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Iodine Deficiency

Iodine is an essential trace element that is required for the production of thyroid hormones. It is a chemical element with the symbol “I” and an atomic number of 53. Deficiency can cause a multitude of thyroid disorders.


Presentation

Goitre

This is the most common presentation. Since the deficiency is endemic, goitres tend to occur in those areas. Goitres present as large swellings in the anterior neck. There usually only have cosmetic consequences, but if they a large then can cause compressive symptoms such as recurrent laryngeal nerve compression causing hoarseness of voice. The goitre may also compress the trachea causing airway obstruction.

Hypothyroidism

This is becoming very rare, and happens in individuals with severe deficiency with goitres. The patient presents with typical symptoms such as weight gain, mental slowing, cold intolerance, menorrhagia and mood disorders.

Cretinism

This is the most catastrophic consequences of these deficiency. The affected children suffer from mental retardation, stunted growth and mutism [8].

Rigor
  • In this context, rigorous monitoring of iodine status is essential to ensure adequate iodisation.[ncbi.nlm.nih.gov]
  • Thyroid function was rigorously assessed by clinical examination, ultrasound and blood tests, including serum thyroglobulin (Tg) and autoimmune antibodies. Iodine intake and the contribution made by unfiltered tap water were estimated by FFQ.[ncbi.nlm.nih.gov]
  • Ideas to Action: Independent research for global prosperity Our Work Our Work With rigorous economic research and practical policy solutions, we focus on the issues and institutions that are critical to global development.[cgdev.org]
  • Rigorous method validation confirmed good linearity (R(2) 0.9998), dynamic range (0.20 to 4.0 μM), accuracy (average recovery of 93% at three concentration levels) and precision for reliable iodide determination in pooled urine specimens over 29 days[ncbi.nlm.nih.gov]
Myxedema
  • Myxedema is a rare but life-threatening complication of hypothyroidism that can be caused by iodine deficiency.[healthline.com]
  • Thus, iodine toxicity can eventually cause iodide goiter, hypothyroidism, or myxedema. Very large amounts of iodide may cause a brassy taste in the mouth, increased salivation, GI irritation, and acneiform skin lesions.[merckmanuals.com]

Workup

Individual tests are usually rare with most tests being done at community levels. The most common system is to measure iodine concentrations in urine; the deficiency is classified as:

  • Mild: 50 to 99mcg/l
  • Moderate: 20 to 49 mcg/l
  • Severe: < 20mcg/l [9]
Glycosuria
  • The incidence of pre-eclampsia, non-proteinuric gestational hypertension, gestational diabetes, glycosuria, anaemia, post-partum haemorrhage, preterm delivery, mode of delivery, being small for gestational age, and large for gestational age did not differ[ncbi.nlm.nih.gov]

Treatment

Supplementation is the mainstay of treatment, but will not reverse the signs, such as goitre or cretinism, but will correct hypothyroidism. Goitres are usually a cosmetic problem, and if there is no indication only supplementation is indicated. Thyroidectomy will be required if there are compressive symptoms. Some nodules may become semiautonomous once iodine levels are normalized, causing hyperthyroidism.

Prognosis

Unfortunately once the consequences of iodine deficiency set in, supplementation will not reverse it. This is true for goitres and cretinism. A continuous supplementation program is required, to avoid these consequences [7].

Etiology

The daily requirement for iodine is approximately 52mcg per day (150mcg/day as per World Health Organisation recommendations) in adults with the highest requirements during pregnancy, when they may reach 250mcg/day. Intake of less than 30mcg over a prolonged period will lead to moderate to severe deficiency. Iodine is found in many food naturally, such as fish, some drinking water and from produce grown in iodine rich soil. Mountainous regions have low levels of iodine in the soil and if there are no other sources of iodine, the inhabitants may become deficient [2] [3].

Epidemiology

There are over 2.2 billion people who are at risk of iodine deficiency. The clinical disorders tend to be worse in areas with other concomitant deficiencies such as vitamin A. The distribution of the deficiency has no race or gender prediction and is totally geographical. The incidence has significantly reduced since the early 20th century due to mandatory iodine supplementation in salt. In many countries uniodinated salt is very rare [4] [5].

Sex distribution
Age distribution

Pathophysiology

Iodine is easily absorbed in the gut as iodide and then actively taken up by the thyroid gland where it is incorporated to form thyroxine and triiodothyronine. Thyroid hormones are important for regulating metabolism, and are essential in neuronal and sexual development in neonates.

If there is deficiency, the body has a number of mechanisms to try and maintain hormone levels. The pituitary releases more thyroid stimulating hormone, when the levels of thyroxine drop. This stimulates the thyroid follicle cells to take up more iodine from circulation to produce more thyroxine. There is also increased production of triiodothyronine which requires less iodine atoms and is more active (this conserves iodine).

Consequences of deficiency

  • Goitre: This is one of the most well-known signs of iodine deficiency. The growth of the goitre is stimulated by the high levels of thyroid stimulating hormone, from the pituitary as a response to low thyroxine level. The chronic stimulation by the stimulating hormone causes follicle cells to proliferate and ultimately increase in the overall size of the goitre. The goitre is initially diffuse but eventually gets nodular with time, due to irregular proliferation.
  • Hypothyroidism: This is extremely rare due to supplementation, but when it does occur there is a goitre. 
  • Cretinism: This is a catastrophic consequence to a neonate. Thyroxine and iodine are required for maturation and development of the fetus. Children born with this, if not treated, will have mental retardation, and developmental problems [6].

Prevention

Continuous population based iodine supplementation is recommended by the World Health Organisation which recommends 150mcg/day in nonpregnant individuals. This has been done in most countries with iodization of salt (In many countries, it is mandatory) [10].

Summary

Alterations in the levels of iodine, deficiency or excess have consequences on thyroid hormone production. Deficiency may impose a variety of consequences, including goitre, intellectual disability and hypothyroidism [1].

Patient Information

Definition

Iodine deficiency is a condition when there is a poor intake of a necessary element called iodine. Low levels of iodine cause imbalance of a hormone called thyroxine which is required for a number of important functions.

Cause

Iodine is usually found in food like vegetables and fish. In some areas there is poor levels of iodine in the soil and therefore the food in those regions has little iodine.

Symptoms

It usually presents with a swelling in the front of the neck due to an enlarged thyroid gland (goitre). The neck swelling is initially smooth but eventually get nodular with time. It can get to a size that it block the air pipes causing difficulty in breathing. The symptoms of low hormones, include weight gain, depression and mental slowing. In children born to mothers with iodine deficiency, there are at risk of mental retardation and poor growth.

Diagnosis

The diagnosis is usually not difficult as the goitres usually come from regions where there is deficiency. These regions tend to have many goitres. The iodine levels may be obtained from urine tests.

Treatment

Treatment includes adding iodine to food. Most countries add iodine to salt, and if you are found deficient you may be given an injection, but it is normally replaced by mouth. This does not reverse the goitre. The goitres are usually removed only if there are causing breathing problems or voice problems.

References

Article

  1. Walker SP, Wachs TD, Gardner JM, et al. Child development: risk factors for adverse outcomes in developing countries. Lancet 2007; 369:145.
  2. WHO Secretariat, Andersson M, de Benoist B, et al. Prevention and control of iodine deficiency in pregnant and lactating women and in children less than 2-years-old: conclusions and recommendations of the Technical Consultation. Public Health Nutr 2007; 10:1606.
  3. Zimmermann MB. Iodine deficiency. Endocr Rev 2009; 30:376.
  4. ICCIDD, UNICEF, WHO. Assessment of iodine deficiency disorders and monitoring their elimination. Geneva, World Health Organization, 2001
  5. Pearce EN, Andersson M, Zimmermann MB. Global iodine nutrition: Where do we stand in 2013?. Thyroid. May 2013;23(5):523-8
  6. Zimmermann MB. Iodine requirements and the risks and benefits of correcting iodine deficiency in populations. J Trace Elem Med Biol. 2008;22(2):81-92
  7. Zimmermann MB, Wegmuller R, Zeder C, et al. Rapid relapse of thyroid dysfunction and goiter in school-age children after discontinuation of salt iodization. Am J Clin Nutr. Apr 2004;79(4):642-5
  8. Cao XY, Jiang XM, Dou ZH, et al. Timing of vulnerability of the brain to iodine deficiency in endemic cretinism. N Engl J Med 1994; 331:1739.
  9. Food and Nutrition Board Institute of Medicine. Dietary reference intake. Washington, DC: National Academy Press, 2001.
  10. Zimmermann MB, Aeberli I, Torresani T, et al. Increasing the iodine concentration in the Swiss iodized salt program markedly improved iodine status in pregnant women and children: a 5-y prospective national study. Am J Clin Nutr. Aug 2005;82(2):388-92.

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Last updated: 2019-07-11 21:36