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.
I would like to know what Pelvic Tuberculosis it.
Tuberculosis is caused by a bacterium known as mycobacterium tuberculosis. It is primarily an infectious process that involves the lungs it is capable of spreading elsewhere (extra-pulmonary TB) It can spread to the woman’s reproductive tract and cause infertility. The commonest site is the Fallopian tubes. From there it can spread to uterine lining (endometrium) and to the ovaries. The lower genital tract (cervix, vagina and vulva can also be affected but this is very rare.
Contrary to popular belief, TB does not spread by surface contact (sharing of utensils or clothes or through touch). Rather it spreads by droplet contamination when you come into contact with an individual who has pulmonary disease, who coughs, spits or sneezes and you come in contact with mycobacterium Tuberculosis. There is a rare form of TB caused by mycobacterium tuberculosis bovis, that spreads through ingestion of infected milk but this usually affects bowel and bone, not the reproductive tract.
While pelvic tuberculosis is a very common cause of infertility in developing countries and in Asia (India in particular), it so rarely causes of infertility in the United States, that the diagnosis is often overlooked here. However, there is good reason to believe that the condition is on the rise in the United States as a result of the influx of immigrants from Asia and other third world countries where tuberculosis is rampant.
Pelvic tuberculosis is often a master of disguise….a silent disease. It may be present for 10 to 20 years without producing any symptoms – the woman remaining in apparent excellent health. Infertility is often one, and sometimes the only, reason that women investigate for the presence of the condition.
Pelvic tuberculosis usually presents with one or more of the following signs and symptoms:
•Pelvic pain, dysmenorrhea (pain with menstruation), dyspareunia (pain with intercourse), chronic lower abdominal pain or discomfort, and chronic back pain
•Absent or irregular menstruation,
•Abdominal distention, usually due to ascites (collection of free fluid in the abdominal-pelvic cavity
•Tuberculosis-related infertility is most commonly due to tuberculous salpingitis (tubal inflammation) which occurs in 75% of cases, ovulation dysfunction that often presents with absent, excessive or non-cyclical menstruation, largely attributable to ovarian involvement (40% of cases) and uterine (endometrial) tuberculosis (30%)
•Sometimes (albeit rarely), local tuberculous lesions may appear on the external genitalia, cervix, and/or vagina.
Diagnosis:
The diagnosis is usually based upon a multitude of signs, symptoms and special tests, there being no magic bullet for diagnosing pelvic tuberculosis.
•Clinical suspicion: Evidence of concomitant, pulmonary tuberculosis, the detection of calcifications on pelvic X-rays, a typical tubal pattern on hysterosalpingogram (dye X-ray test)
•Findings at laparoscopy or laparotomy and the subsequent pathologic examination of biopsy material obtained during these procedures
•Blood tests such as a differential blood count and erythrocyte sedimentation rate
•Microscopic and bacteriologic examination is the primary method for diagnosing pelvic tuberculosis:
•Polymerase chain reaction (PCR) done on biopsied material (usually from a defined tuberculous lesion or from uterine curettings.
1.Most commonly a dilatation and curettage (D&C) of the uterus is performed a few days prior to menstruation. The surgeon takes care to avoid using an antiseptic to clean the vagina and cervix while preparing for the D&C;, lest the antiseptic kill any tuberculous bacilli present in the specimen thereby rendering a falsely negative culture result. Instead a physiologic salt solution is used to cleanse the operative field. Upon collection, the specimen of uterine curetings is immediately divided into two parts. The first is placed in a physiologic salt solution and expeditiously delivered to the bacteriologic lab for culturing. A specialized culture medium (e.g., Loewenstein Jensen medium) is used for this purpose. Some of the curettings are also used for Guinea pig inoculation. While menstrual products can also be cultured, this approach is less effective. The second portion of the specimen is fixed and then stained for the detection of the acid-fast Bacillus, mycobacterium tuberculosis. The Ziel Nielsen stain is one of the methods used.
2.Biopsy specimens of local lesions and endometrial curettings can of can also be subjected to histopathologic examination, culture and guinea pig inoculation
3.PCR: analysis: . PCR is a molecular test, which”
Even in the presence of established tuberculosis, histopathologic examination will only be positive about 50% of the time. Cultures, although more reliable, can also yield false-negative results. And while PCR analysis, conducted under ideal conditions is a highly sensitive and specific method for the detection of the target genes specific to Mycobacterium tuberculosis and has a high positive predictive value, “false positive” results can occur Accordingly, it is often necessary to repeat such tests several times if the diagnosis is strongly suspected.
Treatment
Treatment of TB primarily directed towards the eradication of the infection by means of specific chemotherapeutics such as Para-amino-salicylic acid (PAS), isoniazid (INH), rifampicin (Rifampin) and streptomycin derivatives.
Given the severity and intractability of fallopian tube-TB, natural conception is very unlikely. Pelvic surgery (other than to remove distended or infected lesions and damaged fallopian tubes) has little therapeutic benefit. Provided that the tuberculous inflammatory process has not totally destroyed the basal uterine endometrium (lining) , leaving it capable of responding adequately to estrogen and progesterone, , in vitro fertilization (IVF) following protracted successful anti-bacterial treatment is the only rational method of treating infertility associated with pelvic tuberculosis.
Hope that helps!
Geoff Sher
Dr Sher,
A few more questions for you:
1. After two chemical pregnancies we are doing another cycle with PGS testing. Should we also do karyotyping or is PGS enough?
2. What dose of Lovenox do you recommend (just DVT prophylaxis dose or full anticoagulation?)
3. What thrombophilia work up do you recommend. Is antiphospholid antibody and MTGFR enough to test for? Would you change the Lovenox dose based on a positive result?
Thank you so much!
Rachel
PGS testing involves embryo karyotyping.
As for the dosage of Lovenox ..you need to discuss this with your RE.
St the same time ask him to draw your blood for a Thrombophilia work-up. That will include MTHFR.
Geoff Sher
Hello
I have seen your video re eggs
I have done an ivf but unfortunately stopped at 6 weeks they said my lining was too thin
Is that a cause or what can I do to prevent this to happen again
Will acupuncture help
Thanks
About seventeen years ago, after reporting on the benefit of vaginal Sildenafil (Viagra) for to women who had implantation dysfunction due to thin endometrial linings I was proud to announce the birth of the world’s first “Viagra baby.” For those of you who aren’t familiar with the use of Viagra in IVF, allow me to provide some context.
It was as far back as 1989, when I first published a study that examined the correlation between the thickness of a woman’s uterine lining (the endometrium), and the subsequent successful implantation of embryos in IVF patients. This study revealed that when the uterine lining measured <8mm in thickness by the day of the “hCG trigger” (in fresh IVF cycles), or at the time of initiating progesterone therapy (in embryo recipient cycles, e.g. frozen embryo transfers, egg donation-IVF etc.) , pregnancy and birth rates were substantially improved. Currently, it is my opinion, that an ideal estrogen-promoted endometrial lining should ideally measure at least 9mm in thickness and that an endometrial lining measuring 8-9mm is “intermediate”. An estrogenic lining of <8mm is in most cases unlikely to yield a viable pregnancy.
A “poor” uterine lining is usually the result of the innermost layer of endometrium (the basal or germinal endometrium from which endometrium grows) ) not being able to respond to estrogen by propagating an outer, “functional” layer thick enough to support optimal embryo implantation and development of a healthy placenta (placentation). The “functional” layer ultimately comprises 2/3 of the full endometrial thickness and is the layer that sheds with menstruation in the event that no pregnancy occurs.
The main causes of a “poor” uterine lining are:
1.Damage to the basal endometrium as a result of:
a.Inflammation of the endometrium (endometritis) most commonly resulting from infected products left over following abortion, miscarriage or birth
b.Surgical trauma due to traumatic uterine scraping, (i.e. due to an over-aggressive D & C)
2.Insensitivity of the basal endometrium to estrogen due to:
a.Prolonged , over-use/misuse of clomiphene citrate
b.Prenatal exposure to diethylstilbestrol (DES). This is a drug that was given to pregnant women in the 1960’s to help prevent miscarriage
3.Over-exposure of the uterine lining to ovarian male hormones (mainly testosterone): Older women, women with diminished ovarian reserve (poor responders) and women with polycystic ovarian syndrome -PCOS tend to have raised LH biological activity.. This causes the connective tissue in the ovary (stroma/theca) to overproduce testosterone. The effect can be further exaggerated when certain methods for ovarian stimulation such as agonist (Lupron/Buserelin) “flare” protocols and high dosages of menotropins such as Menopur are used in such cases.
4.Reduced blood flow to the basal endometrium:
Examples include;
a.Multiple uterine fibroids - especially when these are present under the endometrium (submucosal)
b.Uterine adenomyosis (excessive, abnormal invasion of the uterine muscle by endometrial glands).
“The Viagra Connection”
Treatments such supplementary estrogen therapy, aspirin administration and/or administration of high dosage gonadotropin fertility drugs, aimed at improving endometrial development have all yielded disappointing results.
It was in the 90’s that Sildenafil (brand named Viagra) was gaining popularity as a treatment for erectile dysfunction. The mechanism by which it acted was through increasing penile blood flow through increasing nitric oxide activity. This prompted me to investigate whether Viagra administered vaginally, might similarly improve uterine blood flow and in the process cause more estrogen to be delivered to the basal endometrium and thereby increase endometrial thickening. We found that when Viagra was administered vaginally it did just that! However oral administration was without any significant benefit in this regard. We enlisted the services of a compound pharmacy to produce vaginal Viagra suppositories. Initially, four (4) women with chronic histories of poor endometrial development and failure to conceive following several advanced fertility treatments were evaluated for a period of 4-6 weeks and then underwent IVF with concomitant Viagra therapy. Viagra suppositories were administered four times daily for 8-11 days and were discontinued 5-7 days prior to embryo transfer in all cases.
Our findings clearly demonstrated that vaginal Viagra produced a rapid and profound improvement in uterine blood flow and that was followed by enhanced endometrial development in all four cases. Three (3) of the four women subsequently conceived. . I expanded the trial in 2002 and became the first to report on the administration of vaginal Viagra to 105 women with repeated IVF failure due to persistently thin endometrial linings. All of the women had experienced at least two (2) prior IVF failures attributed to intractably thin uterine linings. About 70% of these women responded to treatment with Viagra suppositories with a marked improvement in endometrial thickness. Forty five percent (45%) achieved live births following a single cycle of IVF treatment with Viagra The miscarriage rate was 9%. None of the women who had failed to show an improvement in endometrial thickness following Viagra treatment achieved viable pregnancies.
Following vaginal administration, Viagra is rapidly absorbed and quickly reaches the uterine blood system in high concentrations. Thereupon it dilutes out as it is absorbed into the systemic circulation. This probably explains why treatment is virtually devoid of systemic side effects
Since the introduction of this form of treatment, thousands of women with thin uterine linings have been reported treated and many have gone on to have babies after repeated prior IVF failure.
It is important to recognize that Viagra will NOT be effective in improving endometrial thickness in all cases. In fact, about one third of women treated fail to show any improvement. This is because in certain cases of thin uterine linings, the basal endometrium will have been permanently damaged and left unresponsive to estrogen. This happens in cases of severe endometrial damage due mainly to post-pregnancy endometritis (inflammation), chronic granulomatous inflammation due to uterine tuberculosis (hardly ever seen in the United States) and following extensive surgical injury to the basal endometrium (as sometimes occurs following over-zealous D&C’s).
To be effective, Viagra must be administered vaginally. It is NOT effective when taken orally. We prescribe 20mg vaginal suppositories to be inserted four times per day. Treatment is commenced soon after menstruation ceases and is continued until the day of the “hCG trigger.” While ideally the treatment should be sustained throughout the first half of the cycle, most women will respond within 48-72 hours. For this reason, Viagra can be used to “rescue” a poor lining after the cycle has already started, provided that there is enough time remaining prior to ovulation, egg retrieval or progesterone administration.
If interested in discussing your case with me, please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
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.
Hi Dr. Sher
I am 40 y.o. – no known issues, healthy lifestyle (never smoked, rare drink, healthy diet and exercise.
Husband – 51 y.o. – healthy, takes supplements for thyroid. Latest sperm analysis: 9% morphology (WHO), count 47, motility 66%, DFI 45% (found lycocites and treated with antibiotics, have not tested after the treatment), previous DFI was 37%, did varecocele surgery May 2016. have been taking Proxeed, CQ10 and on very healthy diet.
IVF#1 – April 2, 2016. Stimmed 8 days (from original 10 days, due to good response). 225 Follistim, 74 Menopur, 3 shots of Ganerelix and 1 trigger injection.
Out of 12 folliciles, 9 eggs retrieved, 7 mature ( Fertilized – 3 with IVF and 4 with ICSI) , 6 made it to day 5 (Frozen cycle). Of those only 1 passed PGS – this came from IVF batch.
Are these poor results? Does this mean my eggs are at issue or it could be sperm quality? Eggs fertilized really well, and most made to Day 5.
IVF#2 – Starting today. Will stim for 8 days, the same protocol plus Omnitrop .25 for 8 days. RE suggesting all IVF, since we fertilize really well. I asked about TESA, to get better sperm – she did not advise it. I am really concern about embryo quality at this point. Please advise what should we do next!
Thanks!
Perhaps you were just unlucky but it is not a great yield.
In my opinion, the protocol used for ovarian stimulation, against the backdrop of age, and ovarian reserve are the drivers of egg quality and egg quality is the most important factor affecting embryo “competency”.
Older women as well as those who (regardless of age) have diminished ovarian reserve (DOR) tend to produce fewer and less “competent” eggs, the main reason for reduced IVF success in such cases. The compromised outcome is largely due to the fact that such women tend to have increased LH biological activity which often results in excessive LH-induced ovarian testosterone production which in turn can have a deleterious effect on egg/embryo “competency”.
Certain ovarian stimulation regimes either promote excessive LH production (e.g. short agonist/Lupron- “flare” protocols, clomiphene and Letrozole), augment LH/hCG delivered through additional administration (e.g. high dosage menotropins such as Menopur), or fail to protect against body’s own/self-produced LH (e.g. late antagonist protocols where drugs such as Ganirelix/Cetrotide/Orgalutron that are first administered 6-7 days after ovarian stimulation has commenced).
I try to avoid using such protocols/regimes (especially) in older women and those with DOR, favoring instead the use of a modified, long pituitary down-regulation protocol (the agonist/antagonist conversion protocol-A/ACP) augmented by adding supplementary human growth hormone (HGH). I further recommend Staggered IVF with embryo banking of PGS (next generation gene sequencing/NGS)-normal blastocysts in such cases. This type of approach will in my opinion, optimize the chance of a viable pregnancy per embryo transfer procedure and provide an opportunity to capitalize on whatever residual ovarian reserve and egg quality still exists, allowing the chance to “make hay while the sun still shines”.
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.
•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)
•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?
•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
•Implications of “Empty Follicle Syndrome and “Premature Luteinization”
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
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
Dr Sher
Do you recommend HLA testing for both husband and wife prior to intralipids and steroids (in addition to NK cell testing?) in case there is alloimmume issues?
If the Nka is positive, then DQ alpha/HLA testing is in my opinion, indicated.
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 Failure and Implantation Dysfunction:
•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!
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
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.