IODINE AND GOITER: A CONSEQUENCES DURING PREGNANCY

By: Anie Kurniawan, MD, MSc 1), and Eman Sumarna, MSc 2)
1) Chief, Sub Directorate of Clinical Nutrition
2)
Staff, Sub Directorate of Clinical Nutrition
Directorate of Community Nutrition MOH-RI

I. The Patho physiology of goiter

Goiter or as colloid nodular goiter is thyroid gland enlargement, which is

usually caused by too little iodine in the body. Lack of iodine intake from the
diet, is the primary cause of iodine deficiency, however goitrogens
(substances in the diet which produce goiter due to action on the thyroid
gland), such as thiocyanates can enhance the effect of iodine deficiency.
Iodine is mineral essential for the normal metabolism of cells, which is a
necessary nutrient for production of thyroxin hormones and normal thyroid
function. The healthy human adult body contains 15–20 mg of iodine of which
70-80 percent is in the thyroid gland, which weight only 15-25 gr. Thyroid
gland consisted of three lobes, which located in the neck two lobes were
located behind the throat, with one lobe as conjunction between each lateral
lobes.
Iodine exists in the thyroid gland as in organic iodine, that are 1) In the form
of iodine containing amino acids; Monoiodotyrosine (MIT), Diodotyrosine
(DIT), Thyroxin (T4) and Tri-iodothyronine (T3), 2) In the form of polypeptides
containing thyroxin and 3) In the form of thyroglobulin. Thyroglobulin is the
main constituent of the colloid, which fills the thyroid follicle, as the storage
form of thyroid hormones, and make up 90 percent of the total iodine in the
gland. Iodine exists in the blood as Thyroxin (T4) and Triodothyroxin (T3) and
as in organics iodine. The level of inorganic iodine falls in iodine deficiency
and rises with increase of iodine intake. The dissemination of free T4 is
important to assess the thyroid status and to diagnose hypo or hyper
thyroids. When iodine intake is deficient, the thyroid gland is unable to
produce sufficient thyroid hormone, it may attempt to compensate by
enlarging of thyroid gland, which is called colloid nodular goiter. In otherwise,
when the thyroid is then reexported to iodine, the nodules may produce
thyroid hormone, but occasionally, the nodules may produce too much
thyroid hormone causing thyrotoxitosis, which usually accompanied by
enlargement of thyroid gland, called a toxic nodular goiter. Colloid nodular
goiter is also known as endemic goiters and are
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usually caused by inadequate iodine in the diet. Endemic goiter tends to be
occurred in certain geographical areas with iodine-depleted soil away from
the sea cost.
In Indonesia, endemic goiter occurred mainly in volcanic and mountain area
affecting among population living in this area, such as pregnant women,
newborn babies, under fives and school children. Mapping survey among
elementary school children in 1998 showed that 334 sub districts categorized
as severe endemic area (Total Goiter Rate/TGR > 30%), 278 from 4028 sub
districts as moderate endemic area (TGR 20-24%) and 1167 sub districts as
mild endemic area (TGR 5-19,9%). It revealed that around 45% of sub
districts in Indonesia were risk to have goiter cases. The latest data showed
that TGR among elementary school children, was little bit increased to 11.1%
of national rate, but there was decreased TGR in the severe endemic areas
significantly. The National IDD Evaluation Survey (2003) showed 50 districts
had increased to the better status, while 68 districts had decreased to the
worse status and 150 districts in stable condition.

II. The causes of goiter

Lack of iodine in the diet is the majority cause of endemic goiter, where the
loss of iodine from the soil due to glaciating, erosion, high rain fall, snow and
flooding leads to a low iodine content of all food grown in it. The husbandry
and agriculture production was also lack of iodine content, which will be in
appropriate resources when people in that area consumed it. Inadequate
dietary iodine leads to reduce synthetics of thyroid hormones (T3 and T4).
While the lower level of T4 in the blood stimulates the pituitary gland to
secrete Thyrotrophin Stimulating Hormone (TSH) from the blood to fulfill the
production of thyroid gland hormones. In other word, TSH increases the rate
of pumping iodine by the thyroid from the blood, followed with hyperplasia of
the thyroid gland, as resulted as goiter. Enlargement is regarded as
significant in the human when the size of lateral lobes is greater than
terminal phalanx of the thumb of the person examined.
Thyroid enlargement whether as form of a single small nodule or massive
enlargement is typically symptoms of goiter, which occasionally accompanied
with breathing and swallowing difficulties, cause of the compression of the
trachea and
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esophagus. Neck vein distention and dizziness are occurred when the size of
the thyroid gland rose above the head (large goiter). Chronic severe iodine
deficiency is associated with thyroid hyperplasia. The prevalence of goiter
increased, with the severity of the iodine deficiency and becomes almost
universal in a population when the iodine intake less than 10 μg per day.
Iodine in the food stuff is widely available in seafood, such as “tenggiri” (cod)
sejenis “ikan sungai” (sea bass), nama “ikan laut” (haddock) and ikan “air
tawar berduri” (perch). Kelp or “lumut laut” is the most vegetable seafood
that is a rich source of iodine. Dairy product and plants grown soil that is rich
in iodine are also a good sources of iodine. The risk factors to become goiters
are female, people older than forty, having an adequate dietary intakes,
which living in an endemic area and having a family history of goiter.

III. Iodine deficiency in pregnancy

The term of “goiter” had been used in the past. Presently, the new term of
“Iodine Deficiency Disorders (IDD)”, now been generally adopted as
international health and nutrition environment. The effect of IDD is due to the
impact of hypothyroidism with reduced of T4 levels, and often accompanied
with normal T3 levels and raised TSH levels.
The spectrum of IDD affected among vulnerable groups that are fetus,
neonates, infancy, childhood and adult. The most common effect of IDD in
adults is goiters, while pregnant women who suffered from IDD will had an
impact to their children. In iodine deficient areas, there is an increase rate of
spontaneous abortions and stillbirths in humans, which can be reduced by
correction of the deficiency. Thyroid treatment in pregnant women who are
hypothyroid, also had similar benefits on reducing the abortus and stillbirths.
(Mc. Michael et al, 1980). Study in Zaire and New Papua Guinea indicated
that an increase of stillbirth and infant mortality could be reduced by
controlled with iodine oil injection given during pregnancy. Recent evidence
indicated that the effects of iodine deficiency on the occurrence of abortion,
stillbirth, congenital anomalies, cretins, neonatal goiter and hypothyroidism,
probably arise when mother suffered from iodine deficiency. Thus, it was
indicated
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that the major impact of IDD among pregnant women is on child survival
(Hetzel BS, 1991). The effect of pregnant women with IDD on their children,
continued up to child and adolescent period, however the children had been
supplied with sufficient iodine intake. This condition is due to the impairment
of brain development of the children, which is depending on inadequate
supply of thyroxin since earlier during conception. About one third of normal
brain development occurred before birth and the rest is completed in the first
two years of life. Normal brain development had to be maintained with
normal level of thyroxin hormones that is important both during and after
pregnancy, especially among the first two years of life. Thus prevention of
goiter especially among pregnant women is important, in order to avoid the
iodine deficient during pregnancy toward reducing the impact of IDD on
pregnancy outcomes.

IV. Prevention of goiter

Iodine supplementation is an effective approach to prevent and control goiter

and IDD rapidly. However, commonly the thyroid gland cannot become
smaller, particularly in person who had a big size of thyroid gland. In fact
Iodine oil capsule supplementation targeted to women at reproductive age
including pregnant women living in endemic area, are recommended to
supply the iodine intake fulfill their requirement.
As known that people living in endemic area are risk to have IDD, more over
in pregnant women, who are higher requirement of iodine rather than non-
pregnant women. Two capsules, which contain 200 mg iodine for each
capsule, should be taken once in year by non-pregnant mother, and adding
with one capsule during pregnancy and one capsule during lactation. These
supplements are sufficient to meet the minimum daily requirement of iodine,
which only 100-150 μg per day.
Fortification of salt with iodine is widely used in the world to improve the
iodine intake of the community. It was mandatory that instead of
supplementation, the content of iodine in salt should be more than >30 ppm
KJO3, and all salt producers have to follow that regulation. The advantage of
iodine salt distribution and
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marketed throughout the country is, that iodine salt supplied can reach all
level of social economic status in the community.

V. Conclusion

Pregnant women are risk to have goiters because the requirement of iodine is
increased during pregnancy. Lack of iodine intake will cause iodine deficiency
disorder (IDD), which result goiters when the deficiency are chronically. IDD
in pregnant women will give a harmful effect among their children due to the
congenital anomalies, neurological cretinism, myxoedematous, cretinism,
which influence the quality of human resources in the future generation.
Therefore, iodine oil capsule distributed to women at reproductive age
including pregnant women living in endemic area of goiter have to be
implemented in order to eliminate their child growth impairment. Further
more, the salt producers should distribute and market the iodized salt
particularly in the community who living in endemic area goiter.
Last but not least, every pregnant woman have to visit the health services
routinely for antenatal care, so the enlargement of thyroid gland can be
detected earlier and then they will have an appropriate treatment.
References

1. Mc Michael, AxJx, Potter, JD and het ind Bys. Iodine Deficiency, thyroid
function and reproductive failure. In endemic goiter and endemic
cretinism. (eds JB Stanbury and BS Hetzel) pp 445-60 Willey, New York-
1980)

2. Hetzel BS. The story of iodine deficiency. An international challenge in

nutrition, pp 284-101, Oxford University Press. Oxford 1991

3. Health Encyclopedia: Iodine in diet Adam, p 1-2, 2004

4. Health Encyclopedia, Colloid nodular goiter, Adam p.1-3, 2004

5. American Map Corporation,1984.

6. Iodine Deficiency Disorders (IDD) control program in Indonesia, MOH RI,

2002

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http://www.gizi.net/makalah/Iodine-Goiter.pdf

What is a goiter?
The term “goiter” simply refers to the abnormal enlargement of the
thyroid gland. It is important to know that the presence of a goiter does
not necessarily mean that the thyroid gland is malfunctioning. A goiter
can occur in a gland that is producing too much hormone
(hyperthyroidism), too little hormone (hypothyroidism), or the correct
amount of hormone (euthyroidism). A goiter indicates there is a
condition present which is causing the thyroid to grow abnormally.
What causes a goiter?
One of the most common causes of goiter formation worldwide is
iodine deficiency. While this was a very frequent cause of goiter in the
United States many years ago, it is no longer commonly observed. The
primary activity of the thyroid gland is to concentrate iodine from the
blood to make thyroid hormone. The gland cannot make enough
thyroid hormone if it does not have enough iodine. Therefore, with
iodine deficiency the individual will become hypothyroid.
Consequently, the pituitary gland in the brain senses the thyroid
hormone level is too low and sends a signal to the thyroid. This signal
is called thyroid stimulating hormone (TSH). As the name implies, this
hormone stimulates the thyroid to produce thyroid hormone and to
grow in size. This abnormal growth in size produces what is termed a
“goiter.” Thus, iodine deficiency is one cause of goiter development.
Wherever iodine deficiency is common, goiter will be common. It
remains a common cause of goiters in other parts of the world.
Hashimoto’s thyroiditis is a more common cause of goiter formation in
the US. This is a autoimmune condition in which there is destruction
of the thyroid gland by one’s own immune system. As the gland
becomes more damaged, it is less able to make adequate supplies of
thyroid hormone. The pituitary gland senses a low thyroid hormone
level and secretes more TSH to stimulate the thyroid. This stimulation
causes the thyroid to grow, which may produce a goiter.
Another common cause of goiter is Graves’ disease. In this case, one’s
immune system produces a protein, called thyroid stimulating
immunoglobulin (TSI). As with TSH, TSI stimulates the thyroid gland to
enlarge producing a goiter. However, TSI also stimulates the thyroid to
make too much thyroid hormone (causes hyperthyroidism). Since the
pituitary senses too much thyroid hormone, it stops secreting TSH. In
spite of this the thyroid gland continues to grow and make thyroid
hormone. Therefore, Graves’ disease produces a goiter and
hyperthyroidism.
Multinodular goiters are another common cause of goiters. Individuals
with this disorder have one or more nodules within the gland which
cause thyroid enlargement. This is often detected as a nodular feeling
gland on physical exam. Patients can present with a single large nodule
with smaller nodules in the gland, or may show as multiple nodules
when first detected (see Thyroid Nodule brochure). Unlike the other
goiters discussed, the cause of this type of goiter is not well understood.
In addition to the common causes of goiter, there are many other less
common causes. Some of these are due to genetic defects, others are
related to injury or infections in the thyroid, and some are due to tumors
(both cancerous and benign tumors)

How do you diagnose a Goiter?

As mentioned earlier, the diagnosis of a goiter is usually made at the
time of a physical examination when an enlargement of the thyroid is
found. However, the presence of a goiter indicates there is an
abnormality of the thyroid gland. Therefore, it is important to determine
the cause of the goiter. As a first step, you will likely have thyroid function
tests to determine if your thyroid is under active or overactive (see
Thyroid Function Tests brochure). Any subsequent tests performed will
be dependent upon the results of the thyroid function tests.
If the thyroid is diffusely enlarged and you are hyperthyroid, your doctor
will likely proceed with tests to help diagnose Graves’ Disease (see
Graves’ Disease brochure). If you are hypothyroid, you may have
Hashimoto’s Thyroiditis (see Hypothyroidism brochure) and you may
get additional blood tests to confirm this diagnosis. Other tests used to
help diagnose the cause of the goiter may include a radioactive iodine
scan, thyroid ultrasound, or a fine needle aspiration biopsy

How is a goiter treated?

The treatment will depend upon the cause of the goiter. If the goiter
was due to a deficiency of iodine in the diet (not common in the United
States), you will be given iodine supplementation by mouth. This will
lead to a reduction in the size of the goiter, but often the goiter will not
completely resolve.
If the goiter is due to Hashimoto’s Thyroiditis, and you are hypothyroid,
you will be given thyroid hormone supplement as a daily pill. This
treatment will restore your thyroid hormone levels to normal, but does
not usually make the goiter go completely away. While the goiter may
get smaller, sometimes there is too much scar tissue in the gland to allow
it to get much smaller. However, thyroid hormone treatment will usually
prevent it from getting any larger.
If the goiter is due to hyperthyroidism, the treatment will depend upon
the cause of the hyperthyroidism (see Hyperthyroidism and Graves’
disease brochures). For some causes of hyperthyroidism, the treatment
may lead to a disappearance of the goiter. For example, treatment of
Graves’ disease with radioactive iodine usually leads to a decrease or
disappearance of the goiter.
Many goiters, such as the multinodular goiter, are associated with
normal levels of thyroid hormone in the blood. These goiters usually
do not require any specific treatment after the appropriate diagnosis is
made. If no specific treatment is suggested, you may be warned that
you are at risk for becoming hypothyroid or hyperthyroid in the future.
However, if there are problems associated with the size of the thyroid
per se, such as the goiter getting so large that it constricts the airway,
your doctor may suggest that the goiter be treated by surgical removal.

http://www.thyroid.org/patients/brochures/Goiter_brochure.pdf
Initially a person suffering from goiter notices that she has periods when she is emotionally upset.
With time, these upsets increase in their duration. Other symptoms are weeping and feelings of
depressions, and an inability to concentrate. The patient is edgy and seems close to a nervous
breakdown. Patients also lose weight rapidly and their eyes begin to bulge out. In addition to this
they notice tremors in their hands and a certain inability to perform any task requiring muscular
effort.

With time the goiter becomes bigger causing the neck to look swollen. When the goiter becomes
bigger it compresses the windpipe and the tube which we use to swallow. As a result of this people
suffering from goiter develop symptoms like coughing, a feeling of being unable to breathe and also
the fear that there are food particles stuck in the upper throat.
Some goiters may disappear on their own while others are enlarged. When the thyroid tissue is
destroyed, this leads to the development of hypothyroidism in patients.

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