# A Case of Amiodarone-Induced Thyrotoxicosis Presenting With Methimazole-Induced Agranulocytosis

**Authors:** Neha Meda, Suhail Saad-Omer, Moises Matos, Mustafa Kinaan

PMC · DOI: 10.7759/cureus.63858 · Cureus · 2024-07-04

## TL;DR

A patient with amiodarone-induced thyrotoxicosis experienced complications from methimazole and was successfully treated with surgery and hormone replacement.

## Contribution

This case highlights the challenges in managing AIT and the effectiveness of surgical intervention when medical therapy fails.

## Key findings

- Methimazole treatment was stopped due to agranulocytosis.
- Total thyroidectomy resolved persistent thyrotoxicosis.
- The patient is now euthyroid with levothyroxine therapy.

## Abstract

Amiodarone is a class III anti-arrhythmic drug found to be effective in treating multiple life-threatening arrhythmias, including paroxysmal atrial fibrillation. Despite its effectiveness, amiodarone has been found to result in thyroid dysfunction. Amiodarone-induced thyrotoxicosis (AIT) is classified as type 1, which often develops in those with autoimmune hyperthyroid conditions, or type 2, which occurs because of destructive thyroiditis in an apparently normal thyroid. Differentiating between both types often poses a clinical and therapeutic dilemma, as AIT 1 is treated with thionamides, whereas AIT 2 requires steroids for treatment. We present a case of a patient with AIT who was treated empirically for both subtypes with methimazole and prednisone without clinical improvement. Methimazole was later stopped due to concern for agranulocytosis, and the patient was then treated with cholestyramine, metoprolol, and prednisone. Given persistent thyrotoxicosis, the decision was made to proceed with surgical intervention. The patient underwent a successful total thyroidectomy without complications. The patient‘s condition clinically improved post-surgery and was discharged home on post-operative day 2 in stable condition. Prednisone was tapered over two weeks, and he was started on a weight-based dose of levothyroxine. He continues to follow up in our clinic for postoperative hypothyroidism and is clinically and biochemically euthyroid.

## Linked entities

- **Chemicals:** amiodarone (PubChem CID 2157), methimazole (PubChem CID 1349907), prednisone (PubChem CID 5865), metoprolol (PubChem CID 4171), levothyroxine (PubChem CID 5819)
- **Diseases:** thyrotoxicosis (MONDO:0010138), agranulocytosis (MONDO:0001609), hypothyroidism (MONDO:0005420)

## Full-text entities

- **Diseases:** Thyrotoxicosis (MESH:C566386), thyroiditis (MESH:D013966), AIT (MESH:D000092582), arrhythmias (MESH:D001145), Agranulocytosis (MESH:D000380), AIT 1 (MESH:D056486), AIT 2 (MESH:D006111), paroxysmal atrial fibrillation (MESH:D001281), hypothyroidism (MESH:D007037), thyroid dysfunction (MESH:D013959)
- **Chemicals:** Amiodarone (MESH:D000638), cholestyramine (MESH:D002792), levothyroxine (MESH:D013974), metoprolol (MESH:D008790), Prednisone (MESH:D011241), Methimazole (MESH:D008713), steroids (MESH:D013256), thionamides (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC11297576/full.md

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11297576/full.md

## References

20 references — full list in the complete paper: https://tomesphere.com/paper/PMC11297576/full.md

---
Source: https://tomesphere.com/paper/PMC11297576