Evidence map›Paper›PMID 39100009›Full record

ArticleCureus2024

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

Neha Meda, Suhail Saad-Omer, Moises Matos, Mustafa Kinaan

Abstract readCase Reports
In one paragraph

Article in Cureus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Neha MedaInternal Medicine, University of Central Florida Hospital Corporation of America (HCA) Healthcare Graduate Medical Education (GME), Orlando, USA.
Suhail Saad-OmerInternal Medicine, University of Central Florida Hospital Corporation of America (HCA) Healthcare Graduate Medical Education (GME), Orlando, USA.
Moises MatosEndocrinology, Miami Veterans Affairs Healthcare System, Miami, USA.
Mustafa KinaanEndocrinology, Diabetes, and Metabolism, University of Central Florida Hospital Corporation of America (HCA) Healthcare Graduate Medical Education (GME), Orlando, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

amiodaronedrug-induced agranulocytosisinterleukin-6 (il-6)methimazolethyrotoxicosis

Identifiers

PMID39100009
PMCPMC11297576

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