Robertsonian Translocations

One of our readers left the comments/questions below that were worthy of a post for general consumption by interested readers...

Anonymous has left a new comment on your post "Recurrent Early Pregnancy Loss - 3 - Chromosomal C...": Hi-I am 30 years old and have suffered 3 miscarriages. After my third, my Dr. did a karotype and found that I have a Robertsonian translocation between 13 & 14. From what I've learned researching this topic, is that I have a 50-50 shot of producing an egg with the correct number of chromosomes or with the same translocation as I have. Is that assumption correct?Also, is IVF w/PGD our best bet in having a healthy baby? Is it also true that if I have this translocation that chances are one of my parent's have it and/or my sibling's?Thanks so much!! My anxiety has been sky-high ever since I found this out and I can't see a genetic counselor until November 1st. Gina

Gina, all of these are great questions, and as so much in this world of medicine, not as easily answered as you might like…

Under normal (euploid) circumstances, humans have 46 chromosomes in each of the cells that make up their bodies. The complement of 46 chromosomes is composed of 22 pairs of ‘autosomes’ and 1 pair of sex (either XX = female, or XY = male) chromosomes – half of the total complement being inherited from each parent. Individual chromosomes are quite distinct in their appearance and most have long (= p) and short (= q) ‘arms’ that are connected by a structure called the centromere. When cells replicate to make another cell, they first duplicate their chromosomes and centromeres. The centromeres then connect to the structures in the cell that help separate these duplicated chromosomes from each other so that each new cell which results gets exactly the same chromosomal complement that was present in the ‘mother’ cell. This event is called mitosis.

To produce gametes (ova and sperm), a slightly different process is involved. Following duplication of the chromosomes, the overall complement of chromosomes delivered to each gamete must be reduced to half (23) that found in other cells in the body. This is two-step process called meiosis in which the centromeres also play a key role. During meiosis, the individual chromosomes (that were inherited from each of your parents) segregate more or less randomly into the resulting gametes, providing the great variability seen in our offspring.

Five of our chromosomes (13, 14, 15, 21 and 22) have ‘short arms’ that are very small and which contain no essential genetic material. These 5 chromosomes are called acrocentric chromosomes, or ‘acrosomes.’ Acrosomes have a tendency to fuse at the centromeres with other acrosomes, thus producing a ‘single’ larger chromosome made up of the ‘long arms’ of the chromosomes of origin, connected by a single centromere. When this occurs it is known as a ‘Robertsonian translocation.’ If no essential genetic material is lost (or gained) in the process, the individual with such a chromosome is said to have a ‘balanced’ translocation and appears ‘normal’ although they now have only 45, rather than 46, chromosomes in each cell.

Robertsonian translocations can occur between any of the acrosomes although this is not entirely random and the most common forms of these occur between chromosomes 13 and 14 (75%), 14 and 21 (10%), and 21 and 22. Individuals with Robertsonian translocations can have these as the result of a spontaneous event occurring during the meiosis (in either parent) that produced the egg or sperm from which they were made, shortly after conception, or from the inheritance of the same from one of their parents.

Robertsonian translocations are present in approximately 1/1,000 newborns. Individuals with balanced translocations are usually healthy and often unaware of their condition, especially if there is no prior family history that has led to the diagnosis, and often their chromosomal ‘abnormality’ will not be discovered until they have difficulty having children. The problem arises when individuals with Robertsonian translocations try to make gametes. In the case of our reader, who apparently has a balanced 13;14 translocation, the possible gametes she will produce (don’t ask me to explain why at this point) during meiosis may contain:

• 1) One free copy of chromosome (chr) 13 and one free copy of chr 14.
• 2) The translocation (chr 13;14) chromosome alone (which contains one copy of chr 13 fused with one copy of chr 14).
• 3) Chr 13;14 + one free copy of chr 13 (essentially, a gamete with TWO copies of chr 13 rather than just one).
• 4) One free copy of chr 13 (and NO copy of chr 14).
• 5) Chr 13;14 + one free copy of chr 14 (TWO copies of chr 14 rather than just one).
• 6) One free copy of chr 14 (and NO copy of chr 13).

Obviously, 3 through 6 are gametes that have the incorrect number of chromosomes (either too little or too much genetic material). When these gametes get together with the, presumably, ‘normal’ gametes from her partner (which contain one free copy of chromosome 13 and 14), the following possibilities result (in the same order as above):

• 1) Two free copies of chr 13 + two free copies of chr 14 = NORMAL
• 2) Chr 13;14 + one free copy of chr 13 + one free copy of chr 14 = translocation ‘carrier’ (just like Mom) with NORMAL TOTAL amount of genetic material
• 3) Chr 13:14 + TWO free copies (one EXTRA from Mom and one from Dad) of chr 13 + one free copy (from Dad) chr 14 = TRISOMY 13
• 4) Two free copies chr 13 (one from Mom and one from Dad) + ONE free copy of chr 14 (NONE from Mom and one from Dad) = MONOSOMY 14
• 5) Chr 13:14 + one free copy of chr 13 (from Dad) + TWO free copies (one EXTRA from Mom and one from Dad) chr 14 = TRISOMY 14
• 6) ONE free copy chr 13 (NONE from Mom and one from Dad) + two free copies of chr 14 (one from Mom and one from Dad) = MONOSOMY 13.

Therefore, to answer one of our reader’s questions, mathematically, she has only a 2 in 6 (33.3%) chance of having a baby that has the right TOTAL amount of genetic material; one of these will be entirely chromosomally normal and the other will be a translocation ‘carrier’ just like herself. Two-thirds of her babies are at risk for being chromosomally ABNORMAL.

But, as I mentioned at the outset, things are not quite that simple. Indeed, her actual risk for having a baby with a chromosomal abnormality is much lower than this. The monosomy 13 and 14 embryos will not be successful at all and the trisomy 14 embryos also have very little chance of surviving much of the first trimester. Most trisomy 13 embryos will also be lost early in first trimester and the few that survive will have only a small chance of surviving the pregnancy and even a smaller chance of living more than a few hours or days after birth. These babies all have severe congenital malformations and if they manage to survive birth and the neonatal period, profound metabolic disturbances, and mental retardation. Indeed, the ‘selective forces’ are so strong against these chromosomally abnormal conceptuses that at least two-thirds of her pregnancies in which a pregnancy is actually confirmed will be chromosomally normal and the chances of actually DELIVERING a chromosomally abnormal baby are probably only about 1%! The overall risk of miscarriage is about 25%.

With regard to the question of IVF (in vitro fertilization) and PGD (prenatal genetic diagnosis), I have a significant amount of ambivalence. If you have the money to burn, these are certainly options, but they are very expensive procedures. And, if you have no difficulty conceiving and are willing to trust nature to do the right thing, as pointed out above, the risk for actually having a baby with an unbalanced karyotype is so small, that it is often simply waiting until the dice roll correctly to have a normal baby. I know that can be difficult psychologically and at times physically. However, because there is nothing that can be done to correct a translocation, if one can accept the fact there is an increased risk for miscarriages, and that when these occur, it is probably the result of an aneuploid fetus, dealing with the pain of pregnancy loss may be a little bit easier.

There is a lot we have not discussed about Robertsonian translocations in this post, but I would like to make a few recommendations in closing (and we can always use these other issues as an excuse to write another post). First, I would suggest that any couple with a known Robertsonian translocation, consider having combined first trimester screening for aneuploidy performed and seriously consider a chorionic villus sampling if this is 'abnormal'. Secondly, even if this is reassuring, consider having a fetal karyotype done by amniocentesis. Thirdly, once an individual with a Roberstonian translocation has been identified, I think it is important to let other family members (male or female) of reproductive age know so that they can be screened as well. It may save a lot of anguish down the line.

Anyway, Gina, thanks again for your questions. I am wagering right now that your pregnancy quest will be rewarded in the end. Best of luck to you and your husband and thanks for reading!
Dr T

Labels: aneuploidy, Robertsonian translocation

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Obesity and Birth Defects

The other day, I wrote a post related to rising maternal mortality rates as reported by the National Center for Health Statistics. In that post, I cited obesity as one of the likely contributors to the problem. Today, the Trust for America’s Health (TFAH) foundation released a report, “F as in Fat: How Obesity Policies are Failing in America, 2007.” The results are quite sobering. Obesity, defined in adults as a BMI (BMI = weight in pounds/ height inches x height in inches x 703) > 30, rose in 31 states last year and fell in NONE. Ten of 15 states with the highest rates are in the South. In my own state of South Carolina, the overall rate of adult obesity is now 27.8% (tied for 5th with Tennessee). Accompanying obesity, hypertension is now found in 29.7% and adult-onset diabetes is found in 9.4% of SC state residents. An even more ominous finding is that now, among children ages 10 to 17 in SC, 18.9% are considered overweight (> 95th percentile in weight for age).

Echoing these findings, Dr. James Marks, senior vice president of the Robert Wood Johnson Foundation, which funded the project, commented in a news conference that “The number of states with obesity rates greater than 25 percent has more than doubled in just two years. That's not sending a wake-up call. We're ringing the disaster alarm," he said. "Diseases that used to be considered adult illnesses like type 2 and high blood pressure are becoming increasingly common among children." To put the current epidemic in perspective, in 1991 NO state had an obesity rate in excess of 20%! Jeff Levi, PhD, Executive Director of TFAH, summarized his feelings as follows: “Poor nutrition and physical inactivity are robbing America of our health and productivity.” Indeed, key findings in the report were that “22% of adults admitted to participating in no physical activity and that while every state has school physical education requirements, many are limited in scope or are not enforced.

The statistics above, help to justify the actual reason I sat down to write this post. As part of my comments related to obesity and maternal mortality, one of our residents in OB/GYN couldn’t disagree with my concerns regarding the association of obesity with hypertension, diabetes, and risks for other complications of pregnancy, but challenged my statement regarding the increased risk for fetal abnormalities. Actually, it wasn’t so much a challenge as a request for a specific reference. I did not know one off the top of my head, but the resident wasn’t going to buy my initial response of “in my experience over the last 25 years…” I couldn’t argue the point because these are the days of ‘evidence-based’ medicine and I have to at least try to set a good example. Fortunately, the question was raised on the same day I came a cross an article by Waller and colleagues published earlier this month (Arch Pediatr Adolesc Med. 2007;161:745-50).

In this report, the authors summarized their findings to date from the National Birth Defects Prevention Study, an ongoing multisite case-control study looking specifically at structural birth defects in both overweight and underweight women. Information was gathered from databases in eight states during the time period between October 1997 and December 2002. A clinical geneticist reviewed all cases of birth defects and excluded those found in women with known preexisting diabetes and suspected cases of chromosomal abnormalities or single-gene mutations. An association between congenital abnormalities and obesity was found for spina bifida, congenital heart defects, anorectal atresia, hypospadius, limb reduction defects, diaphragmatic hernias, and omphaloceles with odds ratios ranging from 1.33 to 2.10. It is interesting to note that many of these abnormalities are commonly associated with preexisting diabetes, especially when blood sugar control is poor during the first trimester.

I am not going to speculate on the etiology for the associations at this point. Part of it may be related to previously undiagnosed diabetes or the genetic predisposition for the same, insulin resistance, chronic inflammation, hypercholesterolemia or elevated triglyceride levels, or a host of other problems known to be more common in obese individuals. However, I suspect that a large contribution is simply from the fact that being overweight does not necessarily mean you are in good shape nutritionally. I would not be surprised if studies confirm that levels of folic acid and other vital nutrients that support normal embryogenesis are probably ‘under-represented’ in the obese at the same time certain ‘embryologic toxins’ are present in higher than expected concentrations.

As Dr. Levi from TFAH also pointed out, "If we fail to reverse this epidemic, the current generation may be the first in American history to live sicker and die younger than their parents' generation." With the growing awareness of ‘epigenetic imprinting,’ the condition under which the maternal health status can contribute to the ‘programming’ of the fetus in utero, we may be looking at much more than an impact on the current generation, we may be looking at problems for generations to come!

Labels: congenital anomalies, imprinting, obesity

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Maternal Mortality Rates Rise

• Within the past week the National Center for Health Statistics released its annual report on mortality in the U.S. for the year 2004 (National Vital Statistics Reports. 2007. 55;19) Buried as the last area of comment in the report were the maternal mortality rates for that year and these showed a very troublesome statistic. The mortality rates for women during pregnancy and within 42 days following delivery have risen to 13.1 per 100,000 - the highest in more than 20 years!
  
  Over the past two days, I have read and heard several comments related to this report with statements such as, “This is unexplained…It’s probably the result of the newer methods for gathering statistics…This is incomprehensible in this day and age of modern medicine…This represents only 540 women…” Well, you know what. None of those statements are very appealing to me. They all reflect an attitude of “It’s someone else’s responsibility,” and quite frankly it’s time we face reality and get off our butts and do something about it.
  
  Although this represents “only” 540 women, that is still an increase of 45 over the previous year’s reporting; and I would wager, the real number is greater than that actually reported for a variety of reasons. Furthermore, although the overall rate is 13.1, the rate for blacks is actually 34.7 per 100,000, or 3.7 times the rate in whites. Several recent studies have shown that at least 40% of all maternal deaths are probably preventable. Rather than being “incomprehensible,” there are clearly several factors contributing to the rise in maternal mortality. Below are my thoughts and they are not in a rank order of importance, simply in the order in which they jumped into my head:

• Poor federal funding for uninsured and underinsured women – sorry, but if we can spend $2 billion dollars+ a day in Iraq, we should be able to take care of ALL women who are pregnant or thinking about getting pregnant. Our citizens deserve that and even if a woman is here illegally, her children are going to be U.S. citizens and if not cared for properly, will increase risk to the entire Public Health system. It is an investment in the future of our country and the welfare of ALL citizens.


• Cesarean section rates now exceed 30% - this procedure may not take very long to perform, but it is still a MAJOR operation and as such is accompanied by risks of hemorrhage, infection, and thromboembolic events.


• Vaginal birth after cesarean section (VBAC) is almost history and repeat cesareans are associated with increased risks for the complications noted above and then some.


• Obesity – guess if you take physical education out of the schools, people will get fat – you figure!, and….


• Increased risk for diabetes, hypertension, large babies, birth defects, cesarean section, and attendant complications related to obesity and…


• Delayed child-bearing – older women are having babies and their risks for all the complications above are well-documented.


• Infertile women and women with significant medical problems are achieving pregnancies – ditto to the comments above.


• Medical errors – many related to medication errors, documentation errors, inattention to allergies or unexpected allergic reactions, too few doctors practicing obstetrics and long hours worked, too few nurses, cutbacks with decreased nurse/patient ratios, reliance on ‘technology’ rather than face-to-face patient contact…..


• Lack of a national electonic medical health care record - in this era of Intel, AMD, Microsoft, Apple,...this is a true travesty and providing such a record might vastly improve health care and the acquisition of meaningful statistics that could help us to improve that care.
  
  I am quite certain this list is not complete, but it gives us more than enough areas to which our attention SHOULD be directed to start. The challenge is before us. The only question is will we as health care providers, patients, legislators, and as a nation assume responsibility for our future by addressing these issues proactively….because, quite frankly, they reflect on our health care system and society as a whole.

Labels: cesarean delivery, maternal mortality

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Intrahepatic Cholestasis of Pregnancy - Reprise

On January 10 and 13, 2007, I wrote a couple of posts related to intrahepatic cholestasis of pregnancy (ICP), otherwise know as 'obstetric cholestasis.' ICP affects 1-2 of every 1000 pregnancies and is more common in certain subpopulations around the world, particularly in Scandinavia and South America. Indeed, in the Araucanian Indians in Chile, about 28% of pregnancies are complicated by ICP. As we discussed in the previous posts, this condition usually begins in the third trimester, is associated with intense itching, especially on the palms and soles, and may be accompanied by loss of appetite, sleep deprivation, depression, fatigue, and dark urine (or pale stools). On rare occasions, frank jaundice, right upper quadrant pain, and nausea are present.

ICP is thought to be the result of hepatic dysfunction that results in the decreased clearance and accumulation of bile acids which, subsequently, cause the various symptoms of the condition. Although most women who develop ICP are absolutely miserable, generally, the condition resolves completely following delivery. However, there appears to be a true genetic predisposition to develop ICP and recurrence rates are as high as 90% with subsequent pregnancies. For reasons that are not completely understood, babies of women with ICP are at increased risk for unexplained fetal death in utero as was the case in the patient who was the incentive for my first post on this subject.

Today, I received a comment from the reader below who had several excellent questions related to ICP that were not addressed in my previous posts, so I thought this would be a good time to revisit the condition and provide some additional thoughts for our readers...

At Mon Aug 20, 05:22:00 PM 2007, Rani B said…
I am interested in knowing what I can do to prevent or at least delay the onset of cholestasis of pregnancy. I had cholestasis of pregnancy in 2004 when I was pregnant with my son. I was diagnosed at 35-1/2 weeks and induced for delivery at 37 weeks (because tests showed my bile acids were significantly elevated). Thankfully, my beautiful baby boy was born healthy (though a bit jaundiced). I am now pregnancy (at 19 weeks) with my second child (another boy). So far, so good, but I am watchful for symptoms due to the high rate of recurrence of this condition. I would like to take any steps that I can in terms of diet, exercise, homeopathic treatments, etc. to aid my son's healthy arrival into this world. Do you have any suggestions? For example, should I take water-soluble prenatal vitamins? (and if so, can you recommend one)? Thanks in advance for any guidance you can provide.

At Fri Aug 24, 06:12:00 PM 2007, Kenneth F. Trofatter, Jr., MD, PhD said…
To Rani B Aug 20: You are correct. There is a very high rate of recurrence if you truly had cholestasis because of the genetic predisposition to this condition. There is no way to absolutely prevent its recurrence either. I think you have the right ideas though. I would recommend that you minimize the fat content of your diet (at least during pregnancy), consider the use of a water-soluble PRENATAL vitamin (there are many on the market such as Vegan Prenatal), and try to get some light exercise every day - I suggest walking, swimming, treadmill, stepper or elliptical trainer, or stationary bike. Drink lots of water in your diet and stay away from too much free sugar as well. Although ursodeoxycholate appears to be of some benefit in treating this condition, as far as I know, no one has ever done a study to see if it helps to prevent the RECURRENCE of cholestasis on a prophylactic basis. By the way, for any readers who would like a link to an excellent site that is dedicated to pregnant women with ICP, and explains the salient issues in very comprehensible terms, go to "Itchymoms.com" . Thanks for reading and for VERY good questions! Dr T

Labels: ICP, intrahepatic cholestasis of pregnancy, obstetric cholestasis

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Fetal Cystic Hygromas in First Trimester

Today I received another comment to a post I wrote awhile back on aneuploidy (chromosomal abnormality) from a reader who has a first trimester baby that was found to have a cystic hygroma. With the growing acceptance of first trimester screening for aneuploidy as a 'standard of care' in the U.S. (the rest of the world discovered this several years back!), we are identifying more and more fetal abnormalities early in pregnancy. Since this too is becoming a topic of widespread general interest, I thought it would be worthwhile to highlight three of the comments/questions that were addressed to me so that other readers can hear about real situations and have a point of reference to current thought on this important issue. With apologies to the readers who left the original comments, I have modified the comments as necessary to the best of my understanding so that other readers will more easily understand their concerns...


Sat Jun 09, 09:10:00 AM 2007, Laura said:
My name is Laura and I am 24 years old. Me and my husband went for our first 12 week ultrasound scan a couple of days ago and to our shock we were told that our unborn child has a cystic hygroma, which we are told is fluid underneath the skin at the back of the babies neck (the nuchal translucency) measuring 6 mm. We are devasted at this news because we are told the outlook is not good. It is our first pregnancy and it has taken us so long to get pregnant due to my polycystic ovaries, it just makes it so much harder to deal with. We decided to have a CVS (chorionic villus sampling). They took a biopsy from the placenta which they are now going to test. We should have the rapid test results for Down syndrome, Turner syndrome, and Edwards syndrome by 13th June. We are praying that they will come back clear. They are also going to do routine chromosomal studies to look for other chromosomal abnormalities that are not detected by the rapid test. They said if all the tests are normal, and if the fluid drains away by 18-20 weeks we may have a chance. Its just so hard to understand how some fluid behind the neck could indicate these sort of problems. I am only 24 years old, and so is my husband. We are young, fit and eat a very healthy diet, it just seems so unfair. Do you have any idea of our odds. What is the percentage of babies that do get over this? Have you had any success stories that could give us some hope? Thank you for your time and we hope to hear back soon. Laura

Tues Jun 12, 09:10:00 AM 2007, Kenneth F. Trofatter, Jr., MD, PhD responded:
I know this is hard, especially in a first pregnancy you have had so much trouble getting to because of your polycystic ovary syndrome. Unfortunately, finding the cystic hygroma in first trimester is associated with a very high risk for a baby that has a chromosomal abnormality, most often Down syndrome (trisomy 21 = 47,+21)), Turner syndrome (45XO,missing one sex chromosome), or Edwards syndrome (trisomy 18 = 47,+18). Sometimes cystic hygromas are associated with gene defects and not chromosomal abnormalities per se. Examples of the latter include Noonan syndrome, Roberts syndrome, polysplenia syndrome, multiple pterygium syndrome, and others. At times the baby has no chromosomal abnormality or obvious genetic condition. Under these circumstances, there is an increased risk for a major heart abnormality as an underlying cause, although we do not entirely understand why babies develop cystic hygromas under these circumstances. The prognosis for the baby depends on what problems the baby has, chromosomal, genetic, and/or associated structural. If the baby has no chromosomal abnormality and does not go into heart failure (develop hydrops fetalis), it may well survive the pregnancy. If no syndromic problems, chromosomal mosaicism, or gene defects are discovered after delivery, the baby may have a reasonable chance at doing well. Your doctors will discuss this more with you after they get your test results back. At that point (if they haven't already), they will probably refer you to a genetic counselor to get more information. Good luck to both of you and thank you for reading. By the way, it is highly unlikely that anything you have any control over caused this to happen. If you will, let me know what the tests show and how the pregnancy turns out...


Sun June 24 11:50 AM 2007, Anonymous said:
Dr. Trofatter, I am 41 year old with a 14 week pregnancy. Due to AMA (advanced maternal age) I elected to have a nuchal translucency (NT) scan done and the perinatologist found a large cystic hygroma; I was told extremely large 180mm3 and the doc was not optimistic. He performed CVS that day and we just recieved news that the FISH results were normal. Because there are no genetic defects, I was told we are looking at heart abnormalities, probably severe. My husband and I are deciding whether to terminate but the normal chromosome results makes this decision difficult. I have been doing research on the web for days now and I find myself unable to take care of myself and my family. I am reading the prognosis is poor and if I wait beyond 18 weeks I cannot terminate the pregnancy in my state. My question is can or should I get repeated ultrasound hoping the hygroma goes down and how often is an ultrasound indicated for this? Will the hygroma go down all at once or little by little or how much at a time? Please help me. Thank you

Tues June 26 02:47 PM 2007, Kenneth F. Trofatter, Jr., MD, PhD responded:
Large cystic hygromas have a very poor prognosis, even if the baby is chromosomally normal. Even if the FISH results are reassuring at this point, your baby could have a chromosomal abnormality that was not detected by FISH. Your doctors have counseled you that this baby could also have a major cardiac malformation or other major abnormality that impedes return of fluid and lymph to the heart, even in the absence of a chromosomal abnormality. If the baby develops a condition called hydrops fetalis, this would indicate heart failure for any reason and the prognosis is usually fatal at that point. If the baby is chromsomally normal, has no other genetic or syndromic problem, has no major heart abnormality, and resolves the cystic hygroma, it may well survive and do quite well in the long term. I would recommend another ultrasound before 18 weeks. In many cases, major heart and other abnormalities can be identified by that time and you will have the final results of the fetal chromosome studies back to guide your decision. I am so sorry. It is difficult to be in your situation. If you have not seen a specialist in Maternal-Fetal medicine, I suggest you consider that. Thank you for reading and best wishes to you and your family.


Tues Aug 21 01:55 PM 2007, Ed said:
Doctor, on our 1st trimester baby scan we were told that baby had a 5mm NT (nuchal translucency). We hoped that the consultant could give us some better news on a scan a few days later, but we have the terrible news that it was not simply a wide NT, but a large cystic hygroma of 7mm, extend down the back to the lumbar region. She gave us an 85% chance of choromsome problem and cardiac anomalies even if normal. Also of possible intrauterine death. We are choosing to terminate, we can't wait in hope for a CVS or amniocentesis that MAY indicate the baby is chromosomally normal because it is more likely abnormal. But we have terrible guilt in termination too, as the baby seems ok at the moment. From what I read on the internet, there is a glimmer of hope that the babies do turn out normal. Is this just crazy hope or not?Ed


Wed Aug 22, 04:55:00 PM 2007 Kenneth F. Trofatter, Jr., MD, PhD said...
Although the prognosis is poor, there is always a "glimmer of hope." With your ambivalence and guilt related to pregnancy termination, why don't you have the CVS done and wait just a couple of days. Most labs can give you an answer in as little as 72 hours if they do a "direct prep" for the more common chromosomal abnormalities found with cystic hygromas. If the baby ends up being chromosomally normal, or has a potentially viable condition such as Turner's syndrome, the "glimmer" may improve if the baby survives the first part of the pregnancy....and even if it is chromosomally normal and succumbs, you can walk away having given it the "best shot" and it sounds like that is important for you. Just a thought. Good luck to both of you.


Dr T

Labels: amniocentesis, aneuploidy, CVS, cystic hygroma, first trimester screening

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Group B Strep Colonization and Pregnancy

At Mon Aug 20, 11:32:00 AM 2007, Anonymous said…


Hi there Dr. T. I am 36 1/2 weeks and I just found out that I was GBS+ and I am very concerned about my baby. I wonder, why give antibiotics during labor? Why not now? I have also had many problems with yeast infections during my pregnancy and was wondering if that could have caused the GBS? I don't completely understand why I have it and what I did to get it. Is it caused from something, perhaps the heat? Not being clean enough? Please help me!


One of my very first posts here at “Fruit of the Womb” addressed Group B Streptococcus (GBS) infections and pregnancy. The question from today’s reader gives us good reason to revisit this issue since the concerns expressed in the comment are shared by many, many women....

GBS is a bacterium that colonizes the vagina and lower gastrointestinal tract in as many as one-third of all healthy reproductive age women. It is still the leading cause of serious bacterial infection in newborns and most babies contract the organism at the time of delivery. Indeed, 8,000-12,000 babies per year in the U.S. will develop complications related to GBS and approximately 2,000 infants will die from their infections. There are several well-known situations in which babies are at increased risk for developing a serious GBS infection including:

• Premature labor or rupture of membranes before 37 weeks
• Prolonged rupture of membranes (18 hr or longer) before delivery
• Fever in labor (100.4F or higher)
• History of GBS urinary tract infection during the pregnancy (4-fold risk)
• Previous baby affected by GBS disease (increases risk 10-fold!!!)

Some of the dilemmas we face in dealing with GBS in pregnancy are raised by today’s reader. She appears to have had GBS detected at the time of recommended routine screening, 35-37 weeks. She didn’t just “catch it” at this point; it is probably something she has carried with her through most of the pregnancy (and even before conception). We do NOT know why some people carry GBS and others do not, and we are not entirely clear why far more women actually carry the bacterium than are at risk for having a baby with a serious complication related to it, although the maternal immune response to the bacterium probably plays a key role (see below). But, we also know that if you are colonized with GBS and tend to carry it, even if treated, you have a very high risk of being incompletely ‘decolonized’ by treatment and a similarly high risk for becoming ‘recolonized’ in a relatively short period of time for whatever reasons you have it to begin with!

GBS may come and go, but a negative test within 5 weeks of delivery has a ‘negative predictive value’ of about 95%. This implies that only 5% of women who are negative at 35-37 weeks are likely to acquire GBS between the time of screening and delivery. Interestingly, if GBS is detected at routine screening, the ‘positive predictive value’ of the bacteria actually being found at delivery is only about 87%. This means that as many as 13% of women who were positive at the time of screening will not have the bacterium detectable at the time of delivery.

To answer some of our reader’s concerns, these are reasons we do not treat everyone at the time a positive screening test is done unless they themselves have a significant infection (e.g., urinary tract), a previously affected baby, or are in one of the other risk categories noted above. According to the CDC, women who are GBS positive have about a 50% of having a baby who becomes colonized with GBS at delivery and a 1 in 200 chance of having a baby who develops GBS disease if antibiotics are NOT given, but only 1 in 4000 risk if they are given.

There are 5 major serotypes of GBS (Ia, Ib, II, III, and V). All are capable of causing both maternal and neonatal disease. Babies born to women who do not have antibodies to types II and III seem to be at greater risk for complications. Indeed, at some point, this may be one of the primary factors we can use to differentiate pregnancies at risk from those which are less so. About two-thirds of serious GBS infections are apparent at the time of delivery and 90% of babies who will develop complications do so within the first 48 hr after delivery. This is generally referred to as “early-onset” GBS infection and technically is used to define disease occurring in the first week of life. “Late-onset” disease, frequently associated with serotype III, affects another 10% of newborns, often presents as meningitis with septicemia, and rarely occurs after one month of age. Up to one-third of the survivors of GBS meningitis will develop long-term physical and/or neurological handicaps and in 1 of every 8 of these babies, the handicaps will be severe.

Unless you are in one of the high risk groups noted above, the goal of routine prophylactic antibiotic therapy during labor in those who are found to be colonized with GBS during their pregnancies is to deliver antibiotics to the mother early enough in the course of labor that sufficient drug can be transferred across the placenta to achieve protective levels in the baby prior to birth. The goal is not to cure the GBS infection. That means, the antibiotic selected must not only be able to kill GBS, but it must also be able to cross the placenta. Fortunately, GBS has not yet been found to have developed resistance to the antibiotic of choice, penicillin G, and this drug also readily crosses the placenta. It also has a long and proven safety record for the baby. Ideally, antibiotic therapy is begun, intravenously, at least 4 hr prior to delivery so that at least one or two doses can be administered before the baby is born. If a woman has a serious allergy to penicillin, other otions for therapy exist and the risks and benefits of these are discussed in our previous post on this subject.

Anyway, to close this out, I would only like to say to our reader that 1) I doubt the recurrent yeast infections “caused” the GBS, but they might reflect a subtle deficiency in your immune response to other organisms commonly found in the environment. (People with diabetes and autoimmune conditions frequently experience similar problems or, in your case, this may be simply the response your body has to pregnancy; 2) I don’t completely understand why you have it either, but I doubt the “heat” is contributing to the problem and cleanliness is rarely a concern in people who would worry about that to begin with!

The important things are that your doctors did the right thing by screening you, they have identified a potential problem, and there is a well-proven means of significantly reducing the risks from that problem for both you and your baby at the time of your labor and delivery. Thanks for reading and for the good questions. Best wishes for the rest of your pregnancy!

Dr T on Aug 20, 11:32:00 AM 2007

Labels: GBS and pregnancy

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Diabetes in Pregnancy -3 - Normal Changes in Insulin Sensitivity

In our second post on diabetes in pregnancy, we gave a simple overview of glucose metabolism and discussed the essential role insulin plays in assuring that glucose gets into the cell. Pregnancy alters the normal balances involved in glucose metabolism and insulin production, regulation, and action in a dynamic way that changes throughout gestation. Although, pregnancy is often referred to as a ‘diabetogenic state’ with progressively increasing postprandial (after eating) blood sugar levels, presumably, secondary to an increase in insulin resistance, point in fact is that most pregnant women do not actually develop overt diabetes, and those that do, usually do not do so until late in the second or early in the third trimesters. In normal women, compensatory increases in insulin production overcome the increased resistance to its action.

Interestingly, during the first trimester, insulin requirements usually decrease, resulting in lower blood sugars and a concomitant increase in maternal fat stores. Indeed, early pregnancy can be a particularly dangerous time for long-term diabetics, even if they are under good control before conception, because they may develop an unexpected over-response to the same doses of insulin on which they have been stable, resulting in episodes of hypoglycemia (low blood sugars). Although numerous mechanisms for the decrease in maternal insulin requirements have been proposed, the one that seems to make the most sense to me is that this represents a true increase in sensitivity to insulin (not just an increase in production, although this also occurs in women who are not diabetic and diabetics who are not insulin-dependent). Otherwise it is hard to explain how long-standing “type 1” diabetics, who can make virtually no insulin on their own, experience this effect. It is also one of the main reasons I believe that any woman who has hyperglycemia in first trimester should be classified as a true ‘pregestational diabetic’ even if she did not have the diagnosis of diabetes made prior to the pregnancy.

What causes the increase in insulin sensitivity is really not known. However, it is likely to be pregnancy hormones, and since the early rise and subsequent fall in insulin sensitivity closely parallels the rapid rise and fall in human chorionic gonadotropin (hCG) – THE ‘pregnancy hormone’ measured in all pregnancy tests – my money is that hCG has something to do with it. Nor is it understood what role the increase in insulin sensitivity might play in early pregnancy. Some have proposed that the increase in maternal fat stores resulting from insulin action helps to protect the mother from the metabolic demands of the baby and placenta later in pregnancy. I have often wondered too, since insulin is a potent growth factor, if the increased sensitivity in early pregnancy is somehow related to a role in early placentation, placental growth, and in modulation of the maternal immune response to the pregnancy.

Regardless, by the end of first trimester, a variety of placental and maternal hormones are produced at elevated and increasing levels that have the potential to contribute to the progressively increasing insulin resistance that develops after first trimester. Some of these include progesterone, estrogen, human placental lactogen (hPL), cortisol, and prolactin. In recent years, two other factors produced by the placenta, tumor necrosis factor (TNF)-α and leptin, have also been proposed as mediators of insulin resistance. TNF-α, in particular, has been found by Kirwan and colleagues (Diabetes 2002;51:2207-13) to be inversely correlated with changes in insulin sensitivity from prior to conception through the third trimester and, when analyzed statistically with other placental hormones, alone accounts for about half the variance in the decrease in insulin sensitivity throughout pregnancy.

Just as increased sensitivity to insulin in normal early pregnancy may play an important role in the establishment of a successful pregnancy, decreased sensitivity later in pregnancy must also as well in the maintenance of the baby. Again, looking at this simplistically, if the mother cannot readily process glucose into glycogen and fat stores because of insulin resistance, then it frees it up for the baby to help support its rapid growth and high metabolic resource demands. To the mother’s advantage, insulin resistance also decreases the risk of maternal hypoglycemia. Remember, the baby has demands 24 hours per day (even while in utero) and these do not lessen while the mother is fasting. In the presence of decreased influence of insulin, the liver can increase glucose production to maintain maternal blood sugar levels and to supply the continuous needs of the baby.

In the next post on this topic, we will define the different types of diabetes and the criteria we use for the diagnosis of ‘gestational diabetes’ during pregnancy.

Labels: diabetes; insulin resistance

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Another Late Midtrimester Pregnancy Loss

Soumya has left a new comment on your post "Recurrent Early Pregnancy Loss - 6 - A Special Pat..." (I have modified/revised her comment somewhat to the best of my understanding of her concerns)...


Hi I lost my pregnancy at 24 weeks on July 17. Actually I didn't have any complications during pregnancy. When I didn't feel any movements for 5 days, I went to the hospital and they didn't find my baby's heartbeat. My doctor said that blood results are showing protien C and protien S deficiencies and an MTHFR abnormality. She told me that perhaps these abnormalities caused the blood to clot in the placenta and that I should see a high risk specialist before another pregnancy so that he can give me treatment to help overcome these problems. She also said that after delivery protein C and protein S generally will be reduced.... When I lost my baby I didnt have any other symptoms like bleeding or stomach pain except when the baby moved. There is no family history of blood clotting problems. Can you tell me what would be the reason and if so what will be the treatments for blood clotting? Should I start the medication before another pregnancy or only after getting pregnant?
Fri Aug 10, 11:14:00 PM 2007

Kenneth F. Trofatter, Jr., MD, PhD said...

To Soumya: I am sorry for your loss. The most common causes of late midtrimester fetal demise are fetal chromosomal abnormalities (and, less commonly, genetic abnormalities), infection, congenital birth defects, and abnormalities of placentation (that may be associated with "blood clots," sterile inflammatory changes, and fetal growth restriction). The latter are also often associated with maternal pregnancy-related hypertensive disorders and premature placental separation (abruption).

Usually during pregnancy, protein S levels decrease and protein C levels remain the same or are only slightly lower, so from what you have told me, I cannot be sure the results you describe above are actually 'abnormal' or simply related to the pregnancy itself. It would help me if I knew what tests were done to measure protein S and protein C, the actual test results, and the 'normal' range of test results in the laboratory that did the studies. It would also be helpful if you could give me more specific information regarding the MTHFR abnormality (the specific 'polymorphism(s)' and whether this is heterozygous (one dose), homozygous (two doses), or complex heterozygous (two different abnormal genes)).

Now that you are no longer pregnant, you should go to the specialist BEFORE you get pregnant again to be tested for these and other factors that are associated with pregnancy losses and increased risk for blood clots. The best way to test for protein C and protein S deficiencies is to have a test for "functional protein C and S activity" (don't ask me to explain that here!) BEFORE you get pregnant again. Other studies that can be done to look for autoimmune or genetic thrombophilias (factors that increase your risk for either making blood clots or not breaking them down efficiently) include: antiphospholipid antibodies; lupus anticoagulant; antithrombin III levels; factor V Leiden mutation; factor II (prothrombin) G20210A mutation; and homocysteine levels. On rare occasions, mutations in the plasminogen activator inhibitor-1 (4G/4G) are also associated with increased risk for blood clot formation and pregnancy losses.

Ask the doctor who delivered your baby if the placental pathology showed any specific evidence of infection or blood clot formation (either placental abruption or evidence of vascular abnormalities or inflammatory changes). Without abdominal pain or bleeding, it is unlikely that you had a placental abruption. Was the placenta normal size? Did the baby appear normal and was it a normal size for 23-24 weeks (i.e., what did the baby weigh)? Was there any evidence of the baby having a chromosomal abnormality (and were chromosomal studies sent) or an infection (bacterial, viral, or parasitic)? Did you have any evidence of infection when you were admitted to the hospital (high white blood cell count, fever, bladder infection)? Did you have cultures sent for Group B Streptococcus? Were you or the baby tested for cytomegalovirus or toxoplasmosis infections or other organisms that are known to cause problems in your country?

If any blood clotting problems are found, a specialist in high risk obstetrics or hematology can counsel you regarding the best ways to reduce the risk for a pregnancy complications for both you and the baby. Sometimes this means simply having to take extra folic acid (2-4 mg per day) and/or a baby aspirin (81 mg). In other situations, it may be best to treat you with either prophylactic or even therapeutic levels of anticoagulation therapy (by self-injection of heparin or low-molecular weight heparin) for part or all of the pregnancy. Before you get pregnant again, you might also consider sitting down and talking with a genetic counselor who might help identify risks that may not be so obvious and help you to better understand some of your risks based on the findings of your doctors. I do hope things turn out better for you the next time. Let me know, okay? Thanks for reading and for the good question! Dr T
Fri Aug 17, 12:26:00 PM 2007

Labels: MTHFR, pregnancy loss, thrombophilias

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A Late Midtrimester Loss

On August 12, 2007 Anonymous said...

Hi, approximatly 5 weeks ago I went into preterm labour and my son was 23 weeks gestation. He was too small to survive and passed away 10 minutes after the birth. I have a healthy 20 month old and I never had complications in my first pregnancy. My question is, what are my chances of having this happen again, and why do these things happen? According to my ultrasounds and right until the he was born he was fine? My o.b says that the cause is not known yet. I had to do some bloodwork something about antibodies? I need help trying to understand this, I am lost!

Kenneth F. Trofatter, Jr., MD, PhD said...

To Anonymous Aug 12: I am so sorry for your loss. That is a very difficult time to lose a baby - so near, yet so far. To answer your questions more accurately, it would help to know how long you contracted before coming to the hospital, how dilated was your cervix when you arrived, did you have a fever, was there evidence of a bladder or intrauterine infection (chorioamnionitis, or infection of the cord or baby), were the baby and placenta normally grown, did he have any congenital abnormalities, was your white blood count elevated, had you had any bleeding during the pregnancy, had you been leaking fluid...?

The most common causes of late midtrimester losses are 1) cervical incompetence or uterine abnormalities, 2) intrauterine infection, 3) unrecognized bladder infections, 4) fetal chromosomal abnormalities, 5) fetal or placental abnormalities, 6) on rare occasions severe early onset preeclampsia, and 7) maternal substance abuse (like cocaine). I hope the baby or at least the placenta were sent for evaluation to help answer some of your questions.

If you really had no problems with your first pregnancy and carried to term, then cervical incompetence is unlikely unless you had a cervical laceration at the time of delivery (most often these are caused by forceps or from a precipitous delivery prior to complete dilation). However, if no other cause is found, you should be evaluated for possible cervical incompetence during a subsequent pregnancy. It is also unlikely that you have a congenital uterine abnormality such as a septate uterus. You could have an intrauterine or cervical fibroid or polyp that acted as a site for chronic inflammation or infection. Evaluating the placenta and umbilical cord will usually answer the question if an intrauterine infection precipitated the early labor. Your doctor probably screened you for a bladder infection at the time of admission so that will be an easy factor to rule in or out. Fetal abnormalities that lead to increased amniotic fluid (usually obstructions of the upper gastrointestinal tract) can lead to uterine overdistention, but it doesn't sound like this was an issue either. If the baby was normal size and had normal fluid, an "antibody problem" or thrombophilia are also unlikely causes. It also does not sound like there was any evidence of preeclampsia or placental abruption.

The hardest question to answer is the one related to risk of recurrence. Part of the counseling in that regard depends on the answers obtained related to the loss of this pregnancy. Unfortunately, history tends to repeat itself in this business, but the best thing you've got going for you is the normal first pregnancy. Please let me know what they find out about your son and maybe I can provide some more thoughts. Again, I am sorry for your loss. Thanks for your questions. Dr T

Labels: cervical incompetence, preterm labor

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Two First Trimester Miscarriages

Labels: maternal age, miscarriage, preeclampsia

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Thanks to Dr. Hsien-Hsien Lei for Great Grand Rounds

My belated (I was at the beach too!) thanks to Dr. Hsien-Hsien Lei for his edition of "Grand Rounds at the Beach" published this week in his Eye on DNA website. What a great collection! Thanks for including a link to my guidelines for the management of Anogenital Warts During Pregnancy. There are many pregnant women out there who will appreciate learning that this condition can be treated while they are pregnant and that there may be distinct benefits to doing so.

Labels: anogenital warts, condylomata acuminata

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Diabetes in Pregnancy - 2 - Glucose Metabolism and Insulin Action

To continue the discussion of diabetes in pregnancy, let’s first start with a very simplified review of glucose metabolism and the role of insulin so that we understand what the furor is all about….


Glucose is one of the primary substrates for the production of energy in cells throughout our body, especially, in the brain, muscles, and kidneys. The two main sources of glucose are dietary carbohydrates, primarily, starches (large “sugar” polymers, or complex carbohydrates) from fruits, vegetables, and grains, and disaccharides (made up of only two “sugar” molecules), such as lactose from milk and sucrose from refined sugars. Through the digestion of these carbohydrates in the gut, they are first broken down to monosaccharides (single “sugar” molecules) before they can be absorbed. Once they cross the gut wall, these monosaccharides are transported via the blood to the liver where they are all converted into glucose molecules (also a monosaccharide). The other monosaccharides cannot be used for ‘fuel’ until they are converted into glucose, therefore, the liver’s role is pivotal in the distribution of this primary source of energy to other body tissues.

Once glucose has gotten into cells, several things can happen to it. First, if the cell needs ‘energy’, glucose can be broken down by a series of enzymes that ultimately results in the production of two molecules of pyruvate. (Pyruvate is the substrate for many important reactions that are not necessary for our discussion herein). As a consequence of the production of pyruvate from glucose, there is also the concomitant net production of two molecules of ATP (adenosine triphosphate) which is the common source of ‘fuel’ for most of the metabolic processes in the cell. Secondly, if there is more glucose than the cell needs, glucose can be converted to glycogen (a polymer of glucose) and stored in that form. Only the liver and muscles have the capability to make and store glycogen (interestingly, the brain does not!) but they are limited in how much they can store. Glycogen can rapidly be converted back to glucose when the need arises. Thirdly, if there is an excess beyond the capacity of the liver and muscles to store glycogen, glucose can be converted into ‘fatty acids.’ Fatty acids are stored in fat (adipose) tissues as triglycerides.

So, where does insulin fit into this picture? Well, none of the events above can occur unless glucose can actually get into the cell in the first place. Among insulin’s many functions, its primary role for sake of our discussion is to enhance the ability of cells to get glucose from the blood into the cell. Under normal circumstances, insulin secretion by the pancreatic β-cells in the islets of Langerhans is proportional to the amount of glucose in the blood within a very tight ‘normal’ range for blood glucose levels. (Actual production of insulin within the β-cells is under the influence of many different hormones, including several pregnancy-related hormones). Once insulin is secreted, it is transported in the blood and binds to specific receptors on the cell membrane. Binding of insulin to the cell membrane results in signals that activate several different metabolic processes (specific to the cell type to which the insulin has bound).

One of the messages that insulin sends to the cell by binding to it is to increase the number of plasma membrane glucose transporters, or GLUTs. GLUTs are stored in the cell and are ‘recruited’ to move to the cell membrane by the action of insulin. Once there, they facilitate the transport of glucose from the blood into the cell. GLUTs are continuously being ‘turned over’ and they only hang around in the cell membrane as long as enough insulin is bound to the cell to keep them there. Different GLUTs with different affinities for glucose, characteristically, reside in different tissues: GLUT1 is present in most tissues, GLUT2 is present in liver and pancreatic β-cells, GLUT3 is found in the brain, and GLUT4 is found in the heart, adipose tissue and skeletal muscle. In addition to enhancing glucose transport, insulin stimulates glycogen and fat production, increases amino acid transport into cells, promotes the transcription of specific gene products, and stimulates growth, DNA synthesis, and cell replication.

In our next post, we will discuss how pregnancy alters the ‘normal’ state of affairs with regard to insulin production and action…

Labels: diabetes, insulin

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Diabetes in Pregnancy -1 - Overview of an Epidemic

Today we admitted a 25 year old woman to the hospital that has Class R/F diabetes and is 9 weeks pregnant. I will explain what ‘Class R/F’ means later on but, simply put, it’s not good because both her kidneys and her eyes have suffered severe damage from long-standing poorly-controlled diabetes. The outcome of pregnancies under these circumstances is usually suboptimal for both mother and baby. Anyway, the reason for her admission was to try to get her diabetes under control. She is the third such patient we have cared for in the past month. I will return to her story in a later post, but she has given me the incentive to begin a long overdue series on diabetes in pregnancy, and so we begin….

Diabetes mellitus is a group of conditions characterized by elevated levels of blood glucose (sugar) that results from inadequate amounts of insulin production, defects in insulin action (e.g., ‘resistance’ to its action), or both. Despite the advances that have been made in the management of diabetes over the years, we are now confronting a worldwide epidemic of diabetes that is being promulgated by the comparably worldwide epidemic of obesity. The World Health Organization has estimated that, barring some remarkable changes in lifestyle, eating, and exercise habits, over the next 20 years there will be a 35% increase in the prevalence of diabetes. To put the magnitude of this problem in perspective, according to International Diabetes Federation statistics, in 1985, an estimated 30 million people worldwide had diabetes; in 2000, a little over a decade later, the figure had risen to over 150 million; by 2025, the figure is expected to rise to 380 million. Quite frankly, that may well be a conservative estimate.

In the U.S. between 1980 and 2005, the number of individuals diagnosed with diabetes increased from 5.6 million to 15.8 million. That reflects an increase in crude prevalence of 120% over that time period. Today, 5-6% of all Americans know they have diabetes and it is estimated that one-third or more of individuals who have the condition, currently do not even know it. Although we generally attribute a large percentage of the increase in prevalence of diabetes to the aging population, the mean age of onset of disease is falling and many young women in the child-bearing years are at increased risk for developing diabetes in pregnancy or for having undiagnosed ‘pregestational’ before they conceive. The dangers of this will be addressed later. In the state of South Carolina where I work, more than 8% of the population has documented disease. The condition is more common in Black women and they tend to develop it at younger ages. Diabetes also appears to be rapidly increasing in the rapidly expanding Hispanic population.

Overall, nearly 5% of pregnancies are complicated by diabetes. Ninety percent of these women will have ‘gestational’ diabetes that is not present early in the pregnancy, but develops by late second or early third trimester. Reasons for this will be discussed later as well. Routine screening for diabetes in pregnancy is a ‘standard of care’ and detects 85-90% women with the condition by 28 weeks gestation. Whether pregestational or gestational, diabetes is associated with increased risks for both fetal and maternal morbidity. Although the risks can be reduced almost to that of the nondiabetic population by good control of blood glucose levels, many pregnant women are unable or unwilling to devote the time and effort necessary to achieve that control and, even more sadly, many providers are also either unable, unwilling, or do not have the time or resources it takes to provide the educational support and ongoing care necessary to optimize pregnancy outcome.

In the next several posts, we will focus our discussion on insulin and its action, the physiological changes that occur during pregnancy that help to ‘bring out’ the disease, and on ‘gestational diabetes’ and its diagnosis and management.

Labels: diabetes, gestational diabetes

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