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.
Hello Dr Sher. May I please ask: how is it possible for a doctor to tell the difference between an hemorrhagic cyst and a corpus luteum cyst on ultrasound? I take it both can have blood clots inside right? And can a corpus luteum cyst be painful? Thank you for answering our questions. Kate
Note: by corpus luteum cyst I mean the normal corpus luteum. I am CD21 with a some structure causing ovarian pain.
A hemorrhagic corpus luteum tends to be cystic (enlarged) and be associated with symptoms. Otherwise it is not always possible to distinguish with confidence…in my opinion.
Geoff Sher
Please doctor I was diagnosed with uterus fibroids and it is located outside my womb. Can it affect me in case l try ivf?
It depends on how many, how large they are whether there might be others that are thatb have gone undetected and are protruding into the uterine cavity and whether they are pedunculated (on a stem) or not.
Fibroids or leiomyomas are non-malignant muscle tumors that grow in the uterine wall. They can be found in about one out of every five (1:5) women >30Y of age. Fibroids are far more prevalent in African Americans and women and less frequent in other ethnic groups (i.e. Caucasians and Asians).
Fibroids, enlarge and/or distort uterine configuration. They can produce symptoms such as heavy, painful and prolonged menstrual periods. Other symptoms include pain with intercourse, backache, severe abdominal pain when large fibroids run out of blood supply or when superficial fibroids on a stem (pedunculated) undergo twisting (torsion). Sometimes fibroids will protrude into the uterine cavity, cause severe cramping and bleeding and so irritate the uterine lining as to compromise embryo attachment (anatomical implantation dysfunction). Women with fibroids are also at greater risk of miscarriage, premature delivery, malposition of the baby (mandating cesarean delivery) and an increased risk of bleeding after birth (post-partum hemorrhage)
Diagnosis can be made by one or more of the following symptoms/presentations: Symptomatology, pelvic examination pelvic ultrasound, hysterosalpingogram (HSG), sonohysterogram (HSN), CT-scan or MRI..
Fibroids are classified as:
•Submucosal: Here the fibroid grows just under the lining of the uterine cavity (mucosa) or protrudes into the uterine cavity. They might mold into the underlying uterine muscle (sessile) or be on a stalk (pedunculated). Submucosal fibroids can change the shape of the uterine cavity, irritate the lining and prevent implantation, cause miscarriage. These lesions must be removed in their entirety prior to undertaking embryo transfer, usually hysteroscopically. (see below)
•Subserosal: – Here the tumors grow under the outer layer (serosa) of the uterus. These fibroids will not compromise implantation, but if they are large, causing severe pain, and especially if they are multiple, pedunculated and thus at risk of undergoing torsion (twisting) the3y should be removed, usually laparoscopically. (See below).
•Intramural: – when the fibroids develop within the muscular wall of the uterus. This is the commonest presentation. Unless they are large and multiple and do not encroach on the uterine cavity, they can be left alone Surgical removal is usually by laparoscopy or laparotomy/abdominal open incision (See below)
The uterus is composed of a thick layer of smooth muscle (myometrium) surrounding the endometrial lining into which the embryo implants and which serves to protect and nourish a growing pregnancy. These tumors are rarely malignant (see below). Fibroid tumors, even large ones, can occur without producing any symptoms at all.
For the most part, only those fibroids that impinge upon the uterine (endometrial) cavity (submucosal) affect fertility. Exceptions include large fibroids in the muscle wall of the uterus (intramural) that can block the openings of the fallopian tubes as they enter the uterus, and where multiple fibroids cause abnormal uterine contraction patterns.
In some cases multiple uterine fibroids may so deprive the uterine lining (endometrium) of blood flow, that the delivery of estrogen to the endometrium is curtailed to the point that the lining cannot thicken sufficient to support a pregnancy. This can result in early 1st trimester (prior to the 13th week of pregnancy) miscarriages. Large or multiple fibroids, by curtailing the ability of the uterus to stretch in order to accommodate the spatial needs of a rapidly growing pregnancy, may precipitate 2nd trimester (beyond the 13th week) miscarriages and/or trigger the onset of premature labor.
Sizable fibroid tumors are usually easily identified by simple vaginal examination. However, even the smallest fibroid can be identified by transvaginal ultrasound. Sometimes it is difficult to tell if the fibroid is impinging on the uterine cavity. In such cases, a hysteroscopy (where a telescope like instrument, inserted via the vagina into the uterine cavity) or a sonohysterogram where injected fluid, distends the uterine cavity allowing for examination of its inner configuration can help distinguish between intramural and submucosal fibroids. CT scan and MRI can also be used to distinguish between fibroid tumors and another condition that also involves affects the uterine muscular wall, known as adenomyosis. This condition is characterized by endometrial tissue growing deeply into the uterine wall.. Given the often-diffuse nature of adenomyosis, it can be very difficult to remove surgically. This contrasts with fibroid tumors, which are well defined and are usually easily removed.
Surgical Treatment: The mainstay for the treatment of fibroid tumors is surgical removal (myomectomy). Small, asymptomatic fibroids that do not impinge upon the endometrial cavity will usually not require treatment other than observation and vigilance. Large fibroids and submucosal fibroids should be removed prior to starting fertility treatments such as In Vitro Fertilization (IVF) in order to decrease the chance of implantation failure, miscarriage, pregnancy complications and premature labor. Intramural and subserosal fibroids are readily removable by laparoscopic resection or via an abdominal incision. The former allows for a more rapid convalescence and is ideal for the removal of small and accessible superficial fibroid tumors, while the latter approach is preferred for treating larger and less accessible fibroids.
Myomectomy can affect fertility in several ways. If the endometrial cavity is entered during the surgery, there is a possibility of post adhesions forming within the uterine cavity. This should always be checked by the performance of a hysteroscopy or through a sonohysterogram, prior to beginning fertility treatment. Because myomectomy can be bloody, there is a high likelihood of post-operative abdominal adhesion formation, which could bind down or encase the ovaries, preventing the release of the eggs, or block the ends of the fallopian tubes. For this reason, it is important that myomectomies be formed only by accomplished surgeons, who are familiar with techniques to limit blood loss and prevent adhesion formation.
Regardless of whether the laparoscopic or abdominal approach is employed, adequate closure of the uterine wall is essential in order to reduce the subsequent risk of uterine rupture during pregnancy or labor. This is one of the main arguments used against the use of laparoscopic removal of large, multiple or remotely situated fibroids. While laparoscopic myomectomy requires but a few days (at most) for post-operative convalescence, abdominal myomectomy usually requires 6-8 weeks of recovery time. When myomectomy necessitates or results in the uterine cavity being entered (purposefully or inadvertently), it should always be followed up with a “2nd look” hysteroscopy to rule out scar tissue formation, which occurs frequently in the presence of submucosal fibroids.
Uterine polyps (and in some cases, also submucosal fibroids), can usually be removed hysteroscopically (through the vagina). This eliminates the need for abdominal surgery and greatly reduces the recovery time. Hysteroscopic surgery is only useful if the majority of the fibroid protrudes into the endometrial cavity, ensuring that the tumor defect will not be too large. This surgery is often done under laparoscopic guidance, to reduce the risk of uterine perforation. After hysteroscopic surgery it is often advisable to prescribe cyclical hormonal therapy for a few months to encourage regeneration of the endometrial lining over the area of tumor defect and healing of the uterine muscle. A 2nd look hysteroscopy should be performed a few months later in all cases, to rule out scar tissue formation even if it means delaying or deferring the initiation of definitive fertility treatment.
Medical Treatment: The growth of fibroid tumors is estrogen-dependent. Thus when a woman enters menopause and stops making female hormones, fibroids tend to shrink in size on their own. Conditions that mimic menopause can also reduce the size of fibroid tumors. The most common of theses treatment is with a medication such as leuprolide acetate (Lupron), which shuts off the communication of the brain with the ovaries, preventing hormone production. However, this type of medication can only be taken for a limited period (usually 6 months) and once the medication is stopped the fibroids will usually regain their original size within a few months. The medication is therefore only a “temporary fix,” used mostly to decrease the size of large fibroids in order to make their ultimate surgical removal easier, or to help a woman bridge the gap until spontaneous menopause sets in. For the majority of women there is no major benefit from Lupron therapy prior to surgery.
Embolization of Fibroid Tumors: Myomectomy always carries the small (although infrequent) risk that severe, uncontrollable intra-operative bleeding could require the performance of a hysterectomy (complete removal of the uterus) as a life saving measure. Moreover, some women are poor candidates for surgery. This is where a new procedure known as embolization comes in. Embolization is a procedure in which small particles are injected into the arteries of the uterus under radiological guidance to shut off the blood supply to the fibroids, in the hope that they will “shrink” and perhaps, even disappear.
Embolization is relatively new to the field of gynecology and little is known about its potential effects on future fertility. We are concerned that in the process of shutting off the blood supply to the uterus, it will permanently so reduce endometrial blood flow, as to compromise embryo implantation. For this reason, I do not currently recommend this therapy for women who still wish to conceive and carry a baby in their uterus. At present, it seems best suited for symptomatic women who are finished with their childbearing or who are planning to use a gestational surrogate.
Malignant Change in Fibroid Tumors: Fibroids rarely undergo malignant change. The reported incidence is less than 1 in 2000 cases. Fibroids usually grow very slowly (over a number of years). However, when growth occurs rapidly over a month or two, especially in older women who have large fibroids, it should raise the suspicion of this very rare but extremely serious complication.
Geoff Sher
hi dr Sher
Can we use femoston( white one) and crinone vaginal suppositories together? If not what is the best interval for taking them
Both?
Best regard
Dom
Yes you can!
Geoff Sher
reply
I’m 43 years old and recently had genetic testing done on six embryos, 5 abnormal & 1 inconclusive (testing again-re biopsy). Can you explain why you would not transfer an XYY embryo? I have six frozen embryos: embryo #1 XY male (Abnormal: +1), embryo #2 XX female (Abnormal: -8), embryo #3 XX female (Abnormal: +1, +8), embryo #4 XY male (Abnormal: -7, -21), embryo #5 (Abnormal: XYY) and embryo #6 (Retesting). I’m trying to weight my options with my hubbie since my RE is reluctant in transferring any abnormal embryos. I appreciate your feedback. I reached out to a genetic counselor as well. Thank you for your help.
Be blessed, J
I would use embryos +1 and -8. The XXY could also be transferred.However, I think the chance of this being a “mosaiac” could be lower. Notwithstanding CVS or amniocentesis should be done if pregnancy ensues.
Geoff Sher
Geoff Sher
Hi Dr Sher
It’s been a very long road for me. 7 yrs ttc!! So please please help me.
I have finally made one mosaic embryo. I had three rounds of IVF and produced 11 day 5 embryos and this is th best I have now.
I have had 5 laporscopies last one to remove hydrosplaix and right tube is gone.
Symptoms are mostly pain free though.
I have stage 1 last November 2017.
I have immune issues, high nk cells and cytokines 47. I’ve taken Humira and LIT with mo movement in markers.
I have borderline MTHR. Rest of my profile is good.
No male factors.
This will be my first and more than likely only transfer at the age of 43!!!
Please GOD make this work. I’m terrified.
How do I ensure the best possible transfer without spending months testing and retesting immunes?
My last two retreivals consultant said my uterus didn’t look good. But was unable to clarify. He said usually when he puts int the probe to retrieve eggs it ‘slides in’ however with me it was hard and tough…. I don’t know what this means. Neither did he.
I have a complex cyst that has grown from all the recent IVF. It’s under 2mm. So they are unconcerned.
Would you recommend an era test at this stage?
Or a uterine wash? Glue? Etc?
I see you have used dexamethasone, is that the same as prednisone?
Should I try dexa?
Are intralipids better than LIT/Humira
My mosaic embryo…. is it really only 30% this is so low!
They have traces of trisomy 4 in this embryo. That’s it.
It was NGS tested.
My amh is roughly 4.5
I don’t have pics, low fish or anything..
How do I give myself the best possible chance of success?
I’m am quite run down from all the drugs so far this year.
Looking forward to hearing your feedback
Thanking you kindly.
At 44y, your only good chance would be using an egg donor.Good luck on the transfer. AS far as the immunologic issues are concerned, consider the following.
Unless tests for immunologic implantation dysfunction (IID) are performed correctly and conducted by a one of the few reliable reproductive immunology reference laboratory in the United States, treatment will likely be unsuccessful. . In this regard it is most important that the right tests be ordered and that these be performed by a competent laboratory. There are in my opinion only a handful of reliable Reproductive Immunology Laboratories in the world and most are in the U.S.A. Also, it is my opinion that far too often, testing is inappropriate with the many redundant and incorrect tests being requested from and conducted by suboptimal laboratories. Finally for treatment to have the best chance of being successful, it is vital that the underlying type of IID (autoimmune IID versus alloimmune) be identified correctly and that the type, dosage, concentration and timing of treatments be carefully devised and implemented.
Who Should Undergo IID testing?
When it comes to who should be evaluated, the following conditions should in always raise a suspicion of an underlying IID, and trigger prompt testing:
•A diagnosis of endometriosis or the existence of symptoms suggestive of endometriosis (heavy/painful menstruation and pain with ovulation or with deep penetration during intercourse) I would however emphasize that a definitive diagnosis of endometriosis requires visualization of the lesions at laparoscopy or laparotomy)
•A personal or family history of autoimmune disease such as hyper/hypothyroidism (as those with elevated or depressed TSH blood levels, regardless of thyroid hormonal dysfunction), Lupus erythematosus, Rheumatoid arthritis, dermatomyositis, scleroderma etc.)
•“Unexplained” infertility
•Recurrent pregnancy loss (RPL)
•A history of having miscarried a conceptus that, upon testing of products of conception, was found to have a normal numerical chromosomal configuration (euploid).
•Unexplained IVF failure
• “Unexplained” intrauterine growth retardation due to placental insufficiency or late pregnancy loss of a chromosomally normal baby
What Parameters should be tested?
In my opinion, too many Reproductive Immunologists unnecessarily unload a barrage of costly IID tests on unsuspecting patients. In most cases the initial test should be for NK cell activation, and only if this is positive, is it necessary to expand the testing.
The parameters that require measurement include:
oFor Autoimmune Implantation Dysfunction: Autoimmune implantation dysfunction, most commonly presents with presumed “infertility” due to such early pregnancy losses that the woman did not even know she was pregnant in the first place. Sometimes there as an early miscarriage. Tests required are: a) blood levels of all IgA, IgG and IgM-related antiphospholipid antibodies (APA’s) directed against six or seven specific phospholipids, b) both antithyroid antibodies (antithyroid and antimicrosomal antibodies), c) a comprehensive reproductive immunophenotype (RIP) and, c) most importantly, assessment of Natural Killer (NK) cell activity (rather than concentration) by measuring by their killing, using the K-562 target cell test and/or uterine cytokine measurement. As far as the ideal environment for performing such tests, it is important to recognize that currently there are only about 5 or 6, Reproductive Immunology Reference Laboratories in the U.S capable of reliably analyzing the required elements with a sufficient degree of sensitivity and specificity (in my opinion).
oFor Alloimmune implantation Dysfunction: While alloimmune Implantation usually presents with a history of unexplained (usually repeated) miscarriages or secondary infertility (where the woman conceived initially and thereupon was either unable to conceive started having repeated miscarriages it can also present as “presumed” primary infertility. Alloimmune dysfunction is diagnosed by testing the blood of both the male and female partners for matching DQ alpha genes and NK/CTL activation. It is important to note that any DQ alpha match (partial or complete) will only result in IID when there is concomitant NK/CTL activation (see elsewhere on this blog).
How should results be interpreted?
Central to making a diagnosis of an immunologic implantation dysfunction is the appropriate interpretation of natural killer cell activity (NKa) .In this regard, one of the commonest and most serious errors, is to regard the blood concentration of natural killer cells as being significant. Rather it is the activity (toxicity) of NK cells that matters as mentioned. Then there is the interpretation of reported results. The most important consideration is the percentage of target cells “killed” in the “native state”. In most cases a level of >10% killing should be regarded with suspicion and >12% overtly abnormal. In my opinion, trying to interpret the effect of adding IVIG or Intralipid to the sample in order assess whether and to what degree the use of these products would have a therapeutic benefit is seriously flawed and of little benefit. Clinically relevant NK cell deactivation can only be significantly effected in vivo and takes more than a week following infusion to occur. Thus what happens in the laboratory by adding these products to the sample prior to K-562 target cell testing is in my opinion likely irrelevant.
There exists a pervasive but blatant misconception on the part of many, that the addition of Intralipid (IL) /immunoglobulin-G IVIG) can have an immediate down-regulatory effect on NK cell activity. This has established a demand that Reproductive Immunology Reference Laboratories report on NK cell activity before and following exposure to IVIG and/or IL. However, the fact is that activated “functional” NK cells (NKa) cannot be deactivated in the laboratory. Effective down-regulation of activated NK cells can only be adequately accomplished if their activated “progenitor/parental” NK cells are first down-regulated. Thereupon once these down-regulated “precursor” NK cells are exposed to progesterone, they will begin spawning normal and functional NK cells, which takes about 10-14 days. It follows that to assess for a therapeutic response to IVIG/IL therapy would require that the patient first be treated (10-14 days prior to embryo transfer) and thereupon, about 2 weeks later, be retested. While at 1st glance this might seem to be a reasonable approach, in reality it would be of little clinical benefit because even if blood were to be drawn 10 -14 days after IL/IVIG treatment it would require an additional 10 days to receive results from the laboratory, by which time it would be far too late to be of practical advantage.
Neither IVIG nor IL is capable of significantly suppressing already activated “functional NK cells”. For this to happen, the IL/IVIG would have to down-regulate progenitor (parent) NK cell” activity. Thus, it should be infused 10-14 several prior to ovulation or progesterone administration so that the down-regulated “progenitor/precursor” NK cells” can propagate a sufficient number of normally regulated “functional NK cell” to be present at the implantation site 7 days later. In addition, to be effective, IL/IVIG therapy needs to be combined with steroid (dexamethasone/prednisone/prednisolone) therapy to down-regulates (often) concomitantly activated T-cells.
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation (COS)
•The Fundamental Requirements for Achieving Optimal IVF Success
•Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
•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)
•Intralipid (IL) Administration in IVF: It’s Composition; how it Works; Administration; Side-effects; Reactions and Precautions
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .
*FYI
The 4th edition of my newest book ,”In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoffrey Sher MD
Np, I totally understand. Thank you again for your help.
Best, J