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Table of Contents | | HYPERTHYROIDISM AND PREGNANCY
Many women develop hyperthyroidism during
pregnancy, most commonly in the third trimester. On the other hand, some women
with hyperthyroidism experience a remission while pregnant.
Other women develop hyperthyroidism during
the period after birth when breast feeding. Some women have reported that
stopping breast feeding at this time has caused their hyperthyroidism to go into
remission within a few weeks.
In the coming weeks, this information will
be expanded. Please come back or request further information if you are
pregnant. The following review
summarizes the significant changes that occur in thyroid physiology during
pregnancy.
-
Ann N Y Acad Sci 2000;900:77-88 |
|
Thyroidopathies.
Koutras DA
Athens University School of Medicine, Endocrine Unit, Evgenidion Hospital,
Greece.
Pregnancy affects thyroid physiology in many ways: (a) The renal iodide
clearance rate is increased, hence iodine requirements increase. (b) The
fetal requirements for thyroid hormones and iodide are an additional
problem. (c) Serum thyroxine-binding globulin increases, thus producing an
increase in the levels of total T4 and T3. (d) Chorionic gonadotropin has a
thyroid-stimulating activity. This may be compensated for by a decrease in
TSH, but in some cases gestational thyrotoxicosis occurs. (e) Thyroid
autoimmunity usually subsides during pregnancy, but may rebound a few months
after parturition, and postpartum thyroiditis may occur. Because maternal
antithyroid autoantibodies cross the placenta readily, fetal and neonatal
hyperthyroidism (or hypothyroidism) may develop. Pre-existing thyroid
diseases are influenced. Nontoxic goiter increases in size. Iodine and/or
thyroxine may be required. Graves' disease may remit. If present,
antithyroid drugs should be given in small doses, and quite often they may
be stopped altogether. Hypothyroid patients may require a larger T4 dose.
-
Clin Chem 1999 Dec;45(12):2250-8 |
|
Thyroid function during pregnancy.
Fantz CR, Dagogo-Jack S, Ladenson JH, Gronowski AM
Department of Pathology and Division of Endocrinology, Washington
University School of Medicine, Saint Louis, MO 63110, USA.
BACKGROUND: This Case Conference reviews the normal changes in thyroid
activity that occur during pregnancy and the proper use of laboratory
tests for the diagnosis of thyroid dysfunction in the pregnant patient.
CASE: A woman in the 18th week of pregnancy presented with tachycardia,
increased blood pressure, severe vomiting, increased total and free
thyroid hormone concentrations, a thyroid-stimulating hormone (TSH)
concentration within the reference interval, and an increased human
chorionic gonadotropin (hCG) beta-subunit concentration. ISSUES: During
pregnancy, normal thyroid activity undergoes significant changes,
including a two- to threefold increase in thyroxine-binding globulin
concentrations, a 30-100% increase in total triiodothyronine and thyroxine
concentrations, increased serum thyroglobulin, and increased renal iodide
clearance. Furthermore, hCG has mild thyroid stimulating activity.
Pregnancy produces an overall increase in thyroid activity, which allows
the healthy individual to remain in a net euthyroid state. However, both
hyper- and hypothyroidism can occur in pregnant patients. In addition, two
pregnancy-specific conditions, hyperemesis gravidarum and gestational
trophoblastic disease, can lead to clinical hyperthyroidism. The normal
changes in thyroid activity and the association of pregnancy with
conditions that can cause hyperthyroidism necessitates careful
interpretation of thyroid function tests during pregnancy. CONCLUSION:
Assessment of thyroid function during pregnancy should be done with a
careful clinical evaluation of the patient's symptoms as well as
measurement of TSH and free, not total, thyroid hormones. Measurement of
thyroid autoantibodies may also be useful in selected cases to detect
maternal Graves disease or Hashimoto thyroiditis and to assess risk of
fetal or neonatal consequences of maternal thyroid dysfunction.
The following study shows that chorionic gonadotropin (hCG) is
inversely related to hemoglobin concentration, which means that the more
anemic the woman is during pregnancy, the higher the hCG is.
-
-
Lancet 1994 Feb 26;343(8896):511-3 |
|
Relation between maternal haemoglobin and placental
hormone concentrations in early pregnancy.
Wheeler T, Sollero C, Alderman S, Landen J, Anthony F, Osmond C
Department of Obstetrics and Gynaecology, University of Southampton,
Princess Anne Hospital, UK.
Environmental factors that influence placental development are of
particular interest because of the reported association between adult
hypertension, low birthweight, and large placental size. Maternal anaemia
is one environmental factor that is associated with an increase in
placental size at birth. We have examined the relation between
haematological status and plasma concentrations of chorionic gonadotropin
(hCG) and placental lactogen (hPL) in 175 women at about 10 weeks of
pregnancy. There were significant negative correlations between
maternal haemoglobin concentration and the levels of hCG (p = 0.03) and
hPL (p = 0.02). Although 21% of women had low iron stores (ferritin
< 13 micrograms/L), no relation was found between serum ferritin and
the two placental hormones. There was no association between plasma volume
(calculated from maternal weight and height) and hCG or hPL
concentrations. We conclude that our observations reflect an influence of
the maternal environment on the placenta. The fact that negative
correlations with placental hormone concentrations exist across the normal
haemoglobin range suggest that they reflect a normal aspect of placental
development. We speculate that placental growth is, in part, determined by
maternal factors that prevail before conception. One possibility is that
these factors modify angiogenesis within the trophoblastic villi.
The following study shows that there is a correlation between zinc
levels and hCG levels, at least in women with hyperemesis gravidum (nausea
during pregnancy). This suggests that high zinc levels can lead to high
hCG levels, and consequently to high thyroid hormone levels.
-
Acta Obstet Gynecol Scand 1988;67(7):599-604 |
|
Plasma zinc concentration and thyroid function in
hyperemetic pregnancies.
Lao TT, Chin RK, Mak YT, Panesar NS
Department of Obstetrics and Gynaecology, Prince of Wales Hospital, Shatin,
Hong Kong.
Low zinc concentrations in plasma have been reported in pregnancy
complications such as pre-eclampsia and intra-uterine growth retardation,
as well as in non-pregnant individuals with gastrointestinal and eating
disorders. The present study looked at the plasma zinc concentration in
hyperemetic and normal pregnant women at the same stage of gestation, as
well as total thyroxin concentration in these two groups, since abnormal
thyroid function is a common phenomenon in hyperemetic women. No
difference in plasma zinc concentration was found between normal and
hyperemetic women, which suggests that hyperemesis gravidarum is not
associated with a low plasma zinc concentration. Hyperemetic women did
have, however, significantly higher total thyroxin concentrations, and on
further examination, a significant correlation was found between plasma
zinc concentration and total and free thyroxin, free tri-iodothyronin, and
human chorionic gonadotropin. The significance of our findings is
discussed.
The following study indicates that the rise in hCG during pregnancy is
not due to cadmium toxicity, since exposure to cadmium results in a
decrease in hCG.
-
Teratology 1995 Apr;51(4):266-72 |
|
Cellular adaptation to chronic cadmium exposure:
intracellular localization of metallothionein protein in human trophoblast
cells (JAr).
Breen JG, Nelson E, Miller RK
Department of Obstetrics and Gynecology, University of Rochester Medical
Center, New York 14642-8668, USA.
Trophoblast cells are the first embryonic cells that modulate the transfer
of a variety of compounds (oxygen, amino acids, xenobiotics, metals) from
the maternal to the fetal circulation in the human placenta. Human
placental exposure to the toxic metal, cadmium (Cd) results in a decrease
in the production of human chorionic gonadotropin (hCG), a decrease in the
maternal to fetal transport of zinc (Zn), and trophoblastic necrosis.
Thus, the ability of trophoblast cells to adapt to exposure to the toxic
metal Cd has been considered crucial. In this study, the expression and
intracellular localization of metallothionein (MT), a small molecular
weight, metal binding protein, was examined in trophoblast cells (JAr)
grown in normal media and in cells exposed chronically (6 months) to 2
microM CdCl2. Conventional and confocal fluorescence microscopy were used
to examine the intracellular localization of MT protein in control cells
and cells grown chronically in Cd. In unexposed trophoblast cells, MT
protein was primarily perinuclear with low level, punctate expression in
the cytosol. Following both chronic and 24 hour exposure to Cd, MT protein
levels were increased (at least 3-fold in both chronic and acute
exposures) and the protein was now concentrated inside the nucleus with a
lacy, cytoskeletal pattern of expression in the cytosol. To determine if
the nuclear accumulation of MT protein was dependent on new protein
synthesis, control cells were exposed to CdCl2 (2 microM) and
cycloheximide (2 micrograms/. ml) for 24 hours.
-
Clin Endocrinol (Oxf) 2000 Aug;53(2):177-81 |
Thyroid function in wholly breast-feeding infants whose
mothers take high doses of propylthiouracil.
Momotani N, Yamashita R, Makino F, Noh JY, Ishikawa N, Ito K.
Ito Hospital, Tokyo, Japan. momotani@blue.ocn.ne.jp
BACKGROUND: Propylthiouracil (PTU) might theoretically be preferred over
methimazole (MMI) during breast-feeding because of its lower milk/serum
concentration ratio (0.1 vs. 1.0). The problem is that Graves' disease often
relapses during the postpartum period, and high doses of PTU are sometimes
needed to control maternal hyperthyroidism) during breast-feeding. However,
there are virtually no data on the effects of maternal PTU on thyroid status
of infants whose mothers take more than 300 mg PTU daily and who are wholly
breast-feeding. OBJECTIVES: To investigate whether mothers can breast-feed
without adverse effects on infants' thyroid status while taking 300 mg or
more daily of PTU. SUBJECTS AND DESIGN: Eleven infants who were wholly
breast-fed while their mothers took PTU 300-750 mg daily for Graves'
hyperthyroidism were included in this study. In one of the 11 infants, the
mother also took iodine 6 mg daily for a limited period. Thyroid status in
these infants was evaluated. MEASUREMENTS: Free T4 (FT4), thyrotrophin
(TSH), and TSH binding inhibiting antibody (TBIAb) concentrations were
examined at least once in the age range 6 days to 9 months. Maternal blood
was also examined for FT4 and TBIAb on the same day, or within a week, of
the infants' blood tests. FT4, TSH and TBIAb concentrations at birth were
examined, using cord blood, in cases where antithyroid drugs had been
continued through delivery. RESULTS: Three of the 11 infants had TSH
concentrations higher than the normal range for adults. In one of the three
infants, the TSH concentration, which was determined 19 weeks after birth,
was just above the normal range. In the remaining two infants whose mothers
had taken PTU through delivery, TSH concentrations, determined within 7 days
after birth, were distinctly high, but they became normal while maternal PTU
doses were the same as or higher than those at the initial examination.
Maternal PTU doses or FT4 concentrations were not significantly correlated
with infants' TSH concentrations. CONCLUSION: Mothers can breast-feed while
taking propylthiouracil at doses as high as 750 mg daily without adverse
effects on thyroid status in their infants.
Michelle wrote:
I had my third opinion today from an endo re: remedies for Grave's. (I have
been on Tapazole for 1.5 years - now I am high again). My numbers are: TSH:
less than 0.03. T4: greater than 18, and T3: 580 (unless I have the T4 and T3
mixed up). Does anyone else have these high numbers? what have you done about
it? I don't particularly want RAI or surgery and I also want to start a family
soon and am not too keen on taking either Tapazole or PTU. Subj: Re: [hyperthyroidism] High Levels - should I worry??
Date: 5/16/00 10:40:44 PM Pacific Daylight Time
From: Tina
Reply-to: hyperthyroidism@egroups.com
To: hyperthyroidism@egroups.com
Michelle,
I am SO glad that I am actually reading my 'thyroid' mail tonight! Please bear with
my LONG reply!
You did not mention how long you have NOT been taking Tapazole. At first I had the
impression that you were still taking the Tapazole and ended up with these HIGH
thyroid levels. Since I don't know any more about your situation, than what you have
shared in this post, let me tell you about me.
I, too, have Graves'. I only took Tapazole for 40 days, at MOST, early in 1996.
During that time I gained more than 30 pounds and the only help the endo offered was
to push myself back from the table!! I couldn't stand the stress of the weight gain
(I struggled the year before to lose 40 pounds, now it was back a pound a day!) and
of the 'quack' of a doctor I had, so I did the only thing I thought possible: resort
to denial! HA! That's the first time I've ever said that! Looking back, I know
that I made the right decision for me by running from the things that caused me so
much stress at that time! I believe that it was choosing to end the
STRESSors, that enabled me to figure out what would be the healthiest choice(s) for ME!
I lived the next 3.5 years doing NOTHING for my thyroid. At least once a year my
family doctor would order the usual thyroid panel and refer me to an endocrinologist. I refused to go until after my yearly exam last summer. It was at
that point that I decided I wanted to do whatever it took to be able to have another
baby~all the docs agreed that it was my extremely overactive thyroid that was keeping
me from conceiving! I even considered asking for RAI. It took me more than a month
to get an appt with the only local endo listed on my insurance. When I saw him in
Sept 99, he shared his amazement that I had never needed hospitalization, since my
numbers were so high! They were: T3=498 (up from 398 in 2/98), Free T4=5.4 (down
from 6.04 in 2/98), and TSH=0.02 (<0.03 in 2/98). Other than noticing my heart
beating faster at different times, I really didn't have the typical HYPER symptoms.
The doctor only prescribed a thyroid scan and a beta blocker for my heart rate (which
ALWAYS increases when I'm nervous!) He said to keep watch on my pulse and adjust the
meds accordingly. Well, I think I only took 3-5 day's worth of the meds, since every
time I checked my pulse was NORMAL! How have you been feeling since coming off the
Tapazole? Did you gradually stop taking it or did you quit 'cold turkey'?
Back to last Sept. I found the thyroid list at onelist and joined! Over and over
again I heard, what I call, horror stories of what HYPOthyroid is really like!
Doctors don't tell you the negatives of going hypo, only how easy it is to treat!! I
chose to NOT have another thyroid scan done last fall, figuring WHY subject my body
to ANY unnecessary radiation!! I found power in making my own medical decisions!!
In January of this year I began taking a multi vitamin and a B-complex! Within a
month I had added several other supplements on the supplement list put out by John.
What I did not realize until the end of March, was that I had gotten pregnant in
Feb!! I can not help but believe my body was waiting for some nutrient in those
supplements!!
It took me until the end of April to get an appt with the OB I chose. When he
realized that I had not followed up with the endo the previous fall, he decided that
I was in a crisis! I spent that afternoon waiting for him to 'discuss' my case with
a fellow medical doctor in his office and then talk the endo into seeing me RIGHT
AWAY! I had to see him before I could even have the regular pregnancy blood tests
drawn! Good news is that I got to have a sonogram that day also!! Baby appeared
healthy and measured exactly the right age~11 weeks!
I was surprised to leave the endo's office without orders to fill a prescription for
PTU that day! Instead, he prescribed more beta blockers (only 10 mg doses - said if
I wasn't' pregnant, he'd start me at 100mg doses) and ordered thyroid tests. Last
week when I saw him, here is what I learned: T3=315 (down almost 200 points), Free
T4=4.64 (down from 5.04), TSH=<0.002 (yikes, looks like this has almost stopped
producing!), and Thyroid-Stimulating Immunoglob (???? what is this?????) = 1.7
(should be 0-1.3). That day, he said to start taking 50mg of PTU, 2xs daily. He
commented how worried he is about my T4 number being 'toxic'. I always thought the
T3 was the important level, now I'm confused!! My philosophy is, my numbers have
DECREASED! Isn't this a GOOD thing? I was really hoping to find that my TSH had
RISEN instead of decreasing!
What will the PTU do? How will it affect the baby? This endo, seems to think he'll
end up sending me for surgery during the second trimester! I'm believing that I've
come this far WITH my thyroid and this baby has survived it's first 14 weeks!! That
in itself is a wonderful sign~why risk taking my thyroid OUT!!!! Oh, I forgot to
mention that the day I found out I was pregnant was the day I became ill with strep
throat! I had to take 2 rounds of antibiotics over the course of 3 weeks! I forgot
to ask the endo if being ill or on antibiotics may have caused the drastic change in
my test results. Does anyone know?
I'm scheduled from another round of thyroid blood tests at the end of this week,
before return to endo next week. I have no idea how quickly PTU can make a
difference, but I suppose I'll be an expert by the end of this pregnancy!!!
All in all, Michelle, what I want to share with you the most is that YOU have to live
with YOU! No one else does!! You have to be comfortable with the decisions you make
for your body!! I totally understand your 'fear' and even your desire to start a
family! My husband even considered being tested to see if it was HE who was sterile
since we had not conceived in over two years!!! I can't get over God's timing for
this child! It totally surprised me to discover I was pregnant!! I have to trust
that God will protect this child from negative effects of my excess hormones and/or
the meds that I'm taking!!
I guess in the end, the meds are the only thing I still have some control over. If
he says to take 500mg, I can if I agree, or take less if I don't! Surgery and RAI
are one time decisions for the doctor!! I'm not ready to entrust the rest of my life
to either yet!!
You are in my prayers,
Tina:)
From
Journal
of the American Board of Family Practice
Transient Hyperthyroidism of Hyperemesis Gravidarum: A Sheep in
Wolf's Clothing
CPT Timothy J. Caffrey, MC, USA, US Army Health Clinic
- Vicenza, Italy.
Abstract
Background. Transient hyperthyroidism of hyperemesis
gravidarum (THHG) is a self-limiting hyperthyroidism occurring in the
context of hyperemesis gravidarum.
Methods. A literature search of MEDLINE was undertaken,
and a case report of a woman with THHG in pregnancy is described.
Results and Conclusions. Because thyroid function tests
cannot distinguish Graves disease from THHG, the diagnosis of THHG rests
largely on the concurrent development of hyperemesis and hyperthyroidism
and the absence of signs and symptoms of hyperthyroidism before and
during pregnancy. THHG might be responsible for 40% to 70% of thyroid
function abnormalities in pregnancy. Both the thyroid function
abnormalities and hyperemesis are related to elevated levels of human
chorionic gonadotropin. THHG resolves by 18 weeks of pregnancy without
sequelae. No treatment is required. Diagnosis of THHG by the primary
care provider can prevent unnecessary treatment or referral for
specialty care. [J
Am Board Fam Pract 13(1):35-38, 2000. © 2000 American Board of
Family Practice] |
Email to BU007: I just found out that I have hyperthyroidism. My husband and I were trying to start a family. What would be the side effects to
having a baby with RAI and PTU pills.
Reply:
Hi,
Radiation increases thyroid eye disease, cancer rates, damages the brain, and causes systemic damage throughout the body. It is certainly a bad treatment for what I consider a nutritional deficiency disease. PTU has it's problems too, but at least it doesn't cause the severe damage that radiation does.
However the problem of getting pregnant with hyperthyroidism goes far beyond the question of subjecting yourself to the damage from RAI and PTU. Although I don't have a lot of scientific evidence to support my opinion, I believe that hyperthyroidism is a nutritional deficiency disease. The fact that most people who follow my nutritional recommendations are improving supports that belief. When your body gets to the point where hyperthyroidism begins, you have some very severe nutritional deficiencies, especially in key minerals like copper and iron. These deficiencies lead to anemia, thyroid disorders, and many other problems.
When a woman gets pregnant, the baby will pull all the nutrients that it needs from the mother. If she starts the pregnancy already deficient, the deficiencies just get worse. This is the reason many women become hyperthyroid during pregnancy. Pregnancy and nursing drain the mother of very vital nutrients and this decreases her health. Additionally the baby may suffer from deficiencies and possible genetic disturbances. It may be possible that the baby's genes are affected by the mother's nutritional status. For example if the mother were copper-deficient, the baby's genes to accumulate copper might be turned on so that the baby will accumulate copper so that it doesn't get deficient in its lifetime. This protects the baby from becoming deficient in an environment which "appears" to be deficient in copper. Later in life, the accumulation of copper in this person may cause hypothyroidism, weight gain, etc. because her or his body is accumulating copper in preference to zinc.
While all the effects of getting pregnant while nutrient deficient are unknown, animal studies strongly suggest that there are effects which last generations.
My advice is to get healthy first and then get pregnant. It might take a year or two to get your minerals up to normal, but the wait will be well worth it in added energy and health for both you and your baby.
The other side of the issue is that it seems to be more difficult to get pregnant when copper and iron deficient. You might not even be able to get pregnant until you get these very important minerals replenished in your body.
My best advice is to get these deficiencies corrected now to not only avoid RAI and keep your use of PTU to a minimum, but to get yourself healthy so you can have healthy children who, in turn, can grow up and have their own healthy children. John
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