Society for Gynecologic Investigation – day 1

Here in Orlando, the meeting opened with the President’s Lecture. John J. Moore, a pediatric neonatologist spoke to openthe conference about the miraculous adaptive ability of very low birth weight babies in terms of developing their brain, lungs and immune systems. The challenges to take care of 24 to 26 week premies has sparked interest in their long term outcomes. And, while developmentally delayed in some ways, he presented research to show how remarkably they are able to compensate for their very early entry into the world.

These investiagors were all new investigators, but presented the best of the best here at SGI. The first by Ryan Hodges demonstrated in a sheep model that amniotic cells infused into very premature lambs will protect the lungs from the damage of early ventilation. The remarkable thing about this research was that they took human cells from the amniotic fluid and showed that they incorporated themselves into the sheeps lungs. They were able to see them because of a green fluorescent protein that was expressed. This amazing work shows that there are mechanisms for lung development that probably include ingesting the cells during gestation from the amniotic fluid and that these cells provide part of the lungs developmental process (perhaps). This also provides a novel treatment for respiratory distress that comes from being severely premature.

The third talk was about severe preeclampsia and how it may put women at future risk for heart attack and stroke. The mechanism of this known connection was explored by studying the vascular response in women who were post-partum who either did or did not have pre-eclampsia. The interesting finding that intrauterine growth redaration pregnanies with normal blood pressure, (IUGR) also showed these same changes suggesting that that is also a risk factor for the future health of the mother.

The 4th talk showed that while radiation and chemotherapy to treat cancer can wipe out the ovarian function by killing off the eggs (oocytes), the process for this reduction in eggs was discovered and found to involve a pairing with a protein called Cables1. By blocking the interactions of Cables1 and another protein P63, the investigators showed that the oocytes of treated animals could be protected from this cell death. These are very interesting data for any young woman who might be treated for cancer but who desires to protect her fertility.

There were wonderful posters at the session and too many to discuss in any detail.

There were concurrent sessions on a variety of topics including PCOS, epigenetics and other topics to follow lunch. In the Epigenetics talks it was fascinating to hear that hormone treatments with potent estrogens like DES and geninstein (soy) can alter the DNA in a way that is passed on to the offspring. There were target genes whose expression was altered due to neonatal exposure in early and mid gestation. The active component in soy protein is genistein so these findings may have implications for the consumption of too much soy during pregnancy. That was not the conclusion of the talk but these data in animal models deserve a closer look.

Finally, a new potential treatment for ectopic pregnancies (tubal pregnancies) was presented, showing that the combination of Gefitinib and methotrexate worked better than either alone to kill trophoblast cells and resolve the ectopic pregnancy. The oral agent could mean quicker treatments and lower doses of methotrexate might be required.

SGI Day -1 (It starts tomorrow)

Endometrium Satellite Symposium (Highly technical stuff)

• Judith Bulmer – Newcastle upon Tyne, UK
  Functional aspects of human endometrial leukocytes – The first talk was very relevant to the importance of white blood cells (WBC) in the endometrium and their role during pregnancy. Of the many different kinds present, natural killer cells (NK cells) are perhaps the most interesting. Their numbers increase in the endometrium during implantation and they appear to have a role in both trophoblast (placental cells) invasion and vascular remodeling that occurs during early pregnancy. There are various cytokines (chemical messages) secreted by these cells that combined with the signals from placental cells that change the way the embryonic cells invade or stop invading into the uterus. The pregnancy must invade sufficiently to establish a blood supply but not too much to jeopardize the mother’s health. Some of these action are related to soluble factors from the trophoblast require direct cell to cell interactions. The implications for infertility include the concept that NK cells regulate key factors that help implantation occur normally and changes seen in pathologic conditions like endometriosis or other diseases may alter the ability for embryos to attach and implant. If the embryo only can establish a marginal blood supply, this may predispose to a condition called preeclampsia that may cause preterm delivery. There was a great deal of information provided about the experimental models that Dr. Bulmer and her laboratory use. There is still much to learn about the role of white blood cells and pregnancy outcome.

• The second talk by Sarah Robertson from University of Adelaide, Australia was perhaps even more interesting. There are factors in the male semen that can signal to the maternal endometrium to make it “tolerant” of pregnancy. Dr. Robertson reviewed the many theories about how embryo attach and growth within a woman’s uterus while not being attacked by the mother’s immune system. The factor in the semen that mediates this protection may be a growth factor called TGFb, and it induces a type of immune blood cell called T-regulatory cells that allow the embryo to be recognized and tolerated. There is an alternative state in which the embryo is recognized as foreign and then destroyed by the immune system. The balance between accepting and rejecting the embryo may have broader signficance. In most mammalian species the male cares primarily about establishing as many pregnancies as possible. The female on the other hand, puts her emphasis is on establishing the best pregnancy that is possible. Therefore, this type of recognition and acceptance mechanism may be there to provide maternal quality control of the pregnancy. The other side of this, is that some men may have sperm that do not induce the type of tolerance in the woman required for a successful pregnancy. It would be interesting to see if unexplained IVF failure is due to a lack of these factors and a loss of T-regulatory cells are necessary for a successful outcome in IVF.
• The third interesting talk was by Henry Jabbour from Queen’s Medical Research Institute in Edinburgh, UK. This talk was very relevant to endometriosis as it spoke of the importance of inflammation to the restoration and repair of the uterine lining. After menses, which is very inflammatory process, the endometrium heals and regrows rapidly. There was a great deal of data provided in this talk to emphasize the importance of inflammation in this healing process following menstruation. Importantly, the idea that cells migrate and invade and proliferate during the first half of the menstrual cycle in response to inflammation suggests that inflammation occurring in the second half of the menstrual cycle (due to a condition like endometriosis) could alter the cell behavior and promote worsening of the disease (through proliferation, invasion and migration). Thus, physiological events that normally restore and preserve fertility can be co-opted by disease states (like endometriosis) and explain why this disease is self-promoting.  Dr. Jabbour spoke about anti-inflammatory drugs as a treatment for conditions like endometriosis. Lipoxin A4, an anti-inflammatory compound is a naturally occuring compound that is made by the body. It can be induced by aspirin.  Fish oil and olive oil are precursors to Lipoxin A so these may be good to include in your diet to promote lipoxin A4 production. Finally, adrenal steroids may have a role as an inflammatory agent, so treatment with predisone or equivalent steroids might have a role for fertility preservation in some circumstances.  These studies were very relevant to fertility care but will require followup studies.
• Other talks of the day included discussion of T-regulatory cells in endometriosis by Andrea Braundmeier, discussions of a mouse model of endometriosis and ovarian cancer by Steve Charnock-Jones, and a wonderful talk by Serdar Bulun from Northwestern University about the role of progesterone action and endometriosis.

Hyperprolactinemia

“Hyperprolactinemia” refers to an abnormal elevation in serum prolactin levels.  We see many cases a year of this associated with infertility. It is a highly treatable condition and one that can also be a serious health risk.  The signs of hyperprolactinemia are infertility, irregular menstrual cycles, milky discharge from the breast, headache and sometimes changes in vision. In some cases of severe hyperproctinemia, the estrogen level can be decreased to a point where loss of bone calcium can occur.

Causes of elevated prolactin include:

1. Prolactin secreting tumors (adenomas) are the most common cause
2. Non-prolactin secreting tumors can cause mild elevations in prolactin if large enough
3. Hyperinsulinemia is associated with elevated prolactin
4. Breast augmentation (implants) or other chest wall surgeries can stimulate prolactin production
5. Pregnancy is a cause of prolactin elevation and should always be ruled out first
6. Hypothyroidism can be associated with a rise in prolactin

Treatment of hyperprolactinemia includes medical and possible surgical treatment. The vast majority of cases can be treated medically using a drug that functions to bring the prolactin level down (dopamine agonist therapy). The two most common medications used are parlodil (bromocriptine) and dostinex (carbergoline). These medications are usually well tolerated. The former is used every day the the latter is used twice a week.  Treatment usually continues up until pregnancy occurs and is then discontinued. The risk of regrowth of a pituitary tumor during is low but the obstetrician should be informed of this condition so that signs of a macroadenoma can be looked for. In some cases, a test of visual fields is performed to make sure that bitemporal hemianopsia does not occur (loss of the lateral visual fields due to optic nerve compression). A microadenoma is a tumor in the pituitary less than 1 cm, and a macroadenoma is 1 cm or larger. The larger the tumor, the more likely surgery might be required, but even large pituitary tumors often respond to medical treatment.

Other important things to know:

1. 10% of people have pituitary microadenomas
2. 80% of patients with amenorrhea/galactorrhea with hyperprolactinemia but no demonstrable tumors had menstrual cycles restored with bromocriptine
3. Breast discharge may take longer to resolve than return of normal menstrual cycles
4. Vaginal administration of bromocriptine works well, and can be used if side effects occur using it orally
5. 80% of infertile women with hyperprolactinemia achieve pregnancy with dopamine agonist therapy
6. Breast feeding, if desired, can be experienced normally without fear of stimulting tumor growth
7. Less than 2% of women will experience signs or symptoms of tumor growth during pregnancy
8. One third of patients with galactorrhea and hyperprolactinemia will have normal menses
9. Individuals who have good response to medical treatment for 2 to 5 years can stop treatment but monitoring of prolactin and signs of regrowth of the tumor is advised
10. One third of women with secondary amenorrhea will have hyperprolactinemia

Case: 34 year old with lack of periods and clinical signs of hypothroidism. Breast discharge had started up again, after she had stopped breast feeding her last child. A serum prolactin level of 89 was found (normal < 20 ng/ml).   A test for hypothyroidism was low (TSH) but so was her free T3 and T4 (measures of thyroid hormones). An MRI was performed and the following picture was taken.  The pituitary in the middle of the brain has a tumor in it, surrounded by compressed (white) pituitary tissue.

This is a rare case of a non-prolactin secreting tumor of the pituitary causing hyperprolactinemia (because if interfered with normal pituitary function) but also hypothyroidism and hypogonadotropic hypogonadism (see glossary). The patient went to surgery and had this tumor removed using a transsphenoidal approach and she is now back to normal and conceived 2 months later. She is expecting to deliver in September.

Source material: Clinical Gynecologic Endocrinology and Infertility, Speroff and Fritz, 7th Ed.

Implantation failure

Embryo implantation occurs only during a narrow window of time in a woman’s cycle. Based on a landmark study (1) embryos usually implant 6 to 10 days after ovulation. A major reason of infertility is a defect in “endometrial receptivity”, which means that the lining of the womb does not become receptive to the embryo. Despite having a fertilized egg inside the uterus, pregnancy doesn’t occur.  If the “window of implantation” opens late, then miscarriage might also occur. We think that the ovarian cyst that makes progesterone needs to get the pregnancy signal (hCG) on time and in the case of a late arriving embryo, that process may also be faulty and lead to pregnancy loss.

The causes of implantation failure have been well defined (2). Number one on the list is endometriosis. The presence of endometrium outside the uterus leads to inflammatory changes that alter the balance between estrogen and progesterone action, leading to derangements in the establishment of uterine receptivity. Next, hydrosalpinx (fluid filled, damaged fallopian tubes) can reduce the success in an IVF cycle, but even one blocked tube can reduce fertility and should be removed or opened (3). Fibroids (smooth muscle tumors of the uterus) can also reduce implantation rates.

Biomarkers of endometrial receptivity are available to detect endometrial receptivity problems (4, 5). The loss of these endometrial proteins in unexplained infertility also can be helpful (6).  While integrin are the best characterized proteins for finding defects of implantation, other proteins have been studied as well including HOXA10, leukemia inhibitor factor (LIF) and others. We are currently finding that lack of these proteins may predict IVF failure and could help avoid some of the problems seen with repeated, unexplained lack of pregnancy with IVF, often associated with unsuspected endometriosis (see: http://ow.ly/1gyFk).

1.            Wilcox AJ, Baird DD, Wenberg CR. Time of implantation of the conceptus and loss of pregnancy. N Engl J Med. 1999;340:1796-9.

2.            Donaghay M, Lessey BA. Uterine receptivity: alterations associated with benign gynecological disease. Semin Reprod Med. 2007 Nov;25(6):461-75.

3.            Sagoskin AW, Lessey BA, Mottla GL, Richter KS, Chetkowski RJ, Chang AS, et al. Salpingectomy or proximal tubal occlusion of unilateral hydrosalpinx increases the potential for spontaneous pregnancy. Hum Reprod. 2003 Dec;18(12):2634-7.

4.            Meyer WR, Castelbaum AJ, Somkuti S, Sagoskin AW, Doyle M, Harris JE, et al. Hydrosalpinges adversely affect markers of endometrial receptivity. Hum Reprod. 1997;12:1393-8.

5.            Lessey BA, Castelbaum AJ, Sawin SW, Buck CA, Schinnar R, Bilker W, et al. Aberrant integrin expression in the endometrium of women with endometriosis. J Clin Endocrinol Metab. 1994 Aug;79(2):643-9.

6.            Lessey BA, Castelbaum AJ, Sawin SW, Sun J. Integrins as markers of uterine receptivity in women with primary unexplained infertility. Fertil Steril. 1995 Mar;63(3):535-42.

Are you healthy enough for sexual activity?

You’ll hear this question nightly on ads for erectile dysfunction (ED) that are part of the ubiquitous industry-sponsored direct-to-patient advertising campaign for viagra, cialis and other medications.  This question takes on deeper significance, however, when the physiology and implications of ED are explored.  This blog segment is not just for men, but for the women who love them.  ED appears to be one of the early warning signs of coronary artery disease and risk of heart attack.

Here are some important points about erectile dysfunction you should know:

1) The penile artery is slightly smaller in diameter than the coronary artery.  Atherosclerosis (fatty cholesterol deposits) in the penis reflects atherosclerosis in the heart. It may serve as the canary in the coal mine, so to speak.

2) The risk of heart attack in men with ED is equal to that of a diabetic smoker, with a 1.5 to 2.5 increased risk of developing coronary vascular disease (CVD)

3) In a study of men with CVD, 68% complained of ED before developing angina or having an MI

4) Based on a study prospective Prostate Cancer Prevention trial, men were followed after age 55 and evaluated for ED and CVS. The relationship was so high that the authors concluded that developing ED was greater to equal to the effects of family history of MI, cigarette smoking, or hyperlipidemia.

5) ED is associated with a 50 fold increase in the 10 year incidence of cardiac events in men 49 years or younger

So, ED appears to be an early manifestation of atherosclerosis  and a predictor of coronary artery disease.  Good information especially if you or you partner develop ED under the age of 50.

(source material: Miner et al., Erectile dysfunction: A precursor to cardiovascular disease. SRM 7:27-32 2009)

Aging and Fertility – tic toc, tic toc

Wish me a happy birthday today – I guess that means it’s time to talk about aging.  And the clock is ticking for everyone who still wants to start or extend their family.  For baby boomers the alarms have already gone off, but even for couples in their late thirties, there are concerns as the number of eggs start to decline.  It is probably just denial that allows couples to put off childbearing to a time when it is the most difficult. We feel healthy when we turn 40 and there’s the career to think about.  “I’m sure my eggs will be OK” – don’t be too sure.

I don’t want to spread doom and gloom, especially on my birthday, but here are some things to be aware of:

1) Natural fertility declines in women starting around age 35. The number of women unable to conceive goes up with age

Percent of women remaining childless on no contraception, by age

2) IVF success rates drop steadily with age

Success rates decline with age with in vitro fertilization

3) The chance of having a miscarriage goes up with age

The percent of women who have miscarriage after getting pregnant with IVF goes up with age

4) The male partner may decline as well after age 50, but unlike the female there no absolute age when men cannot father a child (its so unfair!)

The physiology of this process in women is well understood. A woman starts with 1,000,000 eggs at birth, has 400,000 by the time of puberty and uses them up in a continuous fashion, until the peri-menopause when the depletion rate picks up – then there are none left. Nothing can slow it down and nothing speeds up the process.

The evaluation of the female includes an ultrasound to look at “antral follicle count” (see glossary), anti-müllerian hormone (AMH) that goes down with egg number, and day 3 FSH (follicle stimulating hormone) that goes up with loss of eggs. A clomiphene citrate challenge test is often done after age 35: obtain an FSH on day 3 along with an estradiol level, then take clomiphene citrate 100 mg on days 5 to 9 and then get another FSH on day 10. If either FSH is above 13, it is not good news and a level above 15 usually means that there a very low chance for successful pregnancy without donor eggs.

Counseling for older (over 37) women trying to conceive should include assessment of the ovarian reserve and perhaps more aggressive therapies. Time should be optimized for each couple to avoid getting bogged down doing the same thing over and over. (I saw a women recently who have been on clomiphene citrate for 12  months and was approaching 40).

Treatments including ovulation induction with oral medications, oral meds plus gonadotropin injections (sequential therapy) and superovulation with intrauterine insemination. In vitro fertilization (IVF) can be considered if the FSH is not too high. During IVF there are tricks that can be played on the ovaries to get them to respond better, including DHEA-S treatment, a micro-dose flare protocol using lupron®, using estrogen or OCPs before IVF, avoiding lupron® altogether (substituting an GnRH antagonist) and increasing the amount of medication used. Finally, for women who have very high FSH levels, donor eggs can completely resolve the problem and the success rates (in the setting of IVF) are usually very good.

So my advice is not to put off ’til tomorrow what you can do today, especially if it means trying to have a baby.

I hope that wasn’t too depressing. I think I’ll go have a piece of cake.

(Source material: ASRM Practice Guidelines on Aging and Fertility)

Nausea with menstruation?

I always ask about symptoms at or before menstruation, since it can be very informative. Patients with nausea or vomiting around the time of menstruation may think that’s normal but it definitely is not. In my experience that usually is correlated with endometriosis on the bowel. Most often I’ve found endometriosis on the appendix.

Note the endometriosis on the tip of this appendix

Women are far and away more likely to be diagnosed with irritable bowel syndrome (IBS) compared to men. Is this a coincidence, I don’t think so. Retrograde menstruation of the spent endometrium accounts for most cases of endometriosis, putting the menstrual debris into the pelvic cavity where it can attach to and invade into pelvic structures, including the rectum, colon or appendix. It loves to implant on places with a good blood suppy.

When this patient had her appendix removed, her nausea went away entirely. The bowel talks to itself, communicating problems along its entire length using GI hormones. We need to learn to listen to what our patients are telling us and with time, start to understand what we are hearing. One lesson I’ve learned is that bowel symptoms during menses are almost always associated with occult endometriosis on or near the bowel. How many women on medications for IBS really have a gynecologic disease? Most, I think.

Problem solved

 

Why couples lose pregnancies

At the Fertility Center of the Carolinas we see a lot of couples with infertility. We also get referrals for many couples who have repetitive pregnancy loss. It is tragic to lose a pregnancy, but to lose 2 or more pregnancies becomes a heartbreak for couples that is often difficult to bear.  We feel the pressure as well, since many couples are feeling anger, guilt and despair by the time they first meet us.

I go through the list of possible reasons for losing a pregnancy along with the accompanying list of tests that we’d like to do. At the end of the day, a surprising number of couples don’t have any reason that we can assign to account for the loses they are experiencing.

1) Bad luck – a couple trying to conceive has a 20% (0.2) chance of having a miscarriage. Most of these loses is due to an abnormal embryo caused by the wrong number of chromosomes.  That percentage goes up as the female partner ages. To have 2  losses due to chance alone is equal to 0.2 x 0.2 or 0.04 (4%) and to have 3 loses (0.2 x 0.2 x 0.2 = 0.008; > 1%) is very unlikely.

2) Genetic causes – most spontaneous pregnancy loses are genetically abnormal (see reason #1), but paradoxically, most pregnancies from couples with recurrent loses are normal. In cases where repeated loses are due to genetic causes, the problem usually arises in one of the two partners. Parental karyotype (assessment of the chromosome number) is indicated, in my opinion, when couples loses 3 or more pregnancies. The test requires blood from both partners and a problem with the chromosomes is found only 2 to 3% of the time. When one partner is affected, there is nothing to do about it (practically speaking) although one could perform pre-implantation genetic diagnosis (PGD) on embryos in the setting of IVF. Up to half of the time couples with this problem will eventually be successful on their own.

3) Infectious causes of pregnancy loss are uncommon. In our clinic we rarely see this as a primary reason for recurrent loss. Empiric treatment with antibiotics is easier than performing uterine cultures. A biopsy of the endometrium (done for other reasons), might show endometritis (inflammation of the endometrium) but that diagnosis is usually associated with infertility rather than repeated loss.

4) Structural causes of pregnancy loss are diagnosed with sonohysterogram or hysterosalpingogram (HSG). A septum is a connective tissue ridge in the middle of the uterus that should have been resorbed during development but remains in the uterus. The blood supply is poor and embryos attaching to this septum outgrow their blood supply and can be lost. Other structural causes include polyps, fibroids and intrauterine adhesions, all of which can be corrected surgically, once identified.

5) Immunologic – supposedly up to 10% of recurrent loss is due to an immunologic problem. The tests include a lupus anti-coagulant and anti-cardiolipin test on a blood test. I haven’t seen many of these in the last 7 years, leading me to believe that they are uncommon (at least in SC).

6) Thrombophilias – blood clotting disorders are more common in couples that lose pregnancies in the second trimester. The work up includes 8 or 9 different blood tests and will have implications on how the next pregnancy is treated. Baby aspirin and heparin will be the treatments for folks that have this problem. A higher risk for (and family history of…) blood clots are associated with a positive screen for thrombophilias.

7) Hormonal – this is the most common and perhaps the most controversial cause of pregnancy loss. Diabetes mellitus or hyperprolactinemia (high prolactin levels) are treatable causes of pregnancy loss. Thyroid disease (hypo- or hyperthyroidism) should be ruled out. Luteal phase defect (LPD) is designated by a shorted menstrual cycle, when the time after ovulation is shortened. A timed endometrial biopsy or serum progesterone level has been suggested in the workup of this condition, but each have been shown to be invalid recently by prospective studies that examined LPD in fertile controls. Extra progesterone or hCG support is indicated in LPD, because they do no harm and for hCG at least, it appears to help prevent losses.

8)  Idiopathic – this means we don’t know why the couple is losing a pregnancy. This is the most humbling situation I have ever experienced. I have a patient who has lost 3 pregnancies in a row; all developed normally up to a certain point and then the pregnancy suddenly ended. I am glad this is extremely rare. There must be a cause but we don’t know what it is (yet).

9) Endometriosis – I discussed this in a previous blog. The diagnosis of endometriosis should be considered, especially in idiopathic pregnancy loss. The fact that women with endometriosis are infertile should help us understand why they also lose pregnancies. Timing is everything in a successful pregnancy and it appears that endometriosis delays or eliminates the normal window of implantation. In the former it may cause miscarriage in the latter, infertility.

So to end this very long blog, I suggest that the following tests be considered in recurrent loss patients: TSH, day 3 FSH, fasting glucose, prolactin, testosterone, DHEA-S, lupus anti-coagulant, anti-cardiolipin, parental karyotype, and possibly a thrombophilia workup. An HSG or sonohysterogram is necessary as well  If symptoms suggest  endometriosis or if biomarkers for endometriosis are identified, laparoscopy may also be beneficial

The Infertility Workup 101

Although we are very good at what we do, the diagnostic work up is pretty straight forward, for most couples.  I should add, its very important to finish this evaluation before recommending in vitro fertilization (IVF) or other advanced reproductive techniques.  IVF works well for many couples but many couples probably go through IVF who don’t really need it. The worst situation is to go through IVF and not to get pregnant, multiple times.  My first patient like this came to me having spent $25,000 (in 1989 dollars), failing IVF 3 times and still not knowing why she wasn’t getting pregnant. Turns out she had endometriosis and this story repeats itself over and over (http://ow.ly/1bJAb).

So, what I tell my patients when we first meet, is this:

There are 5 basic reasons why couples can’t conceive.

1) Male factor infertility – get a semen analysis

2) Cervical problems (rare in my opinion)

3) Blocked fallopian tubes or problems inside the uterus (get an HSG and/or sonohysterogram)

4) Ovulation problems – obtain hormone testing (TSH, Prl, FSH, estradiol, testosterone, DHEA-S, day 21 progesterone)

5) Endometriosis – consider a laparoscopy for diagnosis AND treatment of endometriosis

That’s it! Most couples will be quickly sorted out using this simple approach. Skip one of these steps and you may end up very unhappy with the results.  Case in point, see the following email I received from a doctor in Kentucky

 To: Bruce Lessey, MD


Subject: Thanks 

Dear Bruce,  Thanks so much for being so kind to my patient Ginger xxx. She is a very nice lady and is a statistics professor at one of the local universities. I wasn’t aware that she was going to call you until she brought a typed summary letter from her conversation with you, to her appointment later that day. I hope her call was not too much of an inconvenience for you. Both she and I appreciated your suggestions regarding treatment, and I thought I would give you a little follow-up on her. As she mentioned to you she has done 3 fresh IVF cycles and one FET which resulted in a biochemical pregnancy with a peak hCG of only 12. In each of her cycles she stimulated well and had good blastocysts, but never had a successful outcome.  In the cycle following her laparoscopy and ablation of endometriosis, she conceived on her own and is now 7 weeks pregnant with a viable IUP!  Needless to say, she is thrilled.

And so are we. Endometriosis Awareness Month starts March 1, please contact us with any questions you may have at fcc@ghs.org

Male Factor Infertility

According to most textbooks on the subject, male factor accounts for up to 40% of infertility. I not so sure. I talked to a gentleman today who called concerned because his semen analysis report had a “significant abnormality”. According to the World Health Organization, normal means 20 million sperm per milliliter, 2 milliliters of ejaculate, 50% motility and the morphology (the way the sperm look) should be normal. We use Kruger strict morphology and this man’s only problem was he had 5% normal forms. It only takes 10% normal forms to be normal. So, in this case, I suspect this isn’t the whole story for this couple because his count and motility was great.

When a man does have significant abnormalities, there are options. Vitamins (Vit C, E and L-carnitine) may help. Intrauterine insemination (IUI) is often done, often with some form of ovulation induction for the female partner. And if all else fails intracytoplasmic sperm injection (ICSI) in the setting of in vitro fertilization (IVF). With ICSI, a single sperm is injected into the cytoplasm of the egg and in many cases fertilization occurs normally and the embryo can be put back into the woman’s uterus. I’ve included a video of this amazing process and I hope it shows the images for you. Without ICSI, IVF did not work well for these couples with severe male factor; with ICSI, everything changed. More on the rest of the work up later.  ICSI