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 Dr. Sher,
I have irregular cycles and my last period
started on 7/20/20. I had a positive ovulation test reading on 8/8 and I am sure that my husband and I conceived on 8/9. I got a positive
home pregnancy test on 8/21 and had an appt to confirm pregnancy with my doctor on 8/31 , which should have been 6w based on my LMP. At this appt, nothing was seen on the ultrasound except for thickened endometrium and my doctor suspected I ovulated late and was actually only in the 4th week of pregnancy. I had beta HCG numbers checked and it was 2706. Two days later, on 9/2, HCG measured 4883 so the doctor surmised that I was just much earlier in the pregnancy than we thought. I have another appt for a repeat sonogram on 9/16 when I should be 6w. Do you agree with this?
Today I’ve had some red spotting when I wipe after going to the bathroom. I have no pain and very very mild cramping. Is this something to be concerned about? My last pregnancy was an ectopic pregnancy that resulted in emergency surgery and removal of my right fallopian tube, so perhaps I’m worried for no reason. I did call my doctor and was told if there’s no pain, there’s nothing to be worried about.
It is very possible that you have another ectopic.
Approximately 1 out of every 100 embryos will implant and grow outside of the uterine cavity (almost always) in a fallopian tube. This is defined as an ectopic pregnancy. Infrequently, an ectopic pregnancy attaches to an ovary or to one or more other pelvic organs. On very rare occasions (1;1,000), one twin attaches and grows in the uterine cavity with the other growing outside the uterus (i.e. a heterotopic pregnancy).
There is an ever present risk that a tubal (ectopic) pregnancy might rupture causing potentially catastrophic internal hemorrhage. Accordingly any symptoms suggesting that such bleeding has started, requires immediate confirmation of the diagnosis followed by emergency treatment.
While on rare occasions, an extrauterine (ectopic) can proceed well into pregnancy, it almost always happens prior to the 8th week. There is an increase in the incidence of ectopic pregnancy after IVF conceptions where it reportedly occurs in about 3% of cases and a woman who has had one ectopic pregnancy has almost four times as great a risk of an ectopic in a future pregnancy. In fact with every subsequent ectopic this risk of a recurrence increases dramatically.
The fertilization of the human egg normally takes place in the fallopian tube. The embryo then travels into the uterus, where it implants into the endometrial lining 5-6 days after ovulation. Anything that delays the passage of the embryo down the fallopian tube can result in the embryo hatching and sending its “root system” into the wall of the fallopian tube and initiating growth within the tube. One of the most common predisposing factors is pelvic inflammatory disease (PID) in which microorganisms, such as Chlamydia, and Gonococcus damage the inner lining (endosalpinx) and eventually also the muscular walls of the tube(s) by the formation of scar tissue. The endosalpinx has a very complex and delicate internal architecture, with small hairs and secretions that help to propel the embryo toward the uterine cavity. Once damaged, this lining can never regenerate. This is one of the reasons why women who manage to conceive following surgery to unblock fallopian tubes damaged by PID, have about a 1:4 chance of a subsequent pregnancy developing within the fallopian tube (ectopic).
Congenital malformations of the fallopian tube, associated with shortening of, or small pockets and side channels within, the tube are capable of interrupting the smooth passage of the embryo down the fallopian tube, is another cause of an ectopic pregnancy.
Since the lining of the fallopian tube does not represent an optimal site for healthy implantation, a large percentage of pregnancies that gain early attachment to its inner lining will usually be absorbed before the woman even knows that she is pregnant. This is often referred to as a tubal abortion.
The advent of advanced sonographic and hormonal monitoring technology now makes it possible to detect an ectopic pregnancy much earlier than previously, …usually well in advance of it rupturing. A decade or two ago, the diagnosis of an ectopic pregnancy, ruptured or not, was an indication for immediate laparotomy to avoid the risk of catastrophic hemorrhagic shock. This often resulted in the affected fallopian tube having to be completely removed, sometimes along with the adjacent ovary. In the late 1980’s, early conservative surgical intervention by laparoscopy began replacing laparotomy (a wide incision made in the abdominal wall) for the treatment of ectopic pregnancy, often allowing the affected fallopian tube to be preserved and shortening the period of post-surgical convalescence. In the 90’s, early detection combined with the advent of medical management with methotrexate (MTX) has all but eliminated the need for surgical intervention in the majority of patients. If administered early enough, MTX will allow spontaneous resorbtion of the pregnancy and a dramatic reduction in the incidence of catastrophic bleeding. This was especially true in ectopic pregnancies arising from In Vitro Fertilization, where the early progress of pregnancy is usually carefully monitored with hormone levels and ultrasound.
Classically women with an ectopic pregnancy present with the following symptoms:
•Missed menstrual period: Although some patients will have spotting or other abnormal bleeding. The pregnancy test will be positive in such cases.
•Vaginal bleeding. When a pregnancy inadvertently implants in the fallopian tube the lining of the uterus undergoes profound hormonal changes associated with pregnancy (primarily associated with the hormone progesterone). When the embryo dies, the lining of the uterus separates. Initially, vaginal bleeding is dark and usually is quite scanty, even less than with a normal menstrual period. In some cases, of ectopic pregnancy will bleeding is more severe, similar to that experienced in association with a miscarriage. This sometimes leads to an ectopic pregnancy initially being misdiagnosed as a miscarriage and is the reason to examine the material that is passed vaginally, for evidence of products of conception.
•Pain. In the early stages this is typically cramp-like in nature, located on one or another side of the lower abdomen. It is caused by spasm of the muscular wall of the fallopian tube(s). When a tubal pregnancy ruptures the woman will usually experience an abrupt onset of severe abdominal followed by light headedness, coldness and clamminess and will often collapse due to shock. Her pulse will become rapid and thready and her blood pressure will drop. Miscarriage. Sometimes the woman will experience pain in the right shoulder. The reason for this is that that blood which tracts along the side of the abdominal cavity finds its way to the area immediately below the diaphragm, above the liver (on the patient’s right side), irritates the endings of the phrenic nerve, which supplies that part of the diaphragm. This results in the referral of the pain to the neck and the right shoulder. The clinical picture is often so typical that making the diagnosis usually presents no difficulty at all. However, with less typical presentations the most important conditions to differentiate from an ectopic pregnancy are: a ruptured ovarian cyst, appendicitis, acute pelvic inflammatory disease (PID), or an inevitable
•Vaginal bleeding. When a pregnancy inadvertently implants in the fallopian tube the lining of the uterus undergoes profound hormonal changes associated with pregnancy (primarily associated with the hormone progesterone). When the embryo dies, the lining of the uterus separates. Initially, vaginal bleeding is dark and usually is quite scanty, even less than with a normal menstrual period. In some cases, of ectopic pregnancy will bleeding is more severe, similar to that experienced in association with a miscarriage. This sometimes leads to ectopic pregnancy initially being misdiagnosis as a miscarriage and is the reason that we often want to examine the material that is passed vaginally, for evidence of products of conception.
The easiest and most common method of diagnosing an ectopic pregnancy is by tracking the rate of rise in the blood levels of hCG. With a normal intrauterine pregnancy, these usually double every two days throughout the first few weeks. While a slow rate of increase in blood hCG usually suggests an impending miscarriage, it might also point to an ectopic pregnancy. Thus the hCG blood levels should be followed serially until a clear pattern emerges.
A vaginal ultrasound examination usually will clinch the diagnosis by showing the ectopic pregnancy within a fallopian tube and if the tube has already ruptured or internal bleeding has occurred, ultrasound examination will inevitably detect the presence of free fluid into the abdominal cavity.
If there has been a significant amount of intra-abdominal bleeding, irritation of the peritoneal membrane will cause the abdominal wall to become hard tense and, depending on the amount of internal bleeding abdominal distention will be evident. Palpation of the abdominal wall will evoke significant pain and when a vaginal examination is done, movement of the cervix will produce excruciating pain, especially on the side of the affected fallopian tube.
Surgical Treatment: In questionable situations laparoscopy is usually performed for diagnostic purposes. If an ectopic pregnancy is in fact detected, a small longitudinal incision over the tubal pregnancy will allow its removal, without necessitating removal of the tube. (linear salpingectomy). Bleeding points on the fallopian tube can usually be accessed directly and appropriately ligated (tied) via the laparoscope. Sometimes the damage to the fallopian tube has been so extensive that the entire tube will require removal.
On occasions where very severe intra-abdominal bleeding heralds a potential catastrophe, a laparotomy (an incision made to open the abdominal cavity) is performed to stop the bleeding post haste. In such cases a blood transfusion is usually required and may be life saving.
Medical Treatment: The introduction of Methotrexate (MTX) therapy for the treatment of ectopic pregnancy has profoundly reduced the need for surgery in most patients. MTX is a chemotherapeutic that kills rapidly dividing cells, such as those present in the “root system” of the conceptus. Extremely low doses of MTX are used to treat ectopic pregnancy. Accordingly the side effects that are often associated with such chemotherapy used for the treatment of other conditions are seldom seen. It is important to confirm that the ectopic pregnancy has not yet ruptured prior to administering MTX.
MTX is given by intramuscular injection. Prior to its administration, blood is drawn to get a baseline blood hCG level. After the injection of MTX the patient is allowed to return home with strict instructions that she should always have someone with her and never be alone in the ensuing week. The concern is that were the patient to be on her own and an intraabdominal bleed were to occur, she might not readily be able to access someone who could get her to the hospital immediately. Instructions are also given to look for early signs that might point towards severe intra-abdominal bleeding such as the sudden onset of severe pain, light-headedness or fainting.
The patient returns to the doctor’s office four days later to check the blood hCG level. Three days later (7 days after MTX), the level is checked again. By this time the hCG level should have dropped at least 15% from the value on day 4. If not, a second MTX injection is given and the blood levels are tested twice weekly until hCG level is undetectable. Once this occurs, vaginal bleeding will usually ensue within a week or two.
It is important to note, especially in cases where more than one embryo or blastocyst has been transferred to the uterine cavity or fallopian tube (as with Tubal embryo transfer –TET/ZIFT), that implantation may occur in two sites simultaneously (i.e. in the fallopian tube as well as inside the uterine cavity). This is referred to as a heterotopic pregnancy. It is therefore important that before administering MTX, which will cause the death and absorption of any early pregnancy, that the physician makes certain that he/she is not dealing with a heterotopic pregnancy. In such cases, surgery is required to treat the tubal ectopic, while every precaution is taken to protect the pregnancy growing within the uterine cavity.
When an ectopic pregnancy occurs following infertility treatment, there is the added advantage that the physician will be on the lookout for the earliest possible signs of trouble. The performance of a vaginal ultrasound within two weeks of a positive blood pregnancy (HCG) test following IVF allows for early detection of the unruptured pregnancy and timely intervention with MTX and/or laparoscopy.
Geoff Sher
Hi Dr. Sher,
I’m 36 with FSH 8 & AMH 0.67 (dropped from 1.22 to 0.67 in 1 year) and have undergone multiple stimulation cycles.
First Attempt: Natural cycle start with Follistim 375 and eventually added Ganirelix. Trigger was 5,000 HCG and Lupron. 4 mature eggs and all arrested after Day 3.
Dr. recommended starting DHEA and CoQ10.
Second Attempt: Started BCP (on Day 3 of cycle); Microdose Lupron Flare Protocol. Active follicle found at baseline (after being on BCP for roughly 18 days). Since I “broke through” the pill, cycle was converted to Estrogen Priming Protocol. I was only on estrogen patches for 4 days before menses began. Antral follicle count at baseline was 22. Began stims with Follistim 375 and Menopur 150, only 3 follicles grew. Triggered with 10,000 HCG and cycle converted to IUI with no success.
Third Attempt: Started BCP again (on Day 1 of cycle); I didn’t break through this time, but cycle was cancelled due to COVID-19.
Fourth Attempt: Started BCP again (on Day 1 of cycle), ultrasound halfway through to ensure no “break through” and unfortunately, I had an active follicle…again. Dr. recommended no longer using BCP.
Fifth Attempt: Co-Flare Protocol where Lupron was started on Day 2 of natural cycle start, followed by Follistim 450 and Menpur 150 and Lupron dosage eventually dropped.
Antral follicle count at baseline was 16. Cycle only yielded 2-3 large follicles. Triggered with 10,000 HCG. Decided to just “try naturally” with no success.
Sixth Attempt: Estrogen Priming Protocol with Ganirelix; Began patches 7 days after ovulation and Ganirelix 8 days after ovulation. I was only on Estrogen and Ganirelix for 4 & 3 days respectively before menses came. I was instructed to take one more last Ganirelix shot on Day 2 of cycle. Antral follicle count at baseline (Day 3) was 18 and estrogen was 19. Began Gonal-F 375 and 150 Menopur. Cycle yielded 4 follicles: 16mm, 2 19mm, and 1 20mm and a couple more around 14-15mm. Triggered with 10,000 HCG.
At retrieval, a total of 4 eggs collected and only 1 was mature. Embryo arrested at Day 3 (Grade 2, 12 cell)
My biggest questions are as follows:
1. Why is my response to stimulation so poor when my antral follicle count is considered normal?
2. Why do I start my menses shortly after being on estrogen patch? It seems like it’s never long enough to properly “prime” the follicles, which I was told should be 8-10 days.
3. Why do I “break through” the pill?
4. Do you believe Menopur is helping or making things worse, considering my first cycle didn’t contain Menopur and that was the only cycle which yielded the most mature eggs?
Thoughts?
Thank you so much!!
1. Why is my response to stimulation so poor when my antral follicle count is considered normal?
A: Very respectfully, I nthink it has to do with the protocols used for ovarian stimulation and their implementation as well as the trigger dosage + timing of hCG.
2. Why do I start my menses shortly after being on estrogen patch? It seems like it’s never long enough to properly “prime” the follicles, which I was told should be 8-10 days.
A: Hard to say. It could be dosage and the type of medication. Personally, I do not think you need estrogen “priming”.
3. Why do I “break through” the pill?
A: You probably need a stronger BCP
4. Do you believe Menopur is helping or making things worse, considering my first cycle didn’t contain Menopur and that was the only cycle which yielded the most mature eggs?
A: Menopur contains equal amounts of LH and FSH. In my opinion, too much LH can lead to over-production of ovarian testosterone which can compromise egg development, especially in women who have diminished ovarian reserve (DOR).
Women who (regardless of age) have diminished ovarian reserve (DOR) have a reduced potential for IVF success. Much of this is due to the fact that such women tend to have increased production, and/or biological activity, of LH. This can result in excessive ovarian male hormone (predominantly testosterone) production. This in turn can have a deleterious effect on egg/embryo “competency”.
While it is presently not possible by any means, to reverse the effect of DOR, certain ovarian stimulation regimes, by promoting excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), can in my opinion, make matters worse. Similarly, the amount/dosage of certain fertility drugs that contain LH/hCG (e.g. Menopur) can have a negative effect on the development of the eggs of older women and those who have DOR and should be limited.
I try to avoid using such protocols/regimes (especially) in women with DOR, favoring instead the use of the agonist/antagonist conversion protocol (A/ACP), a modified, long pituitary down-regulation regime, augmented by adding supplementary human growth hormone (HGH). I further recommend that such women be offered access to embryo banking of PGS (next generation gene sequencing/NGS)-selected normal blastocysts, the subsequent selective transfer of which by allowing them to capitalize on whatever residual ovarian reserve and egg quality might still exist and thereby “make hay while the sun still shines” could significantly enhance the opportunity to achieve a viable pregnancy
Please visit my new Blog on this very site, www. SherIVF.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 Approach
•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)
•Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
•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?
•Blastocyst Embryo Transfers Should be the Standard of Care in IVF
•Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting 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.
•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
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•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
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
•IVF Egg Donation: A Comprehensive Overview
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ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.
If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).
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Geoff Sher
Dear Dr. Sher,
My name is Naita and i live in Australia (Perth).
I first got pregnant when i was 27 years old (one month after i got married) and i heard a heartbeath tick at 5weeks and 4 days. Just one week after i started spotting which switched to blood and i misscaried in the toilet (July 2017).
I then got pregnant again 2 months later and again we found a heartbeath around 6w +2, but i misscaried just 3 days later in the toilet (November 2017).
I got pregnant the third time in February 2018 and found a heartbeath at 6w +4 days, but found out on a ultrasound a few weeks after (should have been 11w) that it stoped at 6w 6+. I then hade my first D&C surgery to remove it for genetic testing (April 2018). The repport came back showing that chromosome 16 was a thriomsy and not a pair. Which the Dr. told me is the most Common reason to misscary and i will have a baby next time. I was threathed for uterus infection after the surgery. During this pregnancy i was taking baby asprin and 200mg 3times a Day progesterone passaries.
In November 2018 i had a biochemical pregnancy which My period was only late for 6 days but i had positiv + on the hometest only!
By this time we started to do ALL test that they could offer, only to found out that everything was showing normal and My AMH results was 16 Which they told me is a Good Number. We even did the karyotype blood and its all fine. We even did a sperm DNA analasys for My husband and that came back fine too.
Then i got pregnant again February 2019 and started to take baby asprin and same amount of progesterone when i got My +. On the ultrasound it showed i had TWIN SAC but No embryo. We decided to do another ultrasound a week later to see IF something would come Up. I started to feel bit sick in mornings and was hoping everything was fine. We came back for the ultrasound and it had No embryos Still, One sac was 5w + and the other One was 7w+. My gynecologist suggested i do another d&c since My Body was not rejecting it off by itself again. On the chomosonal testing it came back with No info since there where No embryos detected.
My previous pregnancy was ended in miscarrige again September 2019, again stoped at 6w + . And we had a d&c done, but the hospital Called and apologized that there was not enough tissue sent of to be able to test for chromosonal abnormalities and this left me heartbroken as i didnt want to do my 3dr d&c but decided to go ahead only to found out what went wrong again. Please NOTE, I had My 3 d&c and Also 3rd time of uterus infection after surgery!
By this time i Saw a 5th gp and my second fertility specialist here in WA (i Saw the top 2 specialist in WA). The 5th gp, found that i had Ureaplasma infection and Said she thinks this might be the issue since she had cases of women having recurrent miscarrige because of it. But the WA fertility percialist Said it has nothing to do with pregnancies and that My case is “bad luck” and a case of My uterus not rejecting bad eggs and that i should do IVF with PGS.
By this time i got threathed for Ureaplasma (November 2019) and had myself tested for NK leva in My blood at a immunologist specialist. The levels where normal (February 2020). I also did a siline infusion to se if i had svara from the d&c and everything looked normal.
I also got my case look at from specialist doctors at Kind Edward hopsital here in Perth, Which is a hospital only for woman with pregnancy complications or high risk. And they recommended to do IVF with PGS. But i asked since i can concive so easy myself why is this nessesery and Will i Keep it if i do this expensive genetic testing and it shows 46 chromosoms. They Said nothing is 100% and it left me angry think after everything, why would i put myself true something that Will give me almost same chance as natrualy conciving.
I am seeing an immunologist at a hospital next week 17 sept due to, When i was pregnant the last Time in sept i had a allergic rection to asprin (but was fine the other two beforehand).
On of the specialist in ivf clinic.said to take Metformin (Helps ovulating he said) but i had diarriea and stoped after only 3 days as i could not understand why i got it in the first place since i ovulate every month. He Also told me to take thyroxine as My thyroid was 2.5 (he wants it to be 2.0 before i get pregnant) and i started to have an ongoing rash on my arms for almost 4 weeks after i stoped taking thyroxin (i was not pregnant, November 2019) .
I have not got pregnant since My last miscarrige as all the reaction from medications after My d&c freaked me out since i was fine with Them all previosuly pregnancies.
Please, i cant find anyone in Perth to help me figure if i have an issue that is making me misscary or IF it can be the Ureaplasma that acctually was the bad Guy in it all.
I know there are some ivf clinics in Sydney that test for immunology presective but during this Times with Corona viruset we can not fly over since the boarder is Closed.
Please, can you give me your professional opinion on my case and maybe some advice for the future pregancies and maybe even if somehow i can take some other blood work i have not done here in Perth (since i am seeing an immunologist specialist) somehow?
Thank You!
Kind Regards
Naita
Hi Dr. Sher,
I had my Day 5 embryo transfer (frozen) on August 24, 2020. I had my first blood test on September 3rd (10 days later) and my hcg level was 173. I’m not sure how to interpret this… my doctor said I’m pregnant and my levels are higher than average! Does this mean mutiples?? I’m just so happy to be pregnant but can’t stop obsessing over if there’s more than 1!!
Your level is good but it is not possible to extrapolate to singleton versus multiple. In addition, the most important issue pertaining to the level, is the rate of the increase. You should repeat the test in 2 days. It should double. Ultimately, it will take an US at the 6th to 7th week to determine whether you have a viable pregnancy.
Geoff Sher
Dear Doctor Sher
I would be very grateful for your advice. I have tested positive for Ureaplasma Urealyticum (both urine test & urethra swab). I was prescribed Erythromycin by my general practitioner (3 times a day for 7 days). I have no symptoms at the moment (infact I didn’t even know I had it, or what it was until yesterday). I read about estimates that 70% of the female population is assumed to have it. I have an FET transfer scheduled late September. As yet, I have not started taking the antibiotics because I’m worried that they may mess with the bacterial “homeostasis” In my body and hence negatively impact the FET chances of success. It usually takes my body weeks to recover from antibiotics :(. Additionally, I read that there is a high antiobiotic-resistance in Ureaplasma Urealyticum, which coukd potentially render the antibiotic treatment as having been a waste. Is a positive Ureaplasma Urealyticum test despite no symptoms detrimental to FET chances? If so, what are the chances that antibiotics will help without causing any negative impact themselves? I’m a bit at a loss what to do, and hence have done nothing in the interim.
Sincerest thanks for all you do and for helping all of us! You are wonderful!!
Kindest regards,
Kate
Ureaplasma urealyticum is a bacterium that belongs to the mycoplasma family. It can be detected in the reproductive tract of as many as 40% of individuals (male and female). Ureaplasma probably does not prevent normal conception in the majority of cases, because by and large, the uterine cavity remains free of such pathogenic bacteria even in women whose cervical mucous cultures positive for the organism. However, when present in the woman’s cervical secretions, the organism can be unintentionally dragged into the uterine cavity through introduction of a catheter into the uterus at the time of embryo transfer (ET) or intrauterine insemination (IUI). Molecular biologists have shown that contamination of rapidly growing cell cultures, by this organism and its close “relative”, mycoplasma hominis rapidly destroys such cells. The implanting embryo is indeed an example of an organism that comprises rapidly growing cells in a biological culture medium (the uterine lining), and as such, the cells of the trophoblast that form the “root system” of the embryo are vulnerable to intrauterine infection with Ureaplasma. However, even if the uterine cavity were to become infected, the infection willl be purged with the shedding of the infected lining at the time of the next menstruation.
While , aside from a non-specific vaginal discharge, infection with Ureaplasma rarely produces symptoms in the woman, it sometimes causes symptomatic prostatitis or epydidimitis in men. Although ureaplasma can be transmitted from one partner to the other by sexual intercourse, it may also be acquired by other means, since a large percentage of couples in monogamous relationships will culture positive for the organism. It is very difficult for the organism to grow in the laboratory. Accordingly, the reproductive secretions of both partners should be evaluated (sperm and cervical mucus) individually. Successful culturing of ureaplasma requires a specialized media in which the specimens can be transported safely from the physician’s office to the microbiology laboratory.
If both partners culture negative, we can assume that there is no infection present. However, if one partner cultures positive and the other negative, we would err on the side of caution, by assuming that the negative result was caused by the difficulty in culturing the organism. When ureaplasma is detected in the reproductive secretions of either partner, both should be treated concurrently with the appropriate antibiotic (doxycycline, zithromax, erythromycin, ciprofloxin, or metronidazole; cleomycin).
Unfortunately, in approximately 30-40% of couples infected ureaplasma urealyticum, the bacteria will have built resistance to mainstay traditional antibiotics such as tetracyclines (e.g. doxycycline) and erythromycin (e.g. Zythromax) derivatives. In such cases, ciprofloxin or metronidazole (Flagyl) therapy might be needed. This is the reason that we prefer to document cure by reculturing each partner prior to beginning ovarian stimulation for an IVF cycle.
Several authors have shown a difference in pregnancy rates among patients with ureaplasma infection who were treated with antibiotics and those who were not. Other reports have not been able to identify an effect on outcome from ureaplasma infection. Thus, until the final verdict is in regarding the roll of ureaplasma with regard to its effect on IVF implantation, we prefer to err on the side of caution and ensure that this organism is absent in cervical secretions and semen before transferring embryos. To this end, my patients all receive prophylactic antibiotic therapy around the time of embryo transfer. This is administered as oral ciprofloxin. A day or two prior to embryo transfer, vaginal cleomycin suppositories are added.
Geoff Sher
I have been trying to conceive for a year and recently had an HSG done. A small hydrosalpinx was found on one tube, while the other was still open. Would you recommend having both tubes removed prior to IVF embryo transfer, or just removal of the one tube that has the hydrosalpinx? And is it okay to get this done after egg retrieval, but prior to embryo transfer?
Ligation and removal of the affected tube(s).
Geoff Sher