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ULY CLINIC

ULY CLINIC

19 Februari 2026, 15:29:11

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Iodine Deficiency Disorders (IDDA)

Iodine Deficiency Disorders (IDD) are a spectrum of clinical conditions resulting from inadequate iodine intake leading to impaired production of thyroid hormones:

  • Triiodothyronine (T3)

  • Thyroxine (T4)

These hormones regulate:

  • Basal metabolic rate

  • Protein synthesis

  • Growth and skeletal maturation

  • Brain development (especially fetal & early childhood)

  • Lipid and cholesterol metabolism

  • Conversion of carotene to Vitamin A

Because the brain depends on thyroid hormones during fetal life and the first 2–3 years of life, iodine deficiency is the leading preventable cause of intellectual disability worldwide.


2. Pathophysiology

When iodine intake is insufficient:

  1. ↓ Iodine → ↓ T3/T4 production

  2. Pituitary releases ↑ TSH

  3. Thyroid gland hypertrophy → Goitre

  4. Chronic deficiency → impaired neuronal migration & myelination

  5. Irreversible brain damage in fetus/infant


3. Spectrum of Iodine Deficiency Disorders

Age Group

Manifestation

Fetus

Miscarriage, stillbirth, congenital anomalies

Neonate

Congenital hypothyroidism

Infant

Cretinism, developmental delay

Child

Learning disability, stunted growth

Adolescent

Goitre, poor school performance

Adult

Goitre, hypothyroidism, reduced productivity


4. Clinical Manifestations


A. Goitre

Enlargement of thyroid gland due to chronic TSH stimulation.

Grades:

Grade

Description

0

No enlargement

1

Palpable but not visible

2

Visible swelling in neck


B. Hypothyroidism

  • Dry skin

  • Cold intolerance

  • Weight gain

  • Puffy face

  • Constipation

  • Fatigue

  • Bradycardia

  • Slow reflexes


C. Hyperthyroid Features (Occasionally after iodine supplementation)

  • Exophthalmos

  • Tachycardia

  • Weight loss

  • Tremor


D. Cretinism (Severe Congenital Deficiency)

Two forms:


Neurological cretinism

  • Severe intellectual disability

  • Deaf-mutism

  • Squint

  • Spasticity


Myxedematous cretinism

  • Dwarfism

  • Puffy face

  • Thick tongue

  • Severe hypothyroidism


5. Risk Factors


Dietary

  • Living in iodine-poor soil regions (highlands, flood plains)

  • Lack of iodized salt

  • Cassava-based diet (goitrogens)

  • Millet, cabbage, cauliflower excess intake


Physiological

  • Pregnancy

  • Lactation

  • Rapid growth (childhood, adolescence)


Socioeconomic

  • Poverty

  • Poor nutrition education

  • Limited access to fortified foods


6. Signs and Symptoms

System

Findings

Endocrine

Goitre

Neurologic

Developmental delay

Metabolic

Fatigue, cold intolerance

Cardiovascular

Bradycardia

Gastrointestinal

Constipation

Growth

Stunting


7. Diagnostic Criteria

Diagnosis may be clinical or biochemical:


Population indicators (WHO)

Indicator

Deficiency

Urinary iodine <100 µg/L

Insufficient intake

Goitre rate >5% school children

Endemic IDD


Individual diagnosis

  • Goitre

  • Hypothyroidism

  • Developmental delay in iodine-deficient region


8. Investigations

Test

Finding

TSH

Elevated

Free T4

Low

Urinary iodine

Low

Thyroid ultrasound

Enlarged gland

Neonatal screening

Congenital hypothyroidism


9. Management


Goals

  1. Restore iodine levels

  2. Prevent brain damage

  3. Correct thyroid dysfunction

  4. Prevent recurrence


A. Non-Pharmacological Management


Dietary Measures

Use iodine-rich foods:

Food

Source

Iodized salt

Primary prevention

Fish & seafood

High iodine

Seaweed

Very high iodine

Dairy products

Moderate iodine

Eggs

Moderate iodine

Drinking water

Depends on soil iodine

Universal salt iodization is the most effective global strategy.


B. Pharmacological Treatment


1. Iodized Oil Therapy

Used in endemic areas when iodized salt unavailable.

Drug

Dose

Duration

Iodinated oil (IM)

Single injection

3–5 years protection

Iodinated oil (PO)

400 mg

Repeat after 1–2 years


2. Lugol’s Solution

  • 3 drops (~21 mg iodine) single dose


3. Hypothyroidism Treatment (if present)

  • Levothyroxine replacement (lifelong in congenital cases)


10. Monitoring

Parameter

Expected Change

Goitre

Reduces in months

TSH

Normalizes

Growth

Improves

School performance

Improves


11. Complications

  • Permanent intellectual disability

  • Deaf-mutism

  • Growth failure

  • Pregnancy loss

  • Infertility


12. Prevention


Public Health Measures

  • Universal salt iodization

  • Monitoring salt iodine content

  • Maternal supplementation programs

  • Neonatal screening


Individual Measures

  • Use iodized salt daily

  • Avoid washing salt before cooking

  • Add salt after cooking (iodine heat-sensitive)


13. Prognosis

Stage

Outcome

Early treatment

Full recovery

Late childhood

Partial recovery

Fetal deficiency

Permanent brain damage

References

  1. World Health Organization. Assessment of iodine deficiency disorders and monitoring elimination programmes. Geneva: WHO; 2007.

  2. WHO, UNICEF, ICCIDD. Indicators for assessing iodine deficiency disorders. Geneva: WHO; 2013.

  3. Zimmermann MB. Iodine deficiency. Endocr Rev. 2009;30(4):376–408.

  4. Pearce EN, Andersson M, Zimmermann MB. Global iodine nutrition: where do we stand? Nutr Rev. 2013;71(9):553–570.

  5. Hetzel BS. Iodine deficiency disorders and their eradication. Lancet. 1983;2:1126–1129.

  6. FAO/WHO. Human vitamin and mineral requirements. Rome: FAO; 2002.

  7. De Groot LJ. Endocrinology Adult and Pediatric. 7th ed. Philadelphia: Elsevier; 2016.

  8. Harrison’s Principles of Internal Medicine. 21st ed. McGraw-Hill; 2022.

  9. UNICEF. Sustainable elimination of iodine deficiency. New York: UNICEF; 2020.

  10. Tanzania Ministry of Health. National Nutrition Guidelines. Dar es Salaam: MoH; 2023.


Imeandikwa:

20 Novemba 2020, 10:54:53

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