Acute Ischemic Stroke Masking Underlying Hyperthyroidism: A Diagnostic Pitfall of Non-Thyroidal Illness Syndrome
https://doi.org/10.15605/jafes.041.S1
- Author:
Ashwin Kaur
1
;
Ooi Chuan Ng
2
Author Information
1. Department of Internal Medicine, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia
2. Department of Internal Medicine, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia;Department of Internal Medicine, Hospital Sultan Abdul Aziz Shah, Universiti Putra Malaysia
- Publication Type:Journal Article
- MeSH:
Euthyroid Sick Syndromes;
Ischemic Stroke;
Hyperthyroidism
- From:
Journal of the ASEAN Federation of Endocrine Societies
2026;41(S1):112-
- CountryPhilippines
- Language:English
-
Abstract:
Introduction:Non-thyroidal illness syndrome commonly occurs during
acute systemic illnesses and is characterized by suppressed
or inappropriately normal thyroid-stimulating hormone
with low or low-normal thyroid hormone levels. This
biochemical pattern may obscure or delay the diagnosis
of underlying hyperthyroidism, especially in mild or
borderline cases. Acute stroke is a recognized trigger of
non-thyroidal illness syndrome, yet its masking effect on
hyperthyroidism is under-recognized in clinical practice.
Case:A 58-year-old Malay male with cardiovascular risk factors
presented with an acute ischemic stroke involving the left
occipital lobe and right internal capsule. He developed
new-onset atrial fibrillation (CHA₂DS₂-VASc 3) and
mild left ventricular systolic dysfunction. Initial thyroid
function tests during the acute stroke phase showed mildly
suppressed thyroid-stimulating hormone (TSH) (0.30
mIU/L) with high-normal free T4 (21.2 pmol/L), interpreted
in the context of acute illness. The patient was clinically
stable without overt thyrotoxic features.
One month post-stroke, repeat testing revealed further TSH
suppression (0.09 mIU/L) and rising free T4 (27.6 pmol/L).
Detailed history uncovered prior Graves’ disease in 2019
with treatment default. Examination revealed a small
diffuse goiter without ophthalmopathy. The biochemical
evolution following recovery from acute illness confirmed
recurrent hyperthyroidism previously masked by nonthyroidal illness syndrome.
Conclusion:Acute stroke can induce cytokine-mediated suppression
of the hypothalamic-pituitary-thyroid axis and altered
peripheral deiodination, leading to misleading thyroid
function tests. In this case, non-thyroidal illness syndrome
blunted the biochemical severity of hyperthyroidism,
delaying recognition despite high-risk features such as atrial
fibrillation and prior Graves’ disease. Reliance on a single
thyroid function test during acute illness may therefore
result in underdiagnosis.
- Full text:2026080508453577551EP_A166.pdf
