Evidence map›Paper›PMID 42545320›Full record

ArticleProblemy endokrinologii2026

Clinical Case Series of Destructive Thyrotoxicosis Associated with Hashimoto's Thyroiditis Misdiagnosed as Graves' Disease: Clinical Patterns, Diagnostic Pitfalls, and Hypothesized Molecular Insights.

Maher Monir Akl, Amr Ahmed

Abstract readCase Reports
In one paragraph

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

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1 · What the graph read from it

What it found

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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

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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

2 authors.

Maher Monir AklNational Research Lobachevsky State University of Nizhny Novgorod.
Amr AhmedThe public health department, Riyadh First Health Cluster, Ministry of Health.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This descriptive clinical case series analyzes five cases of destructive thyrotoxicosis associated with Hashimoto's thyroiditis, historically referred to as hashitoxicosis, initially misdiagnosed as Graves' disease, highlighting a persistent diagnostic challenge in autoimmune thyroid disorders. The series includes four published cases reported between 2000 and 2025 and one unpublished case contributed by the authors. The cohort comprised three females and two males, with a mean age of 55.4 years (range: 21-69). Clinical presentations were heterogeneous, most commonly fatigue (80%), palpitations (60%), and weight changes (40%), while two patients exhibited no overt hyperthyroid symptoms.Biochemical evaluation demonstrated suppressed thyroid-stimulating hormone (TSH) levels in all cases (range: <0.000-0.13 µIU/mL), elevated anti-thyroid peroxidase (anti-TPO) antibodies in 80% (range: 41->1,000 IU/mL), and initially negative thyroid-stimulating hormone receptor antibodies (TRAb/TSI) in 60% of patients. Seroconversion to positive TRAb/TSI was observed in two cases during follow-up, suggesting autoimmune overlap rather than definitive disease transition. Imaging findings, including thyroid ultrasonography and radioiodine uptake (RAI) studies, consistently favored destructive thyroiditis over stimulatory hyperthyroidism, with heterogeneous echotexture observed in 75% of assessed cases and low or normal RAI uptake in all evaluated patients.Misdiagnosis occurred in 80% of cases, predominantly due to reliance on suppressed TSH levels without TRAb confirmation, resulting in inappropriate antithyroid drug administration in 80% and accelerated hypothyroidism in 60%. Immunopathological interpretation based on existing literature supports a predominantly Th1-mediated destructive process, in contrast to the Th2-driven antibody-mediated stimulation characteristic of Graves' disease, with rare Th1-to-Th2 immune shifts reported. Clinical outcomes ranged from spontaneous resolution to surgical intervention.This case series underscores the importance of mandatory TRAb testing, adherence to American and European Thyroid Association guidelines, and early specialist referral to reduce iatrogenic harm and improve diagnostic precision in autoimmune thyroid disease.

Indexed as

Graves DiseaseHashimoto DiseaseThyrotoxicosisAdultAgedAutoantibodiesDiagnostic ErrorsFemaleHumansMaleMiddle AgedThyrotropinYoung AdultAutoantibodiesThyrotropin

Identifiers

PMID42545320
PMCPMC13474369

What Socratic holds

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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 Socratic graph.