Pelvic Inflammatory Disease (PID), Tubal Damage and Hydrosalpinx: Preparing for IVF

Pelvic inflammatory disease (PID) is a condition where inflammation of pelvic structures occurs, as a result of one of the following: sexual transmission via the vagina and cervix, contamination from other inflamed structures in the abdominal cavity (appendix, gallbladder, kidneys, etc.), a foreign body inside the uterus (i.e., the intrauterine device – IUD), contamination of retained products of conception following abortion or child birth, or, rarely, as a result of blood-born bacterial transmission (e.g., pelvic tuberculosis) which is common in developing countries but rare in the United States.

It is estimated that about 1,500,000 women develop PID annually in the United States and the number is growing.  Less than one-third of these women present with symptoms or signs of acute inflammation (e.g. severe pain, malaise, fever, vaginal discharge).  The remaining cases usually go undetected until the woman presents with symptoms or infertility.  In fact, more that 60% of patients who undergo surgery or in vitro fertilization and embryo transfer (IVF/ET) for the treatment of infertility secondary to pelvic inflammatory disease, provide no history of a prior acute episode.

Acute PID: Where pelvic inflammatory disease presents as an acute illness with fever, sever lower abdominal pain, accompanied by a yellow or blood stained, nonirritant, vaginal discharge and vomiting which usually prompts the woman to seek urgent medical attention.

Subacute PID: Here, the onset of PID is gradual, less severe, and often goes unnoticed until superimposed acute PID occurs, or chronic incapacitating symptoms prompt the woman to seek medical attention (see below).

Chronic Pelvic Inflammatory Disease:  Chronic PID is a consequence of untreated or unsuccessfully managed acute and/or subacute PID.  The woman usually presents with symptoms of pelvic pain, heavy and painful menstrual periods, pain with intercourse (dyspareunia) and infertility.

In the vast majority of cases, PID results from the sexual transmission of infecting organisms such as Neisseria Gonorrhea, and Chlamydia Trachomatis, which are readily eradicated through appropriate antibiotic therapy. Sexually transmitted bacteria first infects the cervix (the opening into the uterus) through which it ascends via the uterus to the fallopian tubes, ovaries, and other pelvic structures.

There are several important factors which predispose women towards developing PID:

  1. Exposure to an infected partner
  2. Exposure blood provides and excellent growth medium for bacteria, promoting their proliferation and passage into the fallopian tubes
  3. Relative ill health and poor nutritional status.  It is predominantly for this reason that PID is much more prevalent in lower socioeconomic groups
  4. The fact that previously infected tissues are highly susceptible to re-infection; resulting in women with a past history of PID being highly susceptible to recurrent attacks

While sexually transmitted PID is certainly capable of causing endometritis (inflammation of the uterine lining) the uterus itself is not the main focus of the inflammatory process. Cyclical shedding of most of the uterine lining with menstruation tends to remove infected tissue monthly, thereby preventing the inflammation from taking a hold and causing permanent damage to or scarring of the uterine lining (the endometrium).  The main site/target of inflammation following sexual transmitted PID is the fallopian tube via which other pelvic and abdominal structures may be infected.

PID following pregnancy (childbirth or abortion): This primarily targets the uterine lining, causing endometritis.  Organisms such as Bacteroides, Peptostreptococcus, Beta hemolytic streptococcus, and E.Coli readily proliferate in the products of conception that are sometimes retained in the uterus following childbirth and abortion.  The delayed onset of menstruation after both childbirth and abortion provides an opportunity for the inflammatory process to take hold and progress, sometimes leading to the development of scar tissue in the uterine cavity with the opposing surfaces of the endometrium to fuse together or produce scarring (Asherman syndrome). Sometimes the inflamed endometrium obliterates the opening (in the uterus) into the fallopian tubes and might also damage a small, adjacent segment of the tubes. Less commonly, post-childbirth and post-abortal endometritis infects the entire fallopian tube(s) (salpingitis) as well as causing partial or complete blockage, and/or spreading into the pelvic cavity.

PID from the use of the intrauterine contraceptive device (IUD) for contraceptive purposes:  This most commonly occurs in cases where the device is inserted into the uterus of women concurrently infected with Gonorrhea or Chlamydia. The IUD acts as a foreign body causing local irritation which compromises the normal defense mechanisms that normally protect against infection.  At the same time, the IUD string which protrudes through the cervix into the vagina may act as a “wick” via which infecting organisms gain entrance to the uterus.  As with post-abortal and post-childbirth endometritis, IUD-related uterine infection can cause scarring of the endometrial lining, blockage of the fallopian tubes where they leave the uterus (utero-cornual occlusion, and spread, via the tubes, to other pelvic structures.  IUD-related PID is a potentially life endangering condition capable of causing pelvic abscess formation, the development of peritonitis (inflammation of the peritoneum), systemic infection (septicemia), and shock.

How PID Causes Tubal Infertility: Sexually transmitted PID caused by Gonorrhea or Chlamydia rapidly spreads via the cervix and uterus to the fallopian tube(s).  These organs are highly specialized and are designed to promote the active passage of eggs, sperm, and embryos in a timely manner to and from the uterine cavity.  They contain cells whose function is to protect and nurture eggs, sperm and embryos in transit.  At their ends, the fallopian tubes have small delicate finger-like projections (fimbriae) that approximate, envelope, and “pick-up” the egg(s) from the ovary(s) at the time of ovulation.  Inflammation due to Chlamydia Trachomatis and Neiserria Gonorrhea, damages and often permanently destroys the specialized lining of the fallopian tube(s) and in severe cases results in fusion of the fimbriae thereby clocking the ends of the tube(s) compromising their mobility and their potential to facilitate timely passage of eggs, sperm and embryos. Pus, which accumulated inside the tube(s), often passes into the pelvic cavity producing peritonitis and results in the formation of scar tissue (adhesions) which further disrupts normal pelvic anatomy as well as the relationship between the tube(s) and the ovary(ies). This may prevent the fallopian tubes from collecting the egg(s) during ovulation.

As previously stated, post-abortal and post-childbirth endometritis causes infertility by causing uterine scarring, occlusion of the fallopian tube at its junction with the uterus, and sometimes producing infection along the full length of the tube with resultant tubal damage.

Sexually transmitted PID: This almost invariably affects both fallopian tubes.  Even in cases where a dye x-ray test (hysterosalpingogram) or laparoscopy (a procedure where a telescope-like instrument is passed through the belly button to visualize the pelvic structures) indicates that only one fallopian tube has been infected, the other tube is almost invariably involved.  A new procedure called tuboscopy (where a thin fiberoptic telescope is passed into the fallopian tube(s) to evaluate the inner structure) has confirmed that the tubes of PID victims, who seemingly have normal pelvic anatomy, oftentimes have internal scarring and/or adhesion.  This could account for the low success rate seen with tubal reparative surgeries and the high ectopic pregnancy rate (8-15%) in PID patients who subsequently conceive.

Ureaplasma Urealyticum Infection: Ureaplasma urealyticum infection is an organism which causes a relatively benign form of PID.  Often times neither partner has any symptoms or signs of the condition. It has been implicated as a possible cause of both infertility and early recurrent miscarriages.  The organism is sexually transmitted and infects the lining of the cervical canal. It rarely produces symptoms of severe physical complications in its female victims.  In men, it sometimes causes nonspecific urethritis and/or prostatitis, but in the majority of cases is asymptomatic. Recent research suggests that infection with Ureaplasma urealyticum might be capable of altering the physico-chemical properties of cervical mucus and/or cervical secretions, so that when a catheter is passed into the uterus to transfer embryos or sperm, the organisms gait entry to the uterine cavity, and produce and environment that is inhospitable to embryos.

Management: Emphases should be placed on the prevention of PID by appropriate population screening for sexually transmitted diseases and through the promotion of condom usage in non-monogamous sexual relationships. Acute PID should be vigorously treated with the appropriate antibiotics.  Gonorrhea is usually successfully treated with penicillin derivatives, cephalosporins, erythromycin, ciprofloxin and tetracyclines.  Anaerobic organisms such as Bacteroides and Peptostreptococcus are responsive to metronidazole (Flagyl), ciprofloxin and in some cases to doxycycline. Beta hemolytic Streptococcus and E. coli respond to penicillin derivatives, tetracyclines, and cephalosporins and ciprofloxin. E. coli can also be treated with the gentamicin.  PID due to Chlamydial infection responds well to doxycycline, erythromycin, and ciprofloxin therapy, but will usually not respond to penicillin derivatives or cephalosporins. Ureaplasma urealyticum infections likewise respond well to the same antibiotics and to Flagyl.

All active sexual contact should be treated concurrently and follow up cultures should always be performed to confirm complete eradication of the disease.

The pain, heavy bleeding, and debilitation associated with chronic PID often necessitates removal of the tube(s) and sometimes even hysterectomy, especially in women who have no childbearing aspirations.  Younger women who are desirous of having a child might defer such treatment while enduring ongoing symptoms, in the hope of conceiving in the interim.

Diagnosing Tubal damage due to PID: Tubal blockage can occur anywhere in the fallopian tubes. It sometimes occurs in the part of the Fallopian tube that passes through the wall of the uterus. It can also occur in the mid-section of the tube. Most commonly however, it occludes the far end of the tubes.

A hysterosalpingogram (HSG) is the most widely used screening test for damaged or blocked tubes. It involves the injection of a radio-opaque dye through the cervix into the uterus. Successive x-rays are then taken in rapid succession to track passage of the dye into the uterus and then to determine whether it passes into the Fallopian tubes and then spills into the pelvic cavity. However, a  HSG showing patent tubes, cannot usually diagnose  tubal damage. All it tells you is whether the petal-like fimbriated ends of the tubes have not fused and blocking their ends. It is especially important to take bear this fact in mind whenever the tubes are found to be open, in spite of there being a history of prior PID. A diagnostic laparoscopy is much more reliable for diagnosing both tubal blockage and damage.

Treating Tubal Damage due to PID: Tubal damage is one of the most common causes of infertility. The Fallopian tubes are not merely “pipes”; they are highly complex structures that pick up the ovulated egg and help move it towards the uterus. Normal fertilization occurs in the tube. And, as stated above, damage to Fallopian tubes is most often caused by PID.

During the 1980’s, surgery was regarded as the mainstay of treatment for infertility secondary to PID.  The advent of high success rates with in vitro fertilization as performed in selected centers of excellence has changed all of that. Today, virtually without exception, most fertility specialists would agree that IVF is the treatment of choice for almost all forms of tubal infertility.  

Surgery to unblock fallopian tubes or clear adhesions resulting from an inflammatory process due to infections with gonorrhea or Chlamydia is truly an exercise in futility.  The chances of pregnancy occurring following such an undertaking is less than 2% per month, and less than 25% in three years.  

Then there is the fact that there is a high incidence of ectopic pregnancy following tubal surgery (15-20%) and this can be a life endangering condition. Finally, more than 70% of patients undertaking such an escapade would ultimately need IVF anyway, there is no longer any medical justification to choose tubal surgery over IVF.

Hydrosalpinx: In cases where the ends of the fallopian tubes are blocked, pus may collect and distend the tube(s).  The pus is usually absorbed over time and replaced by clear straw-colored fluid.  The resulting, occluded, fluid-filled, distended, and often functionless fallopian tube(s) is referred to as a hydrosalpinx.. Such distended Fallopian tubes (hydrosalpinges) can leak fluid back into the uterine cavity where the can destroy transferred embryos upon contact. This is why patients who have hydrosalpinges and are considering undergoing IVF, should first have hydrosalpinges surgically removed or at the very least have the affected tube(s) surgically clipped or tied as they emerge through the uterine wall. This will avoid subsequent back flow when IVF is performed. Understandably, it is often hard for patients to come to terms with the fact that following such surgery they no longer have any possibility of having functional Fallopian Tubes. Such women should be counseled that hydrosalpinges are functionless tubes anyway and that any attempt to open such tubes surgically in an attempt to restore fertility would be an exercise in futility, anyway.

In a nutshell: Tubal surgery is a very poor alternative to IVF. Infertility associated with tubal blockage, especially if due to PID, is an absolute indication for IVF. I would go even further in stating that any tubal damage due to PID, whether or not it is associated with blockage is an indication for IVF.

4 Comments

May

I had PID and a lot of endometriosis and my left tube needs to come out. Apparently my other tube is okay. Should I consider just having the one tube out and clearing the endometriosis and trying naturally or should I go for IVF, in which case my doctor said that both tubes would probably be taken out but we’d have a higher chance of conceiving? Also, I got so flustered in the appointment I forgot the rationale for taking both tubes? What would be the benefit of that?

reply
Dr. Geoffrey Sher

I agree! If your tubes are that damaged, both should probably be removed. You need IVF anyway!

When women with infertility due to endometriosis seek treatment, they are all too often advised to first try ovarian stimulation (ovulation Induction) with intrauterine insemination (IUI) ………as if to say that this would be just as likely to result in a baby as would in vitro fertilization (IVF). Nothing could be further from reality It is time to set the record straight. And hence this communication!

Bear in mind that the cost of treatment comprises both financial and emotional components and that it is the cost of having a baby rather than cost of a procedure. Then consider the fact that regardless of her age or the severity of the condition, women with infertility due to endometriosis are several fold more likely to have a baby per treatment cycle of IVF than with IUI. It follows that there is a distinct advantage in doing IVF first, rather than as a last resort.

So then, why is it that ovulation induction with or without IUI is routinely offered proposed preferentially to women with mild to moderately severe endometriosis? Could it in part be due to the fact that most practicing doctors do not provide IVF services but are indeed remunerated for ovarian stimulation and IUI services and are thus economically incentivized to offer IUI as a first line approach? Or is because of the often erroneous belief that the use of fertility drugs will in all cases induce the release (ovulation) of multiple eggs at a time and thereby increase the chance of a pregnancy. The truth however is that while normally ovulating women (the majority of women who have mild to moderately severe endometriosis) respond to ovarian stimulation with fertility drugs by forming multiple follicles, they rarely ovulate > 1 (or at most 2) egg at a time. This is because such women usually only develop a single dominant follicle which upon ovulating leaves the others intact. This is the reason why normally ovulating women who undergo ovulation induction usually will not experience improved pregnancy potential, nor will they have a marked increase in multiple pregnancies. Conversely, non-ovulating women (as well as those with dysfunctional ovulation) who undergo ovulation induction, almost always develop multiple large follicles that tend to ovulate in unison. This increases the potential to conceive along with an increased risk multiple pregnancies.

So let me take a stab at explaining why IVF is more successful than IUI or surgical correction in the treatment of endometriosis-related infertility:
1. The toxic pelvic factor: Endometriosis is a condition where the lining of the uterus (the endometrium) grows outside the uterus. While this process begins early in the reproductive life of a woman, with notable exceptions, it only becomes manifest in the 2ndhalf of her reproductive life. After some time, these deposits bleed and when the blood absorbs it leaves a visible pigment that can be identified upon surgical exposure of the pelvis. Such endometriotic deposits invariably produce and release toxins” into the pelvic secretions that coat the surface of the membrane (the peritoneum) that envelops all abdominal and pelvic organs, including the uterus, tubes and ovaries. These toxins are referred to as “the peritoneal factor”. Following ovulation, the egg(s) must pass from the ovary (ies), through these toxic secretions to reach the sperm lying in wait in the outer part the fallopian tube (s) tube(s) where, the sperm lie in waiting. In the process of going from the ovary(ies) to the Fallopian tube(s) these eggs become exposed to the “peritoneal toxins” which alter s the envelopment of the egg (i.e. zona pellucida) making it much less receptive to being fertilized by sperm. As a consequence, if they are chromosomally normal such eggs are rendered much less likely to be successfully fertilized. Since almost all women with endometriosis have this problem, it is not difficult to understand why they are far less likely to conceive following ovulation (whether natural or induced through ovulation induction). This “toxic peritoneal factor impacts on eggs that are ovulated whether spontaneously (as in natural cycles) or following the use of fertility drugs and serves to explain why the chance of pregnancy is so significantly reduced in normally ovulating women with endometriosis.
2. The Immunologic Factor: About one third of women who have endometriosis will also have an immunologic implantation dysfunction (IID) linked to activation of uterine natural killer cells (NKa). This will require selective immunotherapy with Intralipid infusions, and/or heparinoids (e.g. Clexane/Lovenox) that is much more effectively implemented in combination with IVF.
3. Surgical treatment of mild to moderate endometriosis does not usually improve pregnancy potential:. The reason is that endometriosis can be considered to be a “work in progress”. New lesions are constantly developing. So it is that for every endometriotic seen there are usually many non-pigmented deposits that are in the process of evolving but are not yet visible to the naked eye and such evolving (non-visible) lesions can also release the same “toxins that compromise fertilization. Accordingly, even after surgical removal of all visible lesions the invisible ones continue to release “toxins” and retain the ability to compromise natural fertilization. It also explains why surgery to remove endometriotic deposits in women with mild to moderate endometriosis usually will fail to significantly improve pregnancy generating potential. In contrast, IVF, by removing eggs from the ovaries prior to ovulation, fertilizing these outside of the body and then transferring the resulting embryo(s) to the uterus, bypasses the toxic pelvic environment and is therefore is the treatment of choice in cases of endometriosis-related infertility.
4. Ovarian Endometriomas: Women, who have advanced endometriosis, often have endometriotic ovarian cysts, known as endometriomas. These cysts contain decomposed menstrual blood that looks like melted chocolate…hence the name “chocolate cysts”. These space occupying lesions can activate ovarian connective tissue (stroma or theca) resulting in an overproduction of male hormones (especially testosterone). An excess of ovarian testosterone can severely compromise follicle and egg development in the affected ovary. Thus there are two reasons for treating endometriomas. The first is to alleviate symptoms and the second is to optimize egg and embryo quality. Conventional treatment of endometriomas involves surgical drainage of the cyst contents with subsequent removal of the cyst wall (usually by laparoscopy), increasing the risk of surgical complications. We recently reported on a new, effective and safe outpatient approach to treating endometriomas in women planning to undergo IVF. We termed the treatment ovarian Sclerotherapy. The process involves; needle aspiration of the “chocolate colored liquid content of the endometriotic cyst, followed by the injection of 5% tetracycline hydrochloride into the cyst cavity. Such treatment will, more than 75% of the time result in disappearance of the lesion within 6-8 weeks. Ovarian sclerotherapy can be performed under local anesthesia or under conscious sedation. It is a safe and effective alternative to surgery for definitive treatment of recurrent ovarian endometriomas in a select group of patients planning to undergo IVF

I am not suggesting that all women with infertility-related endometriosis should automatically resort to IVF. Quite to the contrary…. In spite of having reduced fertility potential, many women with mild to moderate endometriosis can and do go on to conceive on their own (without treatment). It is just that the chance of this happening is so is much lower than normal.

IN SUMMARY: For young ovulating women (< 35 years of age ) with endometriosis, who have normal reproductive anatomy and have fertile male partners, expectant treatment is often preferable to IUI or IVF. However, for older women, women who (regardless of their age) have any additional factor (e.g. pelvic adhesions, ovarian endometriomas, male infertility, IID or diminished ovarian reserve-DOR) IVF should be the primary treatment of choice. I strongly recommend that you visit 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. • Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in 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) • 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! • Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas • Should IVF Treatment Cycles be provided uninterrupted or be Conducted in 7-12 Pre-scheduled “Batches” per Year • A personalized, stepwise approach to IVF • How Many Embryos should be transferred: A Critical Decision in IVF? • Endometriosis and Immunologic Implantation Dysfunction (IID) and IVF • Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice. • Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options • Early -Endometriosis-related Infertility: Ovulation Induction (with or without Intrauterine Insemination) and Reproductive Surgery Versus IVF • Treating Ovarian Endometriomas with Sclerotherapy. • Effect of Advanced Endometriosis with Endometriotic cysts (Endometriomas) on IVF Outcome & Treatment Options. • Deciding Between Intrauterine Insemination (IUI) and In Vitro Fertilization (IVF). • Intrauterine Insemination (IUI): Who Needs it & who Does Not: Pro’s & • Induction of Ovulation with Clomiphene Citrate: Mode of Action, Indications, Benefits, Limitations and Contraindications for its use • Clomiphene Induction of Ovulation: Its Use and Misuse! ___________________________________________________________ ADDENDUM: PLEASE READ!! INTRODUCING SHER FERTILITY SOLUTIONS (SFS) Hitherto I have personally performed IVF- treatment and related procedures on patients who, elected to travel to Las Vegas to be managed by me. However, with the launching of Sher-Fertility Solutions (SFS) in April 2019, I have taken on a new and expanded role. Now, rather than having hands-on involvement I confine my services to providing hour-long online Skype consultations to an ever-growing number of patients (emanating from >40 countries), with complex Reproductive problems, who seek access to my input, advice and guidance. All Skype consultations are followed by a detailed written report that meticulously describes and explains my recommendations for treatment. All patients are encouraged to share this report with their personal treating doctor(s), with whom [subject to consent and a request from their doctor] I will, gladly discuss their case with the “treating Physician”.
Through SFS I am now able to conveniently provide those who because of geography, convenience and cost, prefer to be treated at home or elsewhere by their chosen Infertility Physician.
“I wish to emphasize to all patients with whom I consult, that in the final analyses, when it comes to management, strategy, protocol and implementation of treatment, my advice and recommendations are always superseded by that of the hands-on treating Physician”.

Anyone wishing to schedule a Skype consultation with me, can do so by: Calling my concierge (Patti Converse) at 1-800-780-7437 (in the U.S.A or Canada) or 702-533-2691, for an appointment. Patients can also enroll online on my website, http://www.SherIVF.com, or email Patti at concierge@SherIVF.com .
I was very recently greatly honored in receiving an award by the prestigious; International Association of Top Professionals (IAOTP). For more information, go to the press release on my website, http://www.sherIVF.com .

PLEASE HELP SPREAD THE WORD ABOUT SFS!

Geoff Sher

I was very recently greatly honored in receiving an award by the prestigious; International Association of Top Professionals (IAOTP). For more information, go to the press release on my website, http://www.sherIVF.com .

reply
Dr. Geoffrey Sher

Yes… if retained products of conception become infected and the inflammation travels into the tubes.

ADDENDUM:
INTRODUCING SHER FRERTILITY SOLUTIONS (SFS)
Hitherto I have personally performed the actual hands-on treatment of all patients who, seeking my involvement, elected to travel to Las Vegas for my care. However, with the launching of Sher-Fertility Solutions (SFS), I will as of March 31st take on a new and expanded consultation role. Rather than having hands-on involvement with IVF procedures I will, through SFS, instead provide fertility consultations (via SKYPE) to the growing number of patients (from >40 countries) with complex Reproductive Dysfunction (RD) who seek access to my input , advice and guidance. In this way I will be able to be involved in overseeing the care, of numerous patients who previously, because they were unable to travel long distances to be treated by me, were unable to gain access to my input.

Anyone wishing to schedule a Skype consultation with me, can do so by: Calling my concierge (Patti Converse) at 1-800-780-7437 for an appointment,enrolling online on my website, http://www.SherIVF.com, or 702-533-2691; or emailing Patti at concierge@SherIVF.com or . sher@sherivf.com .
I was very recently greatly honored in receiving an award by the prestigious; International Association of Top Professionals (IAOTP). For more information, go to the press release on my website, http://www.sherIVF.com .

PLEASE HELP SPREAD THE WORD ABOUT SFS!

Geoff Sher

reply

Ask a question or post a comment

Your email address will not be published. Required fields are marked *