Amiodarone induced thyrotoxicosis

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Obesity, Sleep & Internal medicine
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Amiodarone-induced thyrotoxicosis
Synonyms	AIT
Pronounce	N/A
Specialty	N/A
Symptoms	Hyperthyroidism, weight loss, palpitations, tremor, anxiety, heat intolerance
Complications	Thyroid storm, heart failure, atrial fibrillation
Onset	Variable, often months after starting amiodarone
Duration	Can be prolonged, depending on treatment
Types	N/A
Causes	Amiodarone use
Risks	Pre-existing thyroid disease, high iodine intake
Diagnosis	Thyroid function tests, ultrasound, radioiodine uptake test
Differential diagnosis	Graves' disease, toxic multinodular goiter
Prevention	Monitoring thyroid function before and during amiodarone therapy
Treatment	Antithyroid drugs, corticosteroids, thyroidectomy
Medication	Methimazole, propylthiouracil, prednisone
Prognosis	N/A
Frequency	10-20% of patients on amiodarone
Deaths	Rare, but can occur if untreated

Amiodarone induced thyrotoxicosis (AIT) is a form of thyrotoxicosis that occurs as a result of treatment with the antiarrhythmic medication amiodarone. Amiodarone is commonly used to treat and prevent a variety of cardiac arrhythmias, but it can have significant effects on the thyroid gland due to its high iodine content and direct toxic effects on thyroid cells.

Pathophysiology

Amiodarone contains a large amount of iodine, approximately 37% by weight, which can lead to alterations in thyroid function. The drug can cause both hypothyroidism and thyrotoxicosis. AIT is classified into two main types:

• Type 1 AIT: This type occurs in patients with pre-existing thyroid abnormalities, such as nodular goiter or latent Graves' disease. The excess iodine from amiodarone leads to increased synthesis of thyroid hormones.
• Type 2 AIT: This type is a destructive thyroiditis, where amiodarone causes direct damage to thyroid follicular cells, leading to the release of preformed thyroid hormones into the circulation.

Clinical Features

Patients with AIT may present with symptoms of thyrotoxicosis, which can include:

• Tachycardia
• Weight loss
• Heat intolerance
• Tremor
• Anxiety
• Palpitations

The clinical presentation can vary depending on the type of AIT and the underlying cardiac condition being treated with amiodarone.

Diagnosis

The diagnosis of AIT is based on clinical suspicion, laboratory tests, and imaging studies. Key diagnostic steps include:

• Measurement of serum thyroid-stimulating hormone (TSH), free thyroxine (FT4), and free triiodothyronine (FT3) levels.
• Thyroid ultrasound to assess the gland's structure and identify nodules or goiter.
• Radioiodine uptake test to differentiate between Type 1 and Type 2 AIT, although this test is often limited by the iodine load from amiodarone.

Management

The management of AIT depends on the type and severity of the condition:

• Type 1 AIT: Treatment may involve the use of thionamides such as methimazole or propylthiouracil to reduce thyroid hormone synthesis. Potassium perchlorate may also be used to block iodine uptake.
• Type 2 AIT: Treatment typically involves the use of glucocorticoids, such as prednisone, to reduce inflammation and hormone release.

In some cases, discontinuation of amiodarone may be necessary, although this must be balanced against the risk of exacerbating the underlying cardiac condition.

Prognosis

The prognosis of AIT varies depending on the type and the patient's response to treatment. Type 2 AIT often resolves more quickly with appropriate therapy, while Type 1 AIT may require prolonged treatment and monitoring.

See Also

• Thyrotoxicosis
• Amiodarone
• Thyroid gland
• Hypothyroidism
• Graves' disease

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