Maternal iodine deficiency — What condition in infants results from iodine deficiency during pregnancy, characterized by stunted growth, deafness, and severe cognitive impairment?

Introduction / Context:
Iodine is essential for thyroid hormone synthesis. During pregnancy, maternal iodine deficiency can disrupt fetal neurodevelopment with lifelong consequences. This question targets recognition of the classic syndrome associated with prenatal iodine deficiency.

Given Data / Assumptions:

• Thyroid hormones regulate neuronal migration, myelination, and skeletal growth.
• Fetal thyroid depends on maternal iodine supply, especially early in gestation.
• Clinical features include growth, hearing, and cognitive defects.

Concept / Approach:
Cretinism (now often termed congenital iodine deficiency syndrome) encompasses irreversible intellectual disability, deaf-mutism, spasticity, and short stature. Prevention relies on adequate maternal iodine intake via iodized salt or supplements in deficiency-prone regions. Early detection and thyroid hormone replacement can mitigate some postnatal consequences but cannot fully reverse prenatal injury.

Step-by-Step Solution:

Verification / Alternative check:
Public health interventions with iodized salt drastically reduce congenital iodine deficiency syndromes in endemic regions, validating causality between iodine status and neurodevelopmental outcomes.

Why Other Options Are Wrong:

• Keshan disease: linked to selenium deficiency and cardiomyopathy.
• Multiple sclerosis: autoimmune demyelinating disorder, not nutritional iodine-related.
• Crohn's disease: inflammatory bowel disease unrelated to iodine status.
• Rickets: vitamin D/calcium deficiency leading to bone deformities, not primarily neurodevelopmental.

Common Pitfalls:
Confusing cretinism with goiter. Goiter is thyroid enlargement; cretinism reflects fetal neuroendocrine deficiency and has distinct outcomes.

Final Answer:
Cretinism (congenital iodine deficiency syndrome).