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,
Thank you for providing a safe space for IVF patients to share their stories and get your feedback.
I just ended my two week wait, it was a complete fail.
My story:
I am 34 years old and have a history of inflammation (dermagraphatitis, hives, chalazia, acne). I tested negative for food allergies. My allergist and other doctors said it was an autoimmune issue, subclinical hypothyroid, even though my TSH was always within range, albeit on the higher side. I started Synthroid, 25 mcg, in December 2015 and it made a difference. My body felt at peace.
I started fertility treatments (male factor) in February 2016 without doing any further autoimmune testing. I was given Lupron to suppress the eggs for 12 days. (During which I experienced a lot of night sweats).
I started STIM which included Menopure (4 shots) and Follistim (150). By day 6 of my STIM I was on 6 shots of menopure and Ganirelex.
12 eggs were retrieved, 8 fertilized successfully, 2 were grade AA and the rest AB. None were genetically tested, all were frozen. I was given a one month break prior to the medicated implantation. During the one month break I felt fine other than the first week post retrieval which I experienced mild OHSS.
For the medicated implantation the doctor increased Synthroid dosage to 75 and started me off with 3 estradiol pills twice a day, 2 estrogen patches, 1 dexamethasone, 1 aspirin, and 1 week of doxycycline. 2 weeks in I started 2 shots of progesterone a day and 5 days later I had my transfer.
During the 19 days prepping for the transfer I recall a few instances of inflammation which I never before had, namely a swollen hand, an icy cold feeling in my calves while walking on tile, muscle cramps in my leg after waking up in the morning. Please keep in my mind that I was on dexamethasone at this time, the symptoms did not last long.
The day of my transfer, while the doctor was inserting the catheter, I felt the tip of the catheter hit my cervix multiple times and it felt like a needle poking me. Both the nurse and doctor were surprised that it was painful. Never before do I recall that type of pain while getting a catheter inserted.
By day 4 post transfer (transfer day being day 1) I was off anti-inflammatory medication. That evening I felt as though I had a sore throat. I paged the doctor and she said I may have caught a cold virus. The next morning is when my body started to attack. My hand went numb, became swollen, and I felt pain radiating to my shoulder. The pain was so extreme it brought me to tears, I went in to see my doctor she said I must have slept on it the wrong way, and was not concerned about the swelling because she could still see my bone.
Anyway, the attacks continued throughout the week. The muscles in my biceps would cramp so tightly I couldnt move it, pressure points on the bottom of my feet would inflame, lymph nodes in my neck would swell. I felt pain/swelling under my arms through the side of my breast.
The experience was surreal. Depending on what I ate, the inflammation would increase. By day 9 post transfer the pain and symptoms died down.
My doctor thinks it’s a result of a remnant of my STIM and the timing was bad. She plans to test me for viruses and will refer me to a rheumatologist to check for lupus and arthritis.
Please keep in mind that in my entire history of inflammation I have NEVER experienced what I did during this implantation cycle. I have never had pain, or an icy pain feeling in my legs and arms.
What do you think this could this be attributed to?
It sounds to me that many of your symptoms were the aftermath of OHSS.
Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
1.Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
2.Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3.The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
4.Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
a.A“ thin uterine lining”
b.A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c.Immunologic implantation dysfunction (IID)
d.Endocrine/molecular endometrial receptivity issues
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
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
•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 Aproach
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting 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)
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•Endometrial Thickness, Uterine Pathology and Immunologic Factors
•The Role of Nutritional Supplements in Preparing for IVF
•Functional” Ovarian Cysts and IVF
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:
Email: Julied@sherivf.com
OR
Phone: 702-533-2691
800-780-7437
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
I’m 41 years old.My ovarie are micropolicitics, fsh 5, amh 4. I made 7 cycle for male problem NOA fsh 24. In the last 8 cycle we can’t do icsi, its happens 3 time for empty follicles or egfs MI.. The last protocol was long: Decapeptyl 3.75+12 days 300 gonalf+ ovitrelle 250. Results: 26 follicles, the day of ovitrelle 7 follicles about 21 mm, after pick up of 17 egg 3 atresici 7 MI and 7 VG. No icsi. Every time more than 50% of eggs MI, in eco and after pick up they see all mature eggs or very mature eggs and than, after denuding, MI and VG eggs. Now they want to try short protocol with antagonist and few gonalf. What do you suggest me? Thanks for tour attention and excuse me for my English. Regards
Hi enny,
We really should talk as I believe I can provide very important insight here. Please read the articles referenced below and you will immediately recognize how important the protocol selected for ovarian stimulation and the type and timing of the “trigger” shot used is to egg quality and outcome.
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
•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 Aproach
•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?
•Why did my IVF Fail
•Implications of “Empty Follicle Syndrome and “Premature Luteinization”
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
•Fertility Preservation (FP) Through Freezing/Banking Human Eggs
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:
Email: Julied@sherivf.com
OR
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
Please let me know if these results mean I will miscarry?!
Beta-Hcg,quantituve
Result 14301
Ref range <5
Units mIU/mL
It does not!
Geoff Sher
Hi Dr. Sher,
I want to say thank you for doing this open forum for women who struggle with IVF. You help me understand there are different approaches and treatment available. I met my RE yesterday, and we reviewed IVF cycle again (first cycle failed), from blood work to embryo development. He gives me a complete new drug with birth control pill to start. After meeting him, you are the first one pop in my head that I want to hear your opinion about it!
We had done all tests, both healthy/normal, hubby (34), me (31). Never get pregnant. Tired of trying, prefer higher chance of getting BFP sooner.
Failed cycle finding: Antagonist protocol, retrieved 6 eggs with 300 menopur only, fertilized but no blasts/bad eggs. After review, RE pointed out, on day 4 baseline check, my E2/FSH/LH both in normal range. However, during swimming my E2 continued to rise but with lower number. E2 level was 2368 on trigger day (8 days after stimming), and follicle sizes were 12, 14, 13, 15, 15, 16, 22, 23mm and couples of 1mm. 6 fertilized embryos, but none made to blast. Transfer one morula on day 5, lining is 12mm on transfer day. RE believes is my lack of E2 causes incompetent eggs, and fail to develop to blasts. This is main finding of failed cycle.
New Protocol: Antagonist protocol, start with BCP, Puregon only (375 to start, later 400, continue to trigger), Orgalutran (add-on 6 day post stimming), then trigger with HCG 10,000.
Here are my concerns, and I would really appreciate hearing your opinion.
1.Failed cycle I used menopur, for new cycle RE will put me on pure FSH only. From baseline check, all my hormone is in normal level. I’m worried if I still need a little LH at end of stimming? Or my body can produce enough to get egg mature? Do you feel confidence about pure FSH protocol idea?
2.What’s difference use Puregon start low at 375 to higher 400, compare to start higher (400) then go down (375) strategy? I asked, he said its better go from low to high or it could be too late/out of control. I saw some RE doing “high to low” with success, as long as patient didn’t get serious OHSS in hospital. I mean, does my RE is little conservative? What’s your opinion on dosages? Which way you suggest?
3.New protocol with birth control pill, I’m scared. I read using BCP could be tricky like over suppressed, lower AMH, and decreased response to ovarian stimulation…I asked RE if we overlapping BCP with Lupron, he said “No.” Is that possible to do BCP without Lupron? How long should I stay on BCP? and how soon start stimulation after finish last pill if go without Lupron. I’m lost….completely.
4.First cycle, I started stimming on cycle day 4. I saw everyone start on cycle day 3. Does it make a difference? In term of egg development.
5.RE wants me to see a naturopathic to help with E2 level/egg quality. I’m already taking supplements, eating healthy; do you think it is necessary?
6.Is there a way to increase estrogen during ivf? Estrogen pills/ patches? I asked RE, he told me there is nothing I can do during stimming, only solution is to see naturopathic adjust body in healthy. Any suggestion?
7.I’m thinking start acupuncture during cycle. Do you believe it help on stimming, and implantation?
8.When to do a pregnancy blood test after 5 days embryo transfer? My clinic norm is 14 days after transfer. They put everyone on progesterone suppositories, but how do doctor find out if I need E2 or other support? Should I insist do blood test early? Does it make a difference to stay on a viable pregnancy?
9.RE is in confidence the second ivf would work for me, so far there is no other issue beside E2 level. Personally, I think menopur is the reason cause my low E2…I’m not so sure, just a feeling. Do you have other thought/suggestion about his new protocol?
Thank you so much from deep of my heart! Emily
1. Failed cycle I used menopur, for new cycle RE will put me on pure FSH only. From baseline check, all my hormone is in normal level. I’m worried if I still need a little LH at end of stimming? Or my body can produce enough to get egg mature? Do you feel confidence about pure FSH protocol idea?
A: Respectfully, I am not persuaded that in a cycle where LH is completely blocked, giving pure FSH alone is optimal.
2. What’s difference use Puregon start low at 375 to higher 400, compare to start higher (400) then go down (375) strategy? I asked, he said its better go from low to high or it could be too late/out of control. I saw some RE doing “high to low” with success, as long as patient didn’t get serious OHSS in hospital. I mean, does my RE is little conservative? What’s your opinion on dosages? Which way you suggest?
A: In my opinion, it is preferable to start higher and then reduce, rather than the other way around.
3. New protocol with birth control pill, I’m scared. I read using BCP could be tricky like over suppressed, lower AMH, and decreased response to ovarian stimulation…I asked RE if we overlapping BCP with Lupron, he said “No.” Is that possible to do BCP without Lupron? How long should I stay on BCP? and how soon start stimulation after finish last pill if go without Lupron. I’m lost….completely.
A: The only way i used the BCP (and it is my preference to launch stimulation coming off the BCP), is to overlap with Lupron on the pill. 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 PAPs 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 and the follicles will not readily respond to gonadotropins (FSH) , thereby delaying follicle development by up to 7 days and compromising egg quality. 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.
4. First cycle, I started stimming on cycle day 4. I saw everyone start on cycle day 3. Does it make a difference? In term of egg development.
A: In my opinion, the earlier you start..the better.
5. RE wants me to see a naturopathic to help with E2 level/egg quality. I’m already taking supplements, eating healthy; do you think it is necessary?
A: In honesty, I do not see how that would help.
6. Is there a way to increase estrogen during ivf? Estrogen pills/ patches? I asked RE, he told me there is nothing I can do during stimming, only solution is to see naturopathic adjust body in healthy. Any suggestion?
A: It is all related to the protocol you are on and how many good follicles you develop. Taking additional estrogen is helpful in very low responders who have severe DOR. Otherwise not.
7. I’m thinking start acupuncture during cycle. Do you believe it help on stimming, and implantation?
A: It will not improve ovarian blood flow…only uterine flow…therefore, in my opinion, the ideal time for accupuncture is around the time of ET.
8. When to do a pregnancy blood test after 5 days embryo transfer? My clinic norm is 14 days after transfer. They put everyone on progesterone suppositories, but how do doctor find out if I need E2 or other support? Should I insist do blood test early? Does it make a difference to stay on a viable pregnancy?
A We do it 8 and 10 days post blastocyst transfer.
9. RE is in confidence the second ivf would work for me, so far there is no other issue beside E2 level. Personally, I think menopur is the reason cause my low E2…I’m not so sure, just a feeling. Do you have other thought/suggestion about his new protocol?
A: See below.
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
•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 Aproach
•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?
•Why did my IVF Fail
•Implications of “Empty Follicle Syndrome and “Premature Luteinization”
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
I invite you to arrange to have a Skype or an in-person consultation with me to discuss your case in detail. If you are interested, please contact Julie Dahan, at:
Email: Julied@sherivf.com
OR
Phone: 702-533-2691
800-780-7437
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
Hi dr sher please i really don’t know where to start because this is bothering me. Am 29yrs old heard 2 dc while i was 20yrs and 21yrs respectively. i been been having irregular periods, i had a scan done and its shows my left ovary has multiple primordal follicles my doctors says its polystic ovary, i also had a hormonal test which also says my prolactin is 30 testosttone is 1.3 while LH is 28. i really want if i can still get pregnant because my doctors says i have go on a drug to reduce my prolactin . please help me. Thank u so much.
I think you can get pregnant (all other things being equal). However, I would repeat the prolactin test >2 weeks after the 1st one to look for accuracy. If it is still elevated, you need to look fore a cause.
Prolactin is a protein hormone (closely related to human growth hormone) that is secreted by specialized cells in the anterior part of the pituitary gland. In addition, the hormone is also produced and secreted by a broad range of other cells in the body, most prominently various immune cells, the brain and the lining of the uterus. Most cells respond to prolactin. In fact it is hard to identify any tissue that does not have prolactin receptors.
Although prolactin’s major target organ is the breast where it stimulates development and milk production, the hormone has many other functions. Several hundred different actions have been reported for prolactin and
Immune cells are rich in prolactin receptors and certain types of lymphocytes in fact synthesize and secrete prolactin. These observations suggest that prolactin may to some extent act as a regulator of the body’s immune activity.
In an area in the brain known as the hypothalamus, a chemical called dopamine is released. Dopamine suppresses prolactin synthesis and release by the pituitary gland. As such it acts as a “hypothalamic brake set” causing prolactin only to be secreted when the “brake” is released.
Several other hypothalamic hormones, including thyroid releasing hormone (TSH) and gonadotropin releasing hormone (GnRH) cause an increase in prolactin secretion Stimulation of the nipples (including but not limited to nursing) leads to hypothalamic activation and prolactin release Estrogens also exerts a positive control over prolactin synthesis and secretion
Common manifestations of increased prolactin secretion (hyperprolactinemia) in women include amenorrhea (lack of menstrual cycles) and galactorrhea (excessive or spontaneous breast secretion of milk). Men with hyperprolactinemia may present with hypogonadism, decreased sex drive, perm dysfunction resulting in infertility and with impotence. Such men also often show breast enlargement (gynecomastia), but very rarely have galactorrhea.
Significantly raised blood prolactin levels (>60ng/ml) might point to a prolactin producing pituitary tumor (adenoma) which may be large (macroadenoma), small or even microscopic (microadenoma). Markedly elevated blood prolactin is also associated with other types of intracranial lesions such as craniopharyngiomas, meningiomas etc. Prolonged treatment with bromocryptine (Parlodel) will usually effectively lower blood concentrations and lead to shrinkage of the tumor. Such treatment is also safe during pregnancy. Other intracranial lesions causing hyperprolactinemia are usually treated by surgical removal.
Certain drugs: (e.g. tranquilizers, ganglion blocker antihypertensives, antidepressants, thiazides and narcotics) can also lead to significant elevations in prolactin. Drug-induced hyperprolactinemia can be reversed by modifying or withdrawing the causative medication. In cases where this cannot safely be done, bromocryptine derivatives can be used.
Elevated Prolactin and Reproductive Performance: It is important to recognize that even modestly raised prolactin levels (20ng/ml-40ng/ml) can interfere with endometrial proliferation as well as ovarian follicle growth and development, thereby reducing the likelihood of successful implantation, and may require treatment with prolactin suppressants such as bromocryptine (Parlodel). A modest elevation in blood prolactin can also point to an underlying state of hypothyroidism which (as explained elsewhere) in women is usually autoimmune in origin and be associated with increased uterine natural killer cell activity (NKa). The latter may profoundly impair implantation leading to “perceived infertility” or recurrent pregnancy loss.
It is important to note that ATA with NKa can be present prior to the development of clinically overt autoimmune hypothyroidism (Hashimoto’s disease). Since such women will often present with an unexplained elevation in blood TSH and/or prolactin levels, it is wise to always test for the presence of antithyroid antibodies (ATA) such as antithyroglobulin and antimicrosomal antibodies. If the ATA level is elevated, a NKa test (K-562 target cell test) should also be done because in 50% of such cases, there will often also be associated reproductive failure that manifests as “unexplained infertility, unexplained (often repeated) IVF failure or recurrent pregnancy loss (RPL)…due to immunologic implantation dysfunction.
What is not often commonly recognized is that even in cases where autoimmune hypothyroidism is clinically overt, treatment with thyroid hormone replacement will usually not solve the reproductive dysfunction which will usually require selective immunotherapy with Intralipid (IL) infusions plus steroid therapy. IL is administered intravenously about 4-7 days prior to ovulation or egg retrieval and then repeated one more time upon biochemical confirmation of early pregnancy. The steroids are continued to the 8th week of pregnancy and then tailed off over 2 weeks.
Geoff Sher