (aneuploidy) originating in the egg (rather than the sperm). In the remaining 20% of cases, the cause is implantation dysfunction which can result from anatomical (lining), immunologic implantation dysfunction (IID) or molecular biochemical abnormalities.
Since egg and embryo aneuploidy occur so frequently as a variant of normal reproductive performance, it follows that early pregnancy loss is likewise normal to the human condition. Moreover, since egg chromosomal irregularities increase with age advancement beyond 34y, starting at about 1:2 eggs/embryos ty about19; 20 (5%) by age 45y. the incidence of embryo aneuploidy will likewise increase as the woman gets older.
Depending upon how early the pregnancy loss occurs, it might manifest as a positive pregnancy test, prior to the emergence of clinical or ultrasound evidence of a pregnancy (a chemical pregnancy) or later after clinical or ultrasound evidence of an established pregnancy has become evident.
The incidence of early pregnancy loss rises dramatically as the women age beyond 40 years such that by the mid 40’s it is greater than 50%. This is largely due to the age-related increase in egg aneuploidy. Such chromosomal early pregnancy losses occur randomly and sporadically so that a woman might have a baby, lose one or two and then have another healthy pregnancy. In other words, they rarely occur repeatedly (>2 in a row). In contrast, early pregnancy losses that are due to implantation dysfunction (i.e. attributable to surface lesions in the uterine cavity, a thin uterine lining or due to IID) tend to be recurrent in nature. In summary, while miscarriages most commonly occur as a result of chromosomal egg-related embryo abnormalities, these rarely present as recurrent losses and thus when recurrent pregnancy loss (RPL) occurs, it is important to consider and rule out implantation dysfunction problems as the primary cause, before proceeding to another IVF attempt.
Women who have repeated IVF failures thus need to be evaluated thoroughly for both embryo competency and implantation dysfunction before and/or in the course of their next IVF attempt. Implantation problems should be evaluated before proceeding to the next IVF cycle. The tests needed include:
1.Evaluation of the anatomical integrity of the uterus. This necessitates performance of a sonohysterogram (saline sonogram), a hysteroscopy or a pelvic MRI (rarely is it necessary to go this far). A hysterosalpingogram (HSG), also known as a dye x-ray, is inadequate because it involves injecting a radio opaque substance into the uterine cavity which can obscure small lesions due to scarring, polyps or fibroids protruding into the uterine cavity.
2.Assessment of endometrial thickness. This can be determined by ultrasound examination around the time of normal ovulation or can be determined based on endometrial thickness as measured in previous cycle. A lining of > 9 mm in thickness is ideal. Less than 8 mm is poor and between 8 – 9 mm in thickness is “intermediate”. In my opinion, embryos should not be transferred into a uterus where the lining measures < 8 mm. The administration of vaginal Viagra (sildenafil) suppositories for at least 72 hours prior to the hCG trigger will often dramatically improve a “thin lining”. 3.Autoimmune and alloimmune causes of immunologic implantation dysfunction should be assessed. Since both allo-and autoimmune implantation dysfunction ultimately are linked to Natural Killer Cell activation, you can start by doing a Natural Killer Cell activity (NKa) test using the K562 target cell test and/or endometrial cytokine analysis, and only proceed to more detailed evaluations if this turns out to be abnormal. Numerous blog articles on this site provide more details on IID and the use of immunotherapy that address/reverse such problems. 4.Testing molecular and biochemical factors in the endometrium. There has been a growing interest in measurement of various endometrial factors as a method to assess implantation potential, including the endometrial receptivity assay (ERA) and other molecular assessments. Frankly, I personally do not share enthusiasm for most such tests which by and large lack concrete evidence of efficacy. Recent advances in egg and embryo karyotyping using Preimplantation Genetic Screening (PGS)- technologies have improved the our ability to identify “competent” chromosomally normal embryos for transfer. This requires biopsying the advanced embryo (blastocyst) and testing its DNA for aneuploidy. When the so tested, embryo transfer must be deferred until a subsequent hormone replacement cycle (staggered IVF) so as to allow enough time for the results of the testing to become available. In such cases the embryos can be vitrified (ultra rapidly frozen) and stored for subsequent dispensation without prejudice. Aside from the above, there are other less common causes of embryo incompetency (e.g., unbalanced embryo chromosomal translocations) and implantation dysfunction (bacterial and parasitic infections, etc.). Geoff Sher
Hi Dr. Sher, besides MDR, what other pharmacies do you recommend for the compound viagra. Thank you!
Sorry Eva, I do not know of any!
Geoff Sher