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AACE Clin Case Rep. 2020 Jan-Feb; 6(1):
e19–e22. Published online 2020 Sep 26.
doi: 10.4158/ACCR-2019-0180
PMCID: PMC7279774PMID: 32984517
HYPOTHYROIDISM AND GOITER IN A YOUNG MALE
WITH SUSPECTED DIETARY IODINE DEFICIENCY
FOLLOWED BY THYROTOXICOSIS AFTER IODINE
SUPPLEMENTATION
Itivrita Goyal, MD,corresponding author1
Manu Raj Pandey, MD,2 and Rajeev Sharma,
MD, FACE1,2
Author information Article notes
Copyright and License information
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Abstract
Objective:
Iodine deficiency disorders (IDDs) remain
a major public health concern in most
parts of the world but are extremely rare
in North America. We describe a case of
goiter in a young male with dietary
history and findings suggestive of IDD.

Methods:
Laboratory and imaging procedures
including thyroid function tests,
autoantibodies, urine iodine, thyroid
ultrasound, and radioactive iodine (RAI)
uptake scan were performed.

Results:
On initial presentation,
thyroid-stimulating hormone (TSH) was
24.4 mIU/L (normal range is 0.4 to 5.0
mIU/L), free thyroxine was <0.4 ng/dL
(normal range is 0.8 to 1.8 ng/dL), and
thyroid peroxidase antibody was positive
at 43 IU/mL (normal range is <35 IU/mL).
He reported consuming strawberries and
peanut butter sandwiches with no intake
of dairy or seafood due to
gastrointestinal issues (abdominal pain,
bloating, and nausea). Physical exam
revealed a diffusely enlarged, palpable
thyroid gland (grade II goiter).
Ultrasound of the neck showed an enlarged
thyroid gland with no nodules. RAI uptake
scan showed diffuse increased uptake
(91%). Given his poor diet, a 24-hour
urinary iodine excretion test was ordered
which was suggestive of very low iodine
intake. He was started on multivitamins
with 150 μg of iodine daily. On follow
up, clinical exam showed grade I goiter
and TSH had normalized to 0.7 mIU/L and
free thyroxine was 1.2 ng/dL. He
continued on iodine supplementation and
tolerated iodine-rich foods. Six months
later, thyroid function tests showed
hyperthyroidism with TSH of <0.002 ng/dL
and free thyroxine was elevated to 2.8
ng/dL. Iodine supplements were stopped.
Conclusion:
Hypothyroidism and goiter due to IDD
should be suspected in the setting of
poor dietary intake. IDDs can be rapidly
diagnosed in a patient on a restricted
diet with multiple urinary iodine
determinations and RAI study. Regular
thyroid labs should be done to monitor
for hyperthyroidism that can develop
after iodine supplementation.

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INTRODUCTION
Iodine is an essential component of the
diet and its deficiency leads to
impairment of thyroid hormone synthesis.
Iodine deficiency disorders (IDDs) are a
gamut of disorders which include multiple
adverse health effects due to iodine
deficiency at various stages of life (1).
The most serious and important
preventable consequence is cognitive
impairment due to its major role on fetal
neurodevelopment.
IDDs are a major public health concern in
certain parts of the world which are
deficient in iodine because of a lack of
a national program for iodine
supplementation. Fortunately, with the
introduction of iodized salt in the
United States in the 1920s, these
conditions were eradicated in North
America to a great extent (2). However,
certain populations like those with
restricted diets, food allergies, or
increased iodine requirement (such as
pregnant and lactating women) might still
be at increased risk of IDD. Only a few
cases of iodine deficiency-induced
hypothyroidism or goiter have been
reported in the literature (3,4). Here,
we describe a case of goiter in a young
male with a dietary history and other
findings suggestive of IDD.

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CASE REPORT
A 27-year-old, Caucasian male was
referred to the endocrinology clinic for
abnormal thyroid function tests and
enlarged thyroid gland. He reported
chronic nausea, bloating, and abdominal
pain. His dietary history was consistent
with eating peanut butter sandwiches and
strawberries for the past few years. He
denied consuming dairy, seafood products,
and multivitamins. He reported low energy
levels with cold intolerance and denied
dysphagia, odynophagia, or hoarseness. He
denied history of upper respiratory tract
infection, radiation exposure, neck pain,
or tenderness. His physical exam revealed
diffusely enlarged thyroid gland (grade
II goiter) with rubbery consistency, but
no nodules were palpated.

Ultrasound (US) of the neck showed

enlarged thyroid gland without nodules
(Fig. 1). Laboratory workup revealed
thyroid-stimulating hormone (TSH) was
increased to 24.4 mIU/L (reference range
is 0.4 to 5.0 mIU/L), free thyroxine
level (FT4) was <0.4 ng/dL (reference
range is 0.8 to 1.8 ng/dL), slightly
increased thyroid peroxidase antibody of
43 IU/mL (reference range is <35 IU/mL),
and negative thyroglobulin antibody. He
was started on levothyroxine
supplementation by his primary care
physician but never took it. Three months
later, his TSH was 6.1 mIU/L, thyroid
peroxidase antibody was negative, and
total triiodothyronine was within normal
limits. FT4 test was not ordered at this
time.

An external file that holds a picture,

illustration, etc.
Object name is i2376-0605-6-1-e19-f01.jpg
Fig. 1.
Ultrasound of the thyroid gland showing
enlarged left lobe measuring about 7.4 cm
at its widest.

The abnormal thyroid function tests

suggested primary hypothyroidism likely
as a sequela of Hashimoto thyroiditis as
he had elevated antibodies at the initial
workup. The TSH was improving, repeat
thyroid peroxidase antibody was negative,
and he was clinically euthyroid, hence no
treatment was initiated at this time. A
radioactive iodine (RAI) uptake scan was
performed which surprisingly showed a
24-hour uptake of 91% with no hot or cold
nodules (Fig. 2).

An external file that holds a picture,

illustration, etc.
Object name is i2376-0605-6-1-e19-f02.jpg
Fig. 2.
Radioactive iodine uptake scan of the
thyroid gland showing diffusely increased
uptake of iodine at 91% over 24 hours.

These findings were initially presumed to

signify the patient was in the recovery
phase of thyroiditis. A repeat US of the
thyroid gland showed enlargement with a
1.5-cm nodule in the left posteroinferior
region. However, given the patient's poor
eating habits, urinary iodine levels were
obtained. Urine testing showed a very low
spot urine iodine level of 4 μg/L
(reference range is 28 to 544 μg/L) along
with low 24-hour urine iodine excretion
of 10 μg/24 hours (performed by LabCorp,
Burlington, NC; reference range is 100 to
460 μg/24 hours). The nontoxic goiter
associated with primary hypothyroidism
was thought to be secondary to severe
iodine deficiency given the patient's low
intake of dietary iodine for many years,
however this was not firmly established
as multiple 24-hour urine iodine or spot
iodine levels were not measured.

The patient was started on a multivitamin

supplement containing 150 μg of iodine
daily and was advised to consume
iodine-rich foods. On follow up in the
clinic 3 months later, the spot urine
iodine levels had improved to 91 μg/L
(performed by LabCorp; reference range is
28 to 544 μg/L). Thyroid function tests
had normalized with TSH within normal
range (0.655 mIU/L) and FT4 normalized to
1.24 ng/dL. Physical exam showed grade I
goiter, but repeat imaging with US or RAI
scan was not performed.

The patient continued to be on daily

iodine supplementation and was now able
to tolerate a varied diet consisting of
eggs, meat, seafood, vegetables and some
breads. He was evaluated in the clinic 6
months later with repeat thyroid function
tests and US of the thyroid gland. He
complained of weight loss, palpitations,
and pedal edema. Laboratory data
suggested primary hyperthyroidism with
TSH <0.002 mIU/L, FT4 elevated to 2.8
ng/dL (reference range is 0.7 to 1.9
ng/dL), and total triiodothyronine
elevated to 326 ng/dL (reference range is
80 to 180 ng/dL). At this time, 24-hour
urine iodine level was normal at 145
μg/24 hours (performed by Quest
Diagnostics, Secaucus, NJ; reference
range is 70 to 500 μg/24 hours). US
showed enlargement of both thyroid lobes
with increased blood flow and a 1.2-cm
nodule in the posteroinferior aspect of
the left lobe. Hyperthyroidism was likely
secondary to increased uptake of iodine
or an underlying autoimmune state leading
to increased hormone production and
secretion. Iodine supplementation was
stopped as his diet had improved.

Go to:
DISCUSSION
The daily iodine requirement according to
the World Health Organization is in the
range of 90 to 150 μg/day, with higher
requirements during pregnancy (220 to 250
μg/day) and lactation (259 to 290 μg/day)
(2,5). Median spot urine iodine
concentration is used to define iodine
status for a population. A median urinary
iodine concentration of 100 to 199 μg/L
is considered adequate iodine intake for
a non-pregnant population, whereas levels
below 100 μg/L indicate iodine deficiency
(5).

Frank iodine deficiency is mostly seen in

underdeveloped and developing countries,
and although iodine intake has been
considered to be adequate in North
America, this assumption is changing (6).
The National Health and Nutrition
Examination Survey (called NHANES)
reported that iodine intake dropped by
50% from the 1970s to the 1990s in the
U.S.A. (7). The median urinary iodine
concentration reported in the 2009 to
2010 survey was 144 μg/L indicating that
the overall U.S.A. population is iodine
sufficient, but iodine intake varies a
lot across the population (8).

Goiter is the enlargement of the thyroid

gland as an adaptation to chronic iodine
deficiency. Iodine deficiency leads to
decreased thyroid hormone production
resulting in increased TSH production by
the pituitary gland. The increased TSH
stimulates thyroid growth and leads to
goiter formation. Our patient had
elevated TSH on presentation along with
enlarged thyroid seen on the US of the
neck. In the initial stages of iodine
deficiency, goiter is diffusely enlarged
but over time it may become nodular by
progressive accumulation of new
follicles. Chronic TSH stimulation may
also lead to “gain-of-function” mutations
of thyroid follicles, seen more commonly
in areas of endemic iodine deficiency
(9,10). This can lead to toxic
multinodular goiter and hyperthyroidism
if iodine deficiency is not very severe.

Cretinism and mental retardation are the

most profound manifestations seen in
infants as a result of severe IDD in
pregnancy. Children in areas with IDD can
have enlarged thyroid glands. Goiter,
hypothyroidism, and toxic multinodular
goiter are commonly seen in the adults of
these areas. In the industrialized world,
primary hypothyroidism is mostly
attributed to autoimmune disorders like
Hashimoto disease and IDD is an
exceedingly rare phenomenon. Since IDDs
are rare in North America with only a few
cases reported (3,11), IDD is not usually
considered as an etiology of
hypothyroidism. However, people with
restricted diets (such as vegans and
those with lactose intolerance), pregnant
women, and lactating women are at
increased risk (2). Given these concerns,
physicians need to be aware of the risk
factors for IDDs. Our patient ate an
extremely restricted diet which was low
in iodine that put him at increased risk
for an IDD. Iodine deficiency should be
considered as a cause of primary
hypothyroidism in such patients.

RAI uptake scan performed in patients

with IDD will show paradoxical finding of
diffusely increased uptake. Furthermore,
RAI uptake scans are not routinely
performed as a part of workup for
hypothyroidism. This often leads to
underdiagnoses of iodine
deficiency-induced hypothyroidism. This
paradoxical finding on the RAI uptake
scan in a euthyroid or a hypothyroid
patient in the setting of iodine
deficiency provides a strong clue to the
diagnosis of IDD.

Our patient had signs and symptoms of

hypothyroidism on presentation but RAI
uptake scan paradoxically showed
increased uptake of 91%. This, in
addition to his history of restricted
diet, prompted us to obtain a 24-hour
urinary iodine level to screen for an
underlying IDD. Since there is
considerable variation in individual
daily iodine intake, it has been
suggested that 10 samples be collected to
determine iodine status (12). Therefore,
a single 24-hour urine iodine
concentration cannot be used to diagnose
IDD. In our patient, since more than one
24-hour urine iodine level was not
measured on his usual diet, the diagnosis
of IDD was only suggestive based on his
dietary history, clinical features of
hypothyroidism, and very low urine iodine
levels.
When diagnosed with IDDs, patients should
be started on daily iodine
supplementation as recommended by the
World Health Organization with careful
monitoring of thyroid function at regular
intervals. Patients should be counselled
on the signs and symptoms of
hyperthyroidism that can often develop
after iodine supplementation (13). A
cross-sectional study had shown that a
Danish population with deficient iodine
intake had a higher lifetime risk for
hyperthyroidism, the most common cause of
which was multinodular goiter (14,15).

As discussed earlier, iodine deficiency

increases the risk of toxic multinodular
goiter by development of autonomous
thyroid cells. Iodine-induced
hyperthyroidism can develop in such
patients if they are exposed to excess
iodine during fortification and if
preexisting iodine deficiency was severe.
This effect is seen more commonly in
adults over 60 years of age with nodular
thyroid (16) and can be reduced by
gradual introduction of iodized salt to
the diet.

Go to:
CONCLUSION
Timely diagnosis of IDDs is important in
patients who are on restricted diets.
This should be performed by obtaining
24-hour urinary iodine levels and RAI
uptake scan. A detailed dietary history
should also be obtained in patients
presenting with goiter or hypothyroidism,
irrespective of the patient's
geographical residence. IDD is a
reversible condition when treated at
early onset with dietary iodine
supplementation.

Go to:
Abbreviations
FT4 free thyroxine
IDD iodine deficiency disorder
RAI radioactive iodine
TSH thyroid-stimulating hormone
US ultrasound
Go to:
Footnotes
DISCLOSURE

The authors have no multiplicity of

interest to disclose.

Go to:
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Articles from AACE Clinical Case Reports
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Association of Clinical Endocrinology
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