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 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 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 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 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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