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Volume 61, Number 8
OBSTETRICAL AND GYNECOLOGICAL SURVEY
Copyright © 2006
by Lippincott Williams & Wilkins
CME REVIEWARTICLE
23
CHIEF EDITOR’S NOTE: This article is part of a series of continuing education activities in this Journal through which a total
of 36 AMA/PRA category 1 creditsTM can be earned in 2006. Instructions for how CME credits can be earned appear on the
last page of the Table of Contents.
Overt and ‘Subclinical’ Hypothyroidism
in Women
Leonard Wartofsky, MD,*† Douglas Van Nostrand, MD,*
and Kenneth D. Burman, MD*†
*Professor of Medicine, Uniformed Services University, Bethesda, Maryland, and †Professor of Medicine,
Georgetown University School of Medicine, Washington, DC
Thyroid disease in general, and hypothyroidism in particular, are very common in women. In the USA, the
most common cause of primary thyroid deficiency is on an autoimmune basis due to lymphocytic (Hashimoto) thyroiditis. Because there are thyroid hormone receptors in virtually every tissue of the body, the
manifestations of hypothyroidism are varied, but problems with abnormal menses, conception, fertility, and
pregnancy can be especially troubling in young women. The single most important diagnostic test is
measurement of serum thyrotropin (TSH). The overwhelming majority of patients with hypothyroidism are
treated with a single daily dose of synthetic levothyroxine with the goal of therapy being restoration of a
normal metabolic state with return of the TSH level down to the range of 0.5 to 1.5 mlU/L. “Subclinical”
hypothyroidism refers to those patients with early or mild thyroid hypofunction manifested as slight elevations of thyrotropin (⬃4–10 mlU/L) although serum thyroxine (T4) and triiodothyronine (T3) levels are within
their reference ranges. The entity is somewhat controversial in regard to its consequences if left untreated,
and whether or not we should be screening patients, at least susceptible populations, for the condition.
Reports indicate an association between subclinical hypothyroidism and poor outcomes of pregnancy, as
well as dyslipidemias, atherogenesis, and increased mortality in the long term. We believe these consequences are sufficiently compelling to warrant screening and treatment with levothyroxine when found to
halt progression to overt hypothyroidism, and improve symptoms, pregnancy outcomes, lipid abnormalities, and cardiovascular function.
Target Audience: Obstetricians & Gynecologists, Family Physicians
Learning Objectives: After completion of this article, the reader should be able to recall that hypothyroidism is
a common disease in women, has many protean manifestations, and can be successfully diagnosed and treated;
explain that the condition of subclinical hypothyroidism can be diagnosed and if treated can prevent many untoward
complications; and state that there should be heightened awareness of the disease so that proper screening tests
can be performed.
Thyroid hormone deficiency from any cause results in
hypothyroidism. The lack of thyroid hormone may be
Dr. Wartofsky has disclosed that he is a consultant/advisor for Abbott
Laboratories. Dr. Van Nostrand has disclosed that he is/was the recipient of grant/research from Genzyme Corporation, Bristol-Myers Squibb,
and Eastern; and is/was a member of the speakers’ bureau for BristolMyers Squibb. Dr. Burman has disclosed that he is/was a consultant/
advisor and a member of the speakers’ bureau for Genzyme Corporation and Abbott Laboratories.
Lippincott Continuing Medical Education Institute, Inc. has identified and resolved all faculty conflicts of interest regarding this educational activity.
Reprint requests to: Leonard Wartofsky, MD, Department of
Medicine, Washington Hospital Center, 110 Irving Street, NW,
Washington, DC 20010. E-mail: [email protected]
primary, ie, resulting from a defect in the thyroid gland
itself, or secondary, ie, resulting from thyrotropin (TSH)
deficiency related to pituitary or hypothalamic disease.
This discussion focuses only on primary hypothyroidism.
In adult women, virtually 95% of all cases of hypothyroidism are the result of primary disease of the thyroid gland,
the most common of which is on an autoimmune basis
and is the result of lymphocytic (Hashimoto) thyroiditis. It is likely that antithyroperoxidase antibodies
present in this condition are cytotoxic and directed
against thyroid follicular cells leading ultimately to
death of the cells, thyroid atrophy, and hypothyroidism.
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Obstetrical and Gynecological Survey
Hashimoto disease is some 5 to 8 times more common in women than men and may coexist with diabetes
mellitus and other diseases in which circulating autoantibodies are found such as Sjögren syndrome, pernicious anemia, systemic lupus erythematosus, rheumatoid
arthritis, primary biliary cirrhosis, and chronic hepatitis.
Rarely, hypothyroidism may also be a manifestation of
a polyglandular endocrine deficiency state in which
various autoantibodies cause impaired function of the
adrenal, parathyroid, and gonads in addition to the
thyroid. Some patients with Hashimoto disease may
present with goiter rather than an atrophic gland, and in
many cases, the goiter is actually the result of lymphocytic infiltrates within the thyroid. Patients will be
euthyroid until there is sufficient loss of functioning
thyroid follicular cells to cause hypothyroidism. In the
earliest stages of evolution, the hypothyroidism may be
“subclinical” (see subsequently). However, even when
still euthyroid, patients with Hashimoto disease may be
uniquely sensitive to exposure to exogenous iodine
excess and develop iodine-induced hypothyroidism.
edema. Fluid may collect in various body compartments, and pleural effusion, pericardial effusion, or
ascites are not uncommon. Goiter may or may not be
present depending on the etiology of the hypothyroidism and, as mentioned previously, the gland is atrophic
and usually not palpable in primary myxedema as a
result of burned out Hashimoto disease.
On physical examination or chest x-ray, the cardiac
silhouette will appear enlarged that may be the result of
either chamber dilatation or pericardial effusion. A
small cardiac silhouette should bring adrenal insufficiency to mind either on a pituitary basis or as a result
of coincident primary adrenal insufficiency (Schmidt
syndrome). Constipation is common as a result of
slowed gastrointestinal motility, and adynamic ileus
may cause megacolon or intestinal obstruction. A psychiatric syndrome (“myxedema madness”) has been
described, and neurologic findings include a delayed or
hung-up relaxation phase of deep tendon reflexes, muscle weakness, and ataxia.
LABORATORY DIAGNOSIS
CLINICAL PRESENTATION
Signs and symptoms of hypothyroidism will vary
greatly depending on the severity and duration of the
thyroid deficiency, the age of the patient, and the
possible coincidence of other systemic illness. Early
symptoms of hypothyroidism are often nonspecific and
insidious in onset and may include fatigue, lethargy,
constipation, cold intolerance, muscle stiffness and
cramping, carpal tunnel syndrome, decreased libido,
depression, hair loss, menstrual irregularity, menorrhagia, and infertility. In the older woman, the symptoms
may be erroneously attributed to the aging process or
to other common disorders of the elderly such as
Parkinson disease, depression, or Alzheimer disease.
Along with apathy, there is slowing in mental agility
and motor activity, reduced memory, and some
weight gain despite a reduced appetite. The skin and
hair become dry, and the hair becomes thinner as it
falls out. Hearing becomes impaired, and edema of
the vocal cords may account for deepening of the
voice. Somnolence is common, and enlargement of the
tongue contributes to a tendency to obstructive sleep
apnea.
With little functional thyroid reserve, the severity of
hypothyroidism can progress to a clinical picture of
florid myxedema. At this stage, patients appear pallid,
depressed, and hypokinetic with a hoarse voice, dull,
expressionless facies, sparse hair, and a large tongue.
The skin is cool to touch, dry, rough, or scaly, and there
is facial and periorbital puffiness and often generalized
The single most important diagnostic test is measurement of the serum TSH, which is increased in
patients with primary thyroid disease. Serum total
and free thyroxine (T4) will be decreased in all forms
of hypothyroidism. Measurement of serum total triiodothyronine (T3) is less useful and may be within
the normal range in the majority of patients with hypothyroidism. Thyroid autoantibodies (anti-TPO and antithyroglobulin less frequently) will be detectable in
the majority of patients. The radioiodine uptake may
be normal to actually elevated in Hashimoto disease
but is usually decreased in overt hypothyroidism.
The uptake can be elevated because the sodium iodide symporter may be intact until late in the disease,
whereas thyroid hormone synthesis is disturbed earlier leading to low levels of serum thyroxine and high
levels of TSH. The high TSH serves to further stimulate the transport of iodine leading to a high uptake.
Other nonthyroid laboratory tests may provide further
clues to the presence of hypothyroidism. Serum triglycerides and total and low-density lipoprotein cholesterol
level are usually elevated in hypothyroidism as well as
levels of carotene, creatine phosphokinase (CPK), aspartate transaminase, and lactate dehydrogenase.
Anemia may be present on the basis of impaired iron
utilization, and in patients with Hashimoto disease,
there may be coincident pernicious anemia in approximately 10% of patients. Electrocardiographic changes
include bradycardia, low-amplitude QRS complexes,
and flattened or inverted T waves, findings that may be
Thyroid Disease in Women Y CME Review Article
most pronounced in the presence of a pericardial effusion. Cardiac contractility is reduced as can be assessed
by systolic time intervals demonstrating a prolonged
preejection period and an increased ratio of the preejection period to the left ventricular ejection time.
TREATMENT OF OVERT
HYPOTHYROIDISM
Levothyroxine is the overwhelming choice of clinicians for the treatment of hypothyroidism, and
monitoring of serum TSH levels is required for appropriate dosage adjustment. The medication has a
narrow therapeutic index, and either underdosage
(“subclinical” hypothyroidism) or excessive dosage
(“subclinical” hyperthyroidism) will be associated
with adverse symptoms and pathophysiological effects and is to be avoided. The consequent necessity
for careful titration of dosage has had impact on the
issue of “switchability” or bioequivalence of the various levothyroxine products marketed. The position
of the American Thyroid Association, American Association of Clinical Endocrinologists, and The Endocrine Society is that only branded preparations (not
generics) should be used; that patients should stay on
the same brand; and TSH should be remeasured in 6
weeks and dosage retitrated if a switch to a different
brand is required.
Patients should require only a single daily dose of
synthetic levothyroxine because of its long (6–7 days)
half-life. Other thyroid hormone preparations are available and include desiccated thyroid extract USP, a
triiodothyronine (T3) preparation, and a mixture of thyroxine and T3 (liotrix). Although once in popular use,
the thyroid extract preparation is no longer recommended for a number of reasons, principal of which is
because of its content of T3 that is so rapidly absorbed that the resultant high serum T3 can cause
worrisome tachycardias or other arrhythmias in elderly patients or those with underlying cardiac disease. Levothyroxine is more stable and has a longer,
more predictable shelf life. Because T4 is converted
to T3 physiologically, ultimately, near-normal concentrations of serum T3 can be restored by administering thyroxine alone. To more closely mimic thyroidal T3 secretion and normal blood levels, oral
supplements of triiodothyronine would need to be
given in frequent divided dosage, a regimen that
makes good compliance problematic. Moreover, convincing arguments or data demonstrating benefit of
concomitant T3 administration are lacking. When
initially diagnosed, most cases of hypothyroidism
have existed for some time, and there is usually (with
537
the exception of myxedema coma) no reason to rapidly correct the thyroid deficiency with aggressive
therapy. In young women, one could start with 75 to
88 ␮g/day. In older patients and especially in those
with underlying heart disease, dosage is gradually
incremented with an initial daily dose of 25 to 50 ␮g
thyroxine increased by 25 ␮g at 4- to 6-week intervals until a normal metabolic state is attained. The
best indication that a normal metabolic state has been
attained is normalization of the TSH level down to
the range of 0.5 to 1.5 mU/L. On average, this will
equate to an ultimate full replacement dose of approximately 1.7 ␮g/kg per day. Patients who have
had a total thyroidectomy, eg, for thyroid malignancy, especially when surgery was followed by
radioiodine ablation, will have no residual thyroid
tissue and their requirement will be closer to 2.1
␮g/kg per day. Although it has been shown in one
small series of patients that full replacement dosage of
T4 may be safely initiated (1), we have argued that this
is potentially dangerous (2), especially in the elderly
and in patients with heart disease, because a sudden
increase in metabolic rate may tax cardiac or coronary
reserve.
In some circumstances, a previously stable dosage of
levothyroxine may need to be increased or decreased.
Increases of 25 to 50 ␮g per day are generally required during pregnancy, as evidenced by increases
in serum TSH, and some workers have advocated
routinely increasing the dose once pregnancy has
been determined (3). Progressive increases in dose
may be required because further atrophy of the gland
occurs in patients with Hashimoto disease or in patients with Graves disease who have been treated with
surgery or radioiodine. On the other hand, a need to
reduce thyroxine dosage may be indicated by the spontaneous disappearance of TSH receptor blocking antibodies in Hashimoto disease or increases in stimulating
TSH receptor antibodies leading to evolution of autonomy in a previously treated Graves gland or emergence
of autonomous hyperfunction in a uninodular or multinodular goiter.
Gastrointestinal absorption of T4 may be slightly
reduced when taken with food or certain other pharmacologic agents that interfere with gastrointestinal
absorption or enhance the metabolic clearance of T4.
Thus, coingestion of Carafate, cholestyramine, colestipol, ferrous sulfate, or calcium carbonate will
result in reduced absorption of T4. Simultaneous
therapy with either phenytoin (dilantin) or carbamazepine (Tegretol) will lead to enhanced metabolism
and disposition of T4, and the dosage will need to be
increased in the absence of any endogenous thyroid
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Obstetrical and Gynecological Survey
reserve. Finally, it is very important to remember that
modest elevations in the TSH can be transient, and
no harm will arise from postponing initiation of
therapy until the high TSH might be confirmed by a
repeat measurement in 8 to 12 weeks (4).
SUBCLINICAL (MILD) HYPOTHYROIDISM
Like with many disorders, patients with hypothyroidism may present earlier or later in the course of their
disease. In its earliest, mild form, hypothyroidism has
been called “subclinical” because the symptoms may be
so mild as to be overlooked. Other designations for this
condition have include “minimally symptomatic hypothyroidism” or “mild thyroid failure” or “early thyroid
failure” (5–7). The significant point is that thyroid failure is present although the routine thyroid function tests
such as total and free T4 or T3 will still be within the
“normal” or reference range, albeit probably lower than
when the patients were truly euthyroid. Consequently,
the diagnosis of subclinical disease rests on the finding
of a slight elevation in serum TSH. These patients with
an isolated slight elevation in serum TSH have been
presumed to be asymptomatic and hence the “subclinical” designation. Designating this clinical entity as
early or mild hypothyroidism makes somewhat more
physiological sense.
Patients with mild thyroid failure have been traditionally thought to be asymptomatic, but they may
present to the gynecologist with menstrual irregularities or infertility. A more detailed history and physical may reveal several symptoms and signs seen in
overt hypothyroidism and potentially attributable to
thyroid hypofunction such as fatigue, depression,
loss of energy, muscle weakness, dry skin, and sleep
disturbances. Several laboratory abnormalities, as described subsequently, could also be attributed to this
condition. In addition to Hashimoto thyroiditis as a
cause of early thyroid failure, other etiologies include
thyroid ablation with radioactive iodine, antithyroid
drugs (eg, PTU), external beam radiation, partial
thyroidectomy, or drugs such as amiodarone, lithium,
or radiographic contrast agents.
A serum measurement of TSH provides us with an
insight into the adequacy of circulating levels of T4
or T3 in the peripheral tissues. Thus, even the slightest elevation in TSH implies a lack of thyroid hormone at the tissue level, the tissue in the case of TSH
measurements being the pituitary gland, which we
infer to be representative of other tissues as well.
Although reference ranges for TSH are often as
broad as 0.3 to 6.5 mU/L, it is our contention that a
truly normal serum TSH ranges between 0.3 and 2.5
with levels between 2.5 and 4.0 being in a “gray
zone” deserving of subsequent follow up and values
of ⬎4.0 as indicative or early or mild thyroid failure
(even if serum T4 and T3 are still within the “normal” range) (8). Usually, it is not possible to know a
given woman’s optimal TSH “set point” because we
are not likely to have any premorbid original TSH
measurement until she presents with suspected thyroid disease.
Laboratory reference ranges are usually based on
the range of values found in a large sample of ostensibly normal subjects. Such populations are contaminated by subjects with occult underlying thyroid
disease who may have antithyroid antibodies or a
family history of autoimmune thyroid disease. When
such subjects are excluded from the “normal” blood
donor pool, the normal reference range becomes 0.4
to 2.5 mIU/L (9). This narrow true normal range is
consistent with findings of the NHANES III study as
well as consensus guideline C.11 of the National
Academy of Clinical Biochemistry (NACB) (10).
(Notably, a letter dated April 10, 2006, from the
outstanding Endocrine Services Reference Laboratory at the University of Southern California, advised
a change in their reference range for TSH from 0.45
to 4.0 to 0.3 to 3.0 mIU/L.)
Should Mild Thyroid Failure Be Treated With
Levothyroxine?
As indicated previously, it remains controversial
whether early or mild thyroid failure is associated
with significant adverse clinical consequences (11).
Those who believe it may have a clinical impact will
recommend initiation of thyroxine therapy (12–15),
whereas those who do not will tend to recommend
observation and follow-up TSH testing (16,17). Recently, an expert panel convened by the Endocrine
Society, American Thyroid Association, and American Association of Clinical Endocrinologists examined the evidence for clinical impact (18). Their
conclusions were controversial in that reviewers representing all 3 sponsoring professional organizations
disagreed with the conclusions of the panel (19).
Both sides of the controversy have since been further
examined (20,21). As indicated previously, an underlying critical issue is the definition of a “normal”
reference range for TSH. NACB guidelines (10) state
that “greater than 95% of healthy, euthyroid subjects
have a serum TSH concentration between 0.4 and 2.5
mU/liter.” They go on further to state that “Ambulatory patients with a serum TSH ⬎2.5 mU/liter, when
confirmed by repeat TSH measurement made after
Thyroid Disease in Women Y CME Review Article
3–4 weeks, may be in the early stages of thyroid
failure, especially if TPO-Ab is detected.” Thus, it
seems logical to us that those patients who are TPOAb-positive should be excluded from populations
used to derive a normal TSH reference range. In
doing so, one recognizes that this TPO-Ab-positive
population has Hashimoto disease, is vulnerable to
progression to overt hypothyroidism, and may be
“contaminating” the otherwise normal population
sampled. Recently revised thyroid disease guidelines
of the American Association of Clinical Endocrinologists proposed a reference TSH range of 0.3 to 3.0
mU/L (22).
Depending on the cutoff value for TSH used to
define “mild thyroid failure,” its prevalence will
vary. With the traditionally used, but in our view too
high, upper level limit cutoff value of 4.5 mU/L, a
prevalence of 1.1% and 4.5% has been found in black
and white women, respectively (9). Prevalence seems
to increase with age, becoming as high as 12.9% by
the eighth decade of life. Factors that are thought to
be associated with increased likelihood of mild hypothyroidism include white race, high iodine intake
(urinary iodide ⬎1 mgm/Gm creatinine), and positive antithyroid antibodies. The greater incidence in
whites than in blacks is consistent with the mean normal values found in the NHANES population of 1.18
mU/L in blacks and 1.40 mU/L in whites (9). Mild
thyroid failure is found more frequently in women with
other autoimmune diseases such as diabetes mellitus. It
is thought, for example, that up to 25% of pregnant
women with diabetes will develop some degree of
autoimmune postpartum thyroiditis (23).
Today, mild thyroid failure is thought to be a relatively common condition and an increasing number of
studies are actively investigating its epidemiology, potential effects, and treatment options. Those clinicians
who lean toward initiating thyroxine therapy will point
out the potential for inexorable progression of mild
thyroid failure into overt hypothyroidism with its attendant symptoms, pathophysiological consequences, and
sequelae. However, not all TSH elevations may be
permanent or progressive. Those patients who have
positive TPO antibodies are at particular risk for progression, often within a few years (24). Patients with
systemic illness of a wide variety of causes will have
initial TSH suppression as part of the “sick euthyroid
syndrome” and subsequently will have modest elevations in TSH during recovery (25,26). Thus, a blood
TSH level measured during the recovery period may
give a false impression of thyroid failure. Consequently, the management of a single mildly elevated
TSH should not be immediate initiation of treatment
539
with thyroxine, but rather confirmation of the elevated
TSH at a follow-up visit 30 to 60 days later. In view of
the effects of illness on thyroid function tests (25), a
diagnosis of subclinical hypothyroidism should not be
made in hospitalized patients, but should be reserved
for the outpatient setting.
The previously mentioned expert consensus panel
(18) concluded that there was good evidence that
patients with slight elevations of TSH ⬎4.5 will
progress to overt hypothyroidism and that levothyroxine therapy would prevent symptoms but felt that
there was little convincing evidence that early treatment provided benefit. Those endocrinologists disagreeing with this conclusion hold that there have
been extensive clinical studies and reviews indicating
both the abnormalities present in mild thyroid failure
and the benefits of thyroxine treatment (12–15,27–
35) as well as more recent studies supporting their
position since the consensus panel was convened
(36–45). They argue further that the panel recommendations are inconsistent in accepting the practice
of achieving a goal or target TSH range of 1.0 to
1.5 mU/L in patients already on thyroxine therapy,
whereas they refuse to accept TSH levels of 3 to 10
mU/L as abnormal in patients not on thyroxine therapy. One thing that all parties to this controversy can
agree on is the need for future large-scale, carefully
constructed and performed studies (18–21). Until
those data become available, consideration of a more
precisely determined reference range for TSH of
0.3 to 2.5 will permit detection of individuals at risk
of overt thyroid disease and should prompt their
further follow up to confirm progression into thyroid
dysfunction and then justify initiation of therapy. We
will likely never have an absolute cutoff value for
TSH distinguishing “normal” from “abnormal.”
However, recognition that the mean of normal TSH
values is 1.18 mU/L in blacks and 1.40 mU/L in
whites (9) and that greater than 95% of the normal
population will have a TSH level less than 2.5 mU/L
(10) clearly implies that anyone with a higher value
should be assessed for early thyroid failure. We believe that a TSH level between 5 and 10 deserves
confirmation and, if confirmed, warrants treatment.
Some of the clinical and laboratory abnormalities
with potential long-term consequences that have
been associated with even mild hypothyroidism include an abnormal lipid profile that can be seem to
improve with T4 treatment (13,34,40). Such abnormalities in both total and low-density lipoprotein
cholesterol and in apolipoproteins presumably could
translate into an increased risk for coronary artery
disease. One study (35) described an increased inci-
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Obstetrical and Gynecological Survey
dence of aortic atherosclerosis (odds ratio [OR]: 1.7)
and myocardial infarction (OR: 2.3) for women who
met the criteria for mild thyroid failure. There was an
even higher odds ratio for risk in those patients with
elevated antithyroid antibodies. Myocardial performance may also be adversely influenced by mild hypothyroidism, and improvement in both systolic and
diastolic function has been documented after treatment
with levothyroxine (28,29). Other studies claim improvement with therapy in symptoms of depression and
in impaired cognitive functions such as memory (46),
improved muscle energy utilization with reduced fatigue, and beneficial effects on infertility and pregnancy
outcomes (47) have been described.
In appropriate dosage, there should be no concerns
about the effects of levothyroxine replacement therapy
on either the cardiovascular system or on bone mineral
density. The evidence available to date indicates that
even suppressive doses of levothyroxine have not been
associated with loss of bone density in premenopausal
women (48). Postmenopausal women are at risk of
loss of bone on high or TSH-suppressive dosage of
levothyroxine, but that risk is significantly attenuated by concomitant estrogen replacement or therapy
with raloxifene or bisphosphonates. There is little
risk of bone loss with replacement dosage (TSH of
0.5–1.5 mU/L) even in postmenopausal women (49).
One controversial question relates to the indications
for finding patients with mild thyroid failure by screening the general population and whether such screening
is cost-effective (50–52). The American Thyroid Association recommends screening by a measurement of
TSH every 5 years for all adults (especially women)
over the age of 35 (53). The American Association
of Clinical Endocrinologists (54) and the American
Academy of Family Practice (55) recommend screening older patients, and the American College of Physicians recommends case finding in women over 50 years
of age (56). The American College of Obstetrics &
Gynecology (ACOG) has not yet come out in favor of
routine screening of pregnant women or women who
plan to become pregnant. The ACOG guidance is consistent with case finding in patients with a history of
thyroid disease or symptoms of thyroid disease (57).
The latter indication would tend to provide broad license to screen because virtually all patients report
fatigue, and fatigue is a symptom of thyroid disease.
Personally, we agree with others (58) who recommend
TSH screening in pregnant women and then measuring
anti-TPO antibodies should the TSH level be ⬎3.0
mU/L. This appears prudent in view of the high frequency of Hashimoto thyroiditis in the United States
and in view of studies (47,59,60) implicating mild thy-
roid deficiency in pregnant women with impaired neuropsychologic development of their newborn, and the
more recent study by Casey et al (61) describing an
association between subclinical hypothyroidism and
preterm delivery. Given the potential impact of even
mild thyroid failure on outcome of pregnancy, we hope
that the ACOG might reconsider its position, although
there continues to be resistance to do so (62).
Danese et al (63) have proposed that screening with
TSH is as cost-effective as screening for breast cancer
or hypertension. Until this argument might be definitively settled, we believe that “screening” should be
confined to individuals who may be at higher risk for
mild thyroid failure. In addition to pregnant women,
this would include the elderly, women over age 35,
those with a family or personal history of thyroid disease, patients with diabetes mellitus, cardiovascular
dysfunction, hypercholesterolemia, and in other disorders that occur with increased frequency in patients
with Hashimoto disease such as diabetes mellitus,
Sjögren syndrome, Addison disease, or pernicious anemia. Most importantly, screening of pregnant women
with any history of autoimmune thyroid disease before
pregnancy is clearly warranted (64).
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