Iodine induced thyrotoxicosis in apparently normal thyroid glands

Area of Science:

• Endocrinology
• Thyroid Research
• Toxicology

Background:

• Thyrotoxicosis, characterized by elevated thyroid hormones, can have various etiologies.
• Iodine is essential for thyroid hormone synthesis, but excessive intake can paradoxically disrupt thyroid function.

Observation:

• Two male patients presented with thyrotoxicosis, exhibiting elevated serum triiodothyronine (T3) and thyroxine (T4) levels.
• Both patients had a history of prolonged iodine exposure (2-10 mg daily for 2-12 months) and high urinary iodine excretion.
• Thyroid radioiodine uptake was low, and no goiter or thyroid antibodies were detected, suggesting no pre-existing thyroid pathology.

Findings:

• Interruption of iodine intake led to a gradual decrease in urinary iodine excretion and normalization of serum T3 and T4 levels.
• Patients became clinically and biochemically euthyroid within 9-11 weeks of iodine withdrawal.
• Thyroid function tests, including radioiodine uptake, TRH-stimulation, and T3-suppression tests, normalized, with normal thyroid gland morphology observed on scans.

Implications:

• This case study highlights iodine-induced thyrotoxicosis as a distinct clinical entity, potentially occurring in individuals without underlying thyroid disease.
• The exact pathogenic mechanism of iodine-induced thyrotoxicosis in these cases remains unclear and warrants further investigation.
• Understanding the role of iodine excess in thyroid dysfunction is crucial for diagnosis and management, particularly in populations with varying iodine intake levels.