Evidence map›Paper›PMID 42220090›Full record

ArticleThe Permanente journal2026

Biphasic Amiodarone-Induced Thyroid Dysfunction: De Novo Hypothyroidism Followed by Delayed Type 2 Thyrotoxicosis: A Case Report.

Nawras M Ibrahim, Sravani Karuchola, Samir Ouais

Abstract readCase Reports
In one paragraph

Article in The Permanente journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Nawras M IbrahimHCA Houston Healthcare, University of Houston, Houston, TX, USA.ORCID 0009-0000-7266-0364
Sravani KarucholaHCA Houston Healthcare, University of Houston, Houston, TX, USA.
Samir OuaisHCA Houston Healthcare, University of Houston, Houston, TX, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amiodarone disrupts thyroid function in 15% to 20% of patients through iodine overload and direct cytotoxicity, with amiodarone-induced thyrotoxicosis (AIT) classified as type 1 (iodine-driven excess synthesis in abnormal glands) or type 2 (destructive thyroiditis in normal glands). Type 2 AIT often manifests late or after drug discontinuation due to amiodarone's prolonged tissue persistence (terminal half-life 26-107 days, mean approximately 53 days), and biphasic patterns where hypothyroidism precedes thyrotoxicosis are rarely reported, particularly

Indexed as

AmiodaroneAnti-Arrhythmia AgentsHypothyroidismThyrotoxicosisAgedAtrial FibrillationHumansMaleThyroxineAmiodaroneAnti-Arrhythmia AgentsThyroxineamiodarone-induced thyrotoxicosisbiphasic thyroid dysfunctioncolor flow Dopplerdestructive thyroiditispost-discontinuationType 2 AIT

Identifiers

PMID42220090
PMCPMC13576005

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.