I attended the 35th Annual Symbosium on Obstetrics & Gynecology on October 29-30th at Washington University in St. Louis, MO. Learning new things is always exciting and it’s good to go to these programs to try to keep some pace with the rapid advancements in medicine. Wash U is considering a bastion of higher education and high quality medical treatment. Having been trained at a university hospital, I appreciate the level of consideration that goes into medical decision making, i.e. evidence-based medicine, that you sometimes don’t get in a rural community-hospital setting. That being said, since my pursuit of a more wholistic approach has been so rewarding, I can see how sometimes the most medically respected minds can be in an ivory tower of isolation, that is sometimes altogether different than everyday practice. So here’s my take on the topics discussed at the symposium. Warning: this is a lengthy post, so unless you are an ob/gyn geek like me, you might want to skim through to find a topic you like!
CONTROVERSIES IN SCREENING & TREATING FOR THROMBOPHILIAS IN PREGNANCY David Stamilio, MD, Maternal Fetal Medicine Specialist at Wash U, STL
This is a very important topic as I see a surprising number of women who have had a venous thromboembolism (VTE), or blood clot, at some point in their lives. It can be quite confusing in terms of whether this was a non-medically induced clot (such as after a car accident), or whether it represents an underlying clotting disorder, and future therapy. Also there are those who have suffered from adverse pregnancy outcomes like pre-eclampsia, a growth-restricted baby, abruption of the placenta, or multiple miscarriages. The questions include: who should be worked up, what should the work-up entail, who should be treated with anti-coagulation during pregnancy? Some highlights:
Should you test for clotting disorders in a woman who has had a blood clot while on oral contraceptive pills (birth control pills, OCPs) and should you anti-coagulate them during pregnancy (a state when your baseline risk for clotting is higher). Dr. Stamilio says NO you should not test because YES you are going to treat (put them on blood thinners during pregnancy and during the post-partum period). His point is that the testing is not going to change the management. My opinion: I would still test them, mostly because I feel it has implications beyond whether to anti-coagulate during pregnancy. This patient will want to know if you should use OCPS ever again, she will want to know about her risks for hormone therapy during menopause, and if she has daughters, what their risk might be.
What if you had a blood clot after a car accident, with no history of a prior clot or family history? No, don’t test, yes, treat them during pregnancy. One study showed that even patients with a temporary risk factor (like an accident) have a higher risk of a repeat clot. My opinion: I would probably not work up this person if they did not have any other risk factors (like they were on OCPs at the time of the accident).
What if you have a pregnant patient with no prior abnormal OB history who has a positive family history of blood clots? Yes, you would test, specifically for Protein C, Protein S, Factor V Leiden, Anti-thrombin III because these are most likely to cause significant clinical problems. You would treat them only if they test positive for a clotting disorder. My opinion: Agree.
What if you have a newly pregnant patient who had an incidental finding on lab work of a clotting disorder? NO DATA, but the recommendation is if you are a homozygote (2 copies of a mutation) or a compound heterozygote (one copy for two different clotting disorders): Yes, treat them. If they test positive for ONE copy of ONE clotting disorder, the recommendation is NO treatment. My opinion: I am not sure if I would be comfortable NOT treating them during pregnancy, after all, there is NO DATA stating one way or another. I also would recommend that this patient NOT TAKE oral estrogen of any kind.
What if you have a patient with a prior 2nd trimester (after 12 weeks) miscarriage and no family history? Not much data support for one first trimester loss, but there is data to support testing for those with a 2nd trimester loss or multiple first trimester losses. His recommendation is NOT to test for familial clotting disorders but to test for acquired clotting disorders like anti-phospholipid syndrome and treat if that is present. My opinion: I don’t see how you justify testing for some clotting disorders and not all. I would test for all.
What if you are pregnant and have a past history of severe preeclampsia and/or abruption pre-term (before 37 weeks)? The literature doesn’t support testing or treating these patients. My opinion: I know a lot of people who would put this patient on aspirin therapy, even without literature support. Any takers on this one?
Overall: Excellent lecture, however I found out that these guys don’t test for MethylTetraHydroFolateReductase mutations (MTHFR). He states many people are positive for these mutations and there is no association with VTE or early miscarriage. This information is very interesting because in my clinical practice I have seen this mutation be the only abnormality in someone with a prior blood clot. Other literature also says this mutation doesn’t mean anything unless the patient also has high homocysteine levels. I don’t know if I am quite ready to quit testing for this, mostly because my response to the finding is to put people on B6/B12/folate, which doesn’t really put them at risk for anything, and may benefit.
PREGNANCY AND LONG TERM HEALTH RISK by Haywood Brown, MD, Professor of OB/GYN at Duke University.
This was the standout lecture of the symposium! I found myself looking back at this guy’s credentials and saying I can’t believe he is advocating for breastfeeding like this! Not to be cynical or anything, I have come across those in the medical establishment who get it, but he was such a breath of fresh air, because you could tell he is one of those minds that wants to know WHY and how to fix problems by avoiding them in the first place! Plus he was a great public speaker, jokes, engaging the audience, etc. Just great!
Dr. Haywood began by talking about the greatly escalating rates of cardiovascular disease, obesity and diabetes general, but specifically in the child-bearing population. His point is that obesity begins in the womb through poor maternal nutrition which results in small birth weight, but initial poor growth is followed by rapid catch-up growth resulting in increased body fat and increased plasma leptin. (Who hasn’t seen a preemie who is now really big, even obese?) The Barker hypothesis is “Adverse influences early in development, and particularly during intrauterine life, can result in permanent changes in physiology and metabolism, which results in increased disease risk in adulthood. Reduced fetal growth is strongly associated with a number of chronic conditions later in life: coronary heart disease, stroke, diabetes & hypertension.”
He also discussed the “Undernourished Fetus: Thrifty Phenotype”: The fetal response to limited nutrients directs calories away from the body to the head, heart and adrenals which results in tissues becoming insulin resistant. Thus low birth weight babies who have accelerated catch up growth are at increased risk for obesity, insulin resistance and cardiovascular disease. Conversely, high birth weight babies are also at increased risk for obesity, diabetes and premenopausal breast cancer. This gives rise to the definition of gestational programming which means that the negative consequences of fetal adaptation (higher risk for developing certain chronic diseases) may remain dormant for decades, until triggered by other negative factors later in life (smoking, obesity, lifestyle).
So what is the answer to all this disturbing information?? BREASTFEEDING!!! Ob/Gyns are on the frontlines for encouraging, educating and supporting breastfeeding which can substantially affect the long-term health for SGA & LGA babies! The Nurses Study showed that those women who have been breastfed had a reduced risk of cardiovascular disease. Breastfed babies also have lower blood pressure and obesity down the road. Preemies who receive mother’s own milk (as opposed to donor milk or preemie formula) have less necrotizing enterocolitis, sepsis and shorter hospital stays.
Having an adverse pregnancy outcome like pre-eclampsia, eclampsia, low birth weight baby, or preterm birth can increase your risk of cardiovascular disease later in life. If you’ve had all three conditions (pre-eclampsia, prematurity and low birth weight), your risk of ischemic heart disease later in life is greatly increased. Women who’ve had a pregnancy complication like previously mentioned have an increased risk of an early cerebrovascular event.
The sum of the lecture was to have a focus on this concept of Interconceptional Care: Intrauterine nutrition, postnatal feeding, and environmental changes are the keys to breaking the cycle of generational adverse health from chronic disease and narrowing the gap in ethnic disparity of disease. i.e. eat well during pregnancy, breastfeed your baby as long as possible, and make healthy lifestyle choices like not smoking, eating well, exercising (and my addition, take your supplements like fish oil, antioxidants, Vit D, CoQ10). A++++ Dr. Haywood!
INTRAPARTUM CONTROVERSIES AND UPDATES – 2009 by George Macones, MD, Professor of OB/GYN, Wash U
The main focus of this lecture was about the new Electronic Fetal Monitoring classification system and VBAC issues.
Contractions: Normal is considered less than or equal to 5 contractions in 10 minutes. Tachysystole is defined as greater than 5 contractions in 10 minutes (terms of hyperstimulation and hypercontractility are to be abandoned).
Decelerations features NOT defined: slow return to baseline, biphasic decels, reflex tachycardia following variables, shoulders or overshoots, FHR fluctuations in the trough of decels, mild/mod/severe decels.
Category I tracings (Normal); must include all of the following: Baseline rate 110-160 bpm, moderate baseline variability, no late or variable decels, earlys may be present or absent, accelerations may be present or absent. Reponse? follow in routine manner.
Category II tracings (Indeterminate): All tracings that are not categorized as I or III (helpful, huh?) Response? continued reevaluation, additional tests (like scalp stim, vibroacoustic stim, transabdominal halogen light), non surgical intervention (stop Pit, check for cord prolapse, maternal oxygen, position change, correct blood pressure problems, amnioinfusion for persistant deep variables).
Category III tracings (Abnormal): Can include either: Absent FHR variability and any of the following recurrent late decels, recurrent variable decels, or bradycardia. OR a sinusoidal pattern for greater than or equal to 20 minutes. Response? predictive of abnormal acid/base balance, prompt evaluation required, resolve the pattern (supportive measures, delivery).
VBAC: Lowest risk of uterine rupture is in those who go into spontaneous labor or those induced without Pitocin or Prostaglandin. More success if cervix ripe (avoid difficult inductions). Avoid high dose Pitocin (as someone who had a uterine window, eminent rupture, on high dose Pit, I agree). Do not use Cytotec, period. My opinion: Pick your patients well, avoid induction, if things aren’t going well STOP, but don’t be afraid of VBAC (sorry not for homebirthers or birth center births). I am grateful for both of my VBACs, but would never consider it safe for outside of the hospital.
SHOULDER DYSTOCIA: THE UNPREDICTABLE EMERGENCY by Haywood Brown, Professor of Ob/Gyn, Duke University
Increase in incidence of shoulder dystocia (after delivery of head, baby is prevented from delivering spontaneously by impaction of the shoulders in the maternal pelvis) from 0.6 percent of births to 1.4% due to increases in birth weight, increasing prevalance of maternal obesity and diabetes. However, the incidence may be more like 4%, 50% of shoulder dystocia in infants less than 4000 gm (8.8 pounds), however, 11 times higher if baby is greater than 4000 gm and 22 times higher if greater than 4500 gm (9.9 pounds).
Risk factors: Macrosomia (diabetes and post-dates), maternal obesity and excessive weight gain, previous baby greater than 4000 gm, diabetes mellitus, prolonged second stage of labor, prolonged deceleration phase (after 8 cm), rapid descent of fetal head, forceps midpelvic delivery.
Main concerns: Brachial plexus injury, to spinal nerves (incidence 4 to 40% following shoulder dystocia, less than 10% permanent), Fracture of clavicle or humerus.
Take home message: You can’t predict shoulder dystocia, so be prepared ahead of time with the proper maneuvers. Have a high degree of suspicision with macrosomia, maternal obesity, gestational diabetes and prolonged gestation. Estimated fetal weights by ultrasound are problematic because of accuracy issues. Dr. Haywood, “C-section for assumed macrosomia is inappropriate.” This was my favorite: A planned cesarean for greater than 4000 gm baby in a non-diabetic mother would result in a 27% increase in the total cesearean rate and would only reduce shoulder dystocia by 42%. It would result in an additional 2345 cesareans at a cost of $4.9 million annually to prevent one permanent injury from shoulder dystocia. Tell it like it is Dr. Haywood!
MANAGEMENT OF PERIPARTUM DEPRESSION by Keith Garcia, MD, PdD, Assistant Professor of Psychiatry, Wash U
I have one word to describe this lecture: CRAP! Sorry, but I just had to get that off my chest. I’m sure Dr. Garcia is considered to be a fine psychiatrist or he wouldn’t have been selected for this lecture…but this might as well have been one paid advertisement for SSRIs. I guess it shouldn’t be surprising since he is a psychiatrist and not an obstetrician/gynecologist, but FOR REAL??? He spent the entire lecture talking about how imperative it is that women even with mild depression be medicated throughout the entire pregnancy, post-partum period, regardless if they are breastfeeding. He discussed using various depression scales to assess women during pregnancy and afterward and I found myself asking what hormonal pregnant woman wouldn’t answer yes to some of these questions (e.g. I have been anxious or worried for no real reason). He significantly downplayed the fetal risks from SSRI when it is clear there are risks to the baby especially in relation to respiratory problems. He seems to think there is no appreciable transmission of SSRIs in breast milk, which I really question. There is definite evidence that one agent, paroxetine or Paxil, when taken in the first trimester is associated with an increased risk of cardiac malformations.
As always, one of my big areas of concern is the impact of hormone imbalance, specifically progesterone deficiency, with regard to depression in general and specifically post-partum depression (please see my post on this for more). I think we have an epidemic of women with progesterone deficiency, who if they are even able to get pregnant since many have sub-fertility, have higher rates of preterm labor, bleeding during pregnancy, miscarriage and post-partum depression. I wouldn’t expect this guy to really be concerned about hormonal issues (beyond the obligatory nod to checking thyroid function) since most Ob/Gyns ignore this important subject as well. My main concern is his blase attitude toward proliferative drug use, perhaps reflecting his skewed patient population. Don’t get me wrong, patients with psychotic disorders, suicide attempts, or multiple disorders need to be under the joint care of a psychiatrist and an obstetrician, and in their case, treatment is most likely to outweigh the risks, which have to be acknowledged. However, in my opinion, this was far too liberal an approach.
WEIGHING IN ON THE OCTOMOM: KEY CONCEPTS IN EMBRYO TRANSFER – PRACTICES OF IVF AND SUPPORTING FAMILIES THROUGHOUT THE PROCESS by Emily Jungheim, MD, Instructor in Ob/Gyn at Wash U & Kelly Ross, MD, Assistant Professor of Pediatrics, Wash U
Octomom has been a hot topic…how far can the human body really stretch?? In our Guiness Book of World Records mentality, it seems as if we will always have those patients and doctors willing to push the envelope farther when it comes to human reproduction. While it is hard not to be shocked and dismayed at this modern feat of assisted reproductive technology, I find it interesting that the “get your hands of my uterus” crowd didn’t mind voicing their displeasure at Octomom. It seems that only applies if you are bringing less children into the world rather than more.
Here’s what we know: Only the 2nd live born set of octopulets in the US. 6 frozen embryos were implanted, two split into twins. She had 6 other children, all born after IVF. We have been told that she is also single and receiving public assistance, that she asked for multiple embryos to be implanted and that her REI doctor regularly implanted this many to augment his poor success rates. Apparently he has been kicked out of ASRM, see below, for routinely transferring more than the recommended amount of embryos for a woman’s age. The medical board of California hasn’t taken any steps against him, because as I noted above, he doesn’t appear to have broken any laws and was apparently doing what the patient requested.
The American Society of Reproductive Medicine (ASRM) and the Society for Assisted Reproductive Technology (SART) have both been pushing for physicians to strive toward implanting fewer embryos with more emphasis on single embryo transfer. So far these have been recommendations and not mandates understanding that this is a process fraught with troublesome issues: infertile couples wanting to get pregnant but not really understanding the risks of multiples, limited resources and limited cycles that couples are willing to undergo and able to afford, what to do with excess embryos. Naturally the best time to discuss all this is before undergoing IVF, but this is difficult. As another speaker said, the couples come in wanting a baby, not to wade through a 27 page consent form. I disagree with their recommendation that after IVF is the time to discuss what happens if you end up with higher order multiples (more than twins): issues such as whether you would consider abortion or selective reduction (picking which one of your tiny babies you’re going to “sacrifice” for the benefit of the others). Surely a discussion of this magnitude should take place before undergoing any procedures: the list of what-ifs grows longer by the day in the field of reproductive medicine.
If you’re not able to prevent them, then get ready to SUPPORT them, says Dr. Ross, herself a pediatrician and the mother of IVF-produced triplets. Between 1980 and 1998, the triplet rate increased by 400%, mostly because of IVF. Most higher order multiples are going to be preterm births and require NICU stays. “The stresses and experiences of parents of multiples who have undergone multiple fertility treatments diffre from those who have unplanned or spontaneous multiples.” Think Jon & Kate Plus 8? You go from the stress of not being able to get pregnant, to the stress of being pregnant with higher order multiples with the physical, mental, and emotional stressors and the 5 times higher risk of complications, to the stress of a most-frequently surgical delivery, to babies in the NICU, financial stress, higher risk of death and cerebral palsy as well as other complications from prematurity…plus a higher rate of post-partum depression.
Another good quote: “To a woman who has been unable to get pregnant with one baby, discussing her risks of getting pregnant with 3,4, or 5 is like discussing her risks of winning the Powerball.” It is hard to wrap your mind around it…but the discussion must take place ahead of time. And this one, “A history of infertility makes these new mothers feel as if they have ‘no right’ to complain about common experiences other new mothers complain about.”
Support for women with a multifetal pregnancy: Refer to a true specialist in higher order multiples, strongly encourage joining a support group MOST (Mothers of Supertwins), www.MOSTonline.org, Triplet Connection. What if you lose one of those babies: CLIMB (Center for Loss in Muliple Births) and SHARE. Collect memories, www.nowIlaymedowntosleep.com and www.3littleangels.com.
THE INFERTILITY EVALUATION: EVOLUTION AND REVOLUTION by Marc Fritz, MD, Professor of Reproductive Endocrinology and Infertility, University of North Carolina at Chapel Hill
Ovarian factor: 1. Day 20 serum progesterone, standard. This guy thinks you shouldn’t put much credence in it because of problems with fluctuation of hormone levels, different cycle lengths etc. To which I say, test in saliva! You still have to take into consideration the cycle length issue, but it is well correlated to endogenous production of progesterone. This very important issue was drastically underplayed. 2. Urinary LH monitoring, frequently used, not always reliable, expensive. Optimal time for testing: 4 to 10 PM, due to pulsatile LH surge. 3. Serial transvaginal ultrasound – Probably only useful if you are using ovulation induction agents.
Male factor: Semen analysis: Morphology is the best current predictor of sperm function and predicts poor or failed fertilization in IVF cycles. Males should be referred for hormonal testing if they have oligospermia (less than 10 million/mL) or sexual dysfunction (decreased libido or impotence). Of course, they recommend FSH, total testosterone, free testosterone, LH, prolactin. I would also recommend estradiol, cortisol, DHEA and TSH along with that. Males with low sperm count should be referred for urologic testing to rule out obstruction, other problems. Don’t get Dr. Sherman Silber started on this topic. He is a world-renowned fertility specialist who thinks people waste a lot of time at the urologist’s office instead of getting plugged in quickly to the right procedure for male subfertility. Sometimes an abnormal semen analysis also warrants a genetic evaluation for things like Cystic Fibrosis or chromosomal abnormalities.
Cervical factor: Postcoital test, not used or recommended anymore. My favorite cervical factor trick: Guaifenesin, which thins all secretions, including semen to facilitate sperm mobility. Especially important for people taking Clomid, which can thicken cervical mucous.
Uterine factor: Hysterosalpingogram (HSG) or dye study to evaluate the uterine cavity and the prescence of uterine anomalies or structural problems like fibroids. Ultrasound is also used to evaluate the uterus. If an abnormality is indicated, hysteroscopy of the uterus is helpful for diagnosis and treatment of intrauterine abnormalities. Sonohysterogram is also helpful and may save a surgical procedure. Throw out the endometrial biopsy, it is no longer recommended.
Tubal factor: HSG to establish that the tubes are open so the egg and sperm can get to each other. Chromotubation is where dye to put through the tubes at the time of laparoscopy to estalish tubal patency. Some people start with a Chlamydia antibody test to determine whether to do an HSG, as this common infectious organism causes tubal scarring.
Peritoneal factor: Evaluation for endometriosis and adhesions which can cause scarring, blockage or structural abnormalities. Evaluated by laparoscopy. Only do if there are symptoms, risk factors, or an abnormal HSG or ultrasound. Otherwise the yield is low and doesn’t warrant the expense or risk of surgery.
Ovarian Reserve: Indicated for age 35 or over, 1st degree relative with premature menopause, Previous ovarian insult (surgery, chemo, radiation), smoking, poor response to ovarian stimulation, unexplained infertility, candidate for IVF. Cycle Day 3 FSH/estradiol: FSH greater than 10-15 Iu/L, Estradiol greater than 75-80 pg/mL. If abnormal, prognosis is poor, if normal, corelates with age. Clomid challenge seems to be falling into disfavor.
Overall, a nice overview. I differ by performing hormone testing on everyone who has infertility. With so many endocrine disruptors in our lives, it is rare to see a completely normal hormone profile, especially progesterone, which as I have repeatedly stated is essential for fertility.
RISKS OF ADVANCED REPRODUCTIVE TECHNOLOGIES: WHAT PHYSICIANS AND PATIENTS NEED TO KNOW by Randall Odem, MD Professor of Ob/Gyn, Reproductive Endocrinology and Infertility, Wash U
The primary problem is being able to address all the different forms of ART and all the individual risks associated with each facet of it. It can be confusing for doctors, let alone patients. I’m not going to review all the risks of every part of the ART process but rather will try to highlight those I think are most important to communicate.
Risks of the process: We touched on this earlier. The patient needs to be fully informed regarding the specifics of the procedure she is undergoing, the cost of the cycle, and the age-related success rates for the procedure. She needs to be informed of the chances of multiple gestations, a clear and explicit discussion of how many embryos are to be transferred and why, and what is going to become of any leftover embryos. A good IVF clinic is going to have a counselor who spends a good amount of time with the patient and her family regarding these issues. Certainly the process of IVF is mentally challenging, time-consuming, expensive and emotionally draining and the psychosocial aspects of it need to be addressed.
Risks of the pregnancy: The risk of multiples extends not just to babies but to the mother who must carry the pregnancy and be subjected to likely complications. This entails more frequent than average doctors visits, more ultrasounds, more possibility of maternal complications, more chance of a surgical delivery. However, what is more disturbing in my mind, simply because I think it is unrecognized with the focus on multiples, is the higher risk of pregnancy complications in women who conceive ONE baby after IVF. According to one meta-analysis, those increased risks include gestational diabetes, placenta previa, preeclampsia, stillbirth and neonatal death. Another study showed a nearly 3 fold increase in the risk of placenta previa and nearly 2.5 fold increase in placental abruption. Is this from the IVF process itself, or is this simply a reflection of older moms or women with fertility problems being higher risk in general? We don’t have the answer to that.
Risk to the Offspring: Certainly, twins and higher run the routinely higher risk of premature births. However, there are non-prematurity risks with IVF. In the normal population, the risk of birth defects is 2-3%. In the IVF population, it is 2.6-3.9% While this might be felt to be a marginally higher risk, the data does seem to show that babies conceived through ICSI (Intracytoplasmic Sperm Injection, used primarily in male factor infertility) have a higher birth defect rate as well as an increase of sex chromosome abnormalities. One of the hypotheses is that an inherent paternal problem leading to infertility when overcome by ART procedures is possibly magnifying these genetic abnormalities.
Overall, a sobering topic…or some might say, “IVF: Enter At Your Own Risk.” Here’s my pet peeve: the REI doctors’ main concern is getting someone pregnant (which they often do for lots of money, since many IVF procedures are not covered by insurance)…then they are transferred to a regular OB or a high risk OB specialist, who then has to assume the care and the liability for these often extremely high risk pregnancies. And often they only get the same global OB fee. It’s not about the money, sure, but you create these incredibly high risk patients…and then punt them off and they become someone else’s problem…I just think REI docs need to consider not just the burden to the patient, but to the other doctors.
RECURRENT EARLY PREGNANCY LOSS by Marc Fritz, MD, Professor of REI, University of North Carolina, Chapel Hill
Early pregnancy loss affects 12-15% of clinically recognized pregnancies, 60% of all conceptions (many unrecognized). 60% or more may be related to chromosomal abnormalities, most commonly trisomies. Miscarriage rate certainly increases with age.
Recurrent early pregnancy loss is defined as 3 or more losses before 20 weeks, affects less than 1% of couples, and 50-70% ultimately go on to have a live birth. Indications for work-up include 3 or more losses or 2 losses in women older than 35, history of subfertility, normal chromosomes on miscarriage, or loss after heart tones are detected.
Genetic causes include parental chromosomal abnormalities. Testing products of conception for chromosomes after miscarriage is problematic/not always accurate. Can be age-related chromosomal problems in older moms. Preimplantation testing for chromosomal abnormalities prior to IVF is not currently advocated for screening, only in those with a known chromosomal abnormality are the risks considered acceptable (if the parents would even consider themselves).
Anatomic causes include congenital uterine anomalies, fibroids or adhesions. Usually diagnosed by HSG, sonohysterogram or MRI. Miscarriage rate is highest for septate uterus, it is also the most common anomaly. Repair improves outcomes. Only large fibroids disrupting the uterine cavity seem to be the biggest risk and warrent removal. Adhesions can usually be easily removed.
Endocrine causes include undertreated/subclinical hypothyroidism (this is very common), hyperthyroidism (not so common), poorly controlled diabetes. The most common endocrine abnormality in women: PCOS (polycystic ovarian syndrome), although it more frequently causes infertility rather than recurrent early pregnancy loss (PCOS is extremely common in my practice). Luteal phase deficiency due to inadequate progesterone support. He really underplayed this as a risk and again talked about not testing progesterone because it was not reliable to which I say, BUNK!! My opinion: Every women with a history of miscarriage (even if it just one) warrants progesterone support in the first trimester (in my practice, I document their low progesterone level which is easy with saliva testing). You have nothing to lose and everything to gain!
Immunologic factors include lupus and anti-phospholipid syndrome. Optimize control of the disease before conception and anti-coagulation (ASA and heparin or LMWH) if you have the antibodies. Other auto-immune disease may contributre to risk. Inherited clotting disorders has some association: Worse ones are Factor V Leiden and prothrombin mutations. Treat during pregnancy with anti-coagulation.
Infectious factors: not straightforward but there may be more risk with Mycoplasma infections and chronic or recurrent bacterial vaginosis. Treat if found but looking for it has low yield.
Environmental factors include excessive alcohol, smoking, environmental toxins like heavy metals, organic solvents, hyperthermia, radiation, certain medications. Assess for and address.
Up to 70% of women have no identifiable cause or predisposing risk factor. Support women, encourage women and keep looking. Although this expert doubts the true success of progesterone supplementation, again there is no risk in using it and those of us in clinical practice know it works. The use of prophylactic ASA is also contraversial, no data to support using it, but many people do, usually it is low risk, not always.
CLOMIPHENE (CLOMID): KEEPING IT SIMPLE – USING IT WISELY by Valerie Ratts, MD, Associate Professor of Ob/Gyn, Wash U
Interesting drug: has some estrogen-stimulating characteristics, some estrogen-antagonizing characteristics. Essentially fools the ovary into recruiting eggs. Not always effective is women who are low in estrogen to start with. Some start at 50 and go up every month to 250 until ovulation is achieved (seems kind of aggressive to me, but OK). Some use basal body temperatures, LH predictor kits. (I use cervical mucous! Temps are retrospective, predictor kits are expensive and you can miss some good fertile days this way.) She disputes using progesterone, which just amazes me. Risk of multiple gestation is 7-10%, usually twins. Also has side effects on cervical mucous, hot flashes, mood swings, ovarian cysts. 20-30% of people either don’t ovulate or don’t pregnant even if they ovulate with Clomid. PCOS patients benefit from Metformin and Clomid together (Agree!) Aromatase Inhibitors do not signficantly improve ovulation rates over Clomid. Many use Clomid in patients who ovulate, to “optimize eggs” to be combined with intrauterine insemination. She talks about adding estrogen support after last day of Clomid, but poo-poos progesterone (?!?). I would never use Clomid without progesterone, it just doesn’t make physiologic sense.
Alright, well, that’s a lot of information to process so I’ll leave you to that for now. Stay tuned for Part Two which will address issues in gynecology and oncology. You get to hear my opinion of the highly esteemed (by the establishment, that is) Wulf Utian, Executive Director of the North American Menopause Society (NAMS) regarding hormone therapy. Readers of this blog will guess which direction that is going!