Dry eye disease in thyroid eye disease: A narrative review of pathogenic mechanisms and therapeutic implications
4 affiliations
- 1Department of Oculoplastic and Orbital Surgery, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran
- 2Department of Ophthalmology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
- 3Department of Ophthalmology, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran
- 4Student Research Committee, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Abstract
Dry eye disease (DED) is a common and persistent manifestation of thyroid eye disease (TED), often remaining symptomatic despite apparent control of orbital inflammation or systemic thyroid dysfunction. This narrative review synthesizes current evidence within an integrated mechanistic framework relating the overlapping contributors to TED-associated DED to disease phenotype, therapeutic limitations, and opportunities for more targeted management. A literature review was conducted using PubMed and Scopus through March 2026, using broad MeSH and free-text terms related to TED, DED, ocular surface disease, and treatment, with manual screening of relevant references. Current evidence suggests that DED in TED reflects coordinated disruption of tear film homeostasis involving glandular, evaporative, inflammatory, epithelial/mucin, and neuro-sensory pathways rather than a single mechanism such as exposure or reduced tear production. The relative contribution of these pathways may vary according to disease activity and individual ocular surface phenotype. Recognition of the dominant contributors in individual patients may support a shift from uniform symptom-directed lubrication toward phenotype-directed ocular surface management. Emerging neuro-regenerative and regenerative therapies remain investigational because TED-specific evidence is limited.
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BibTeX
@article{rafizadeh2026disease,
title = {{Dry eye disease in thyroid eye disease: A narrative review of pathogenic mechanisms and therapeutic implications}},
author = {Seyed Mohsen Rafizadeh and Enes Eroglu and Ali A. Haydar and Haniyeh Zeidabadinejad and Mostafa Heidari and Mohammad Taher Rajabi and Amirhossein Aghajani and Ali Davarpanah and Kamran Rezaei and Mohammad Soleimani},
journal = {Therapeutic Advances in Ophthalmology},
year = {2026},
month = sep,
doi = {10.1177/25158414261491563},
url = {https://doi.org/10.1177/25158414261491563},
note = {CC BY-NC 4.0},
}
RIS
TY - JOUR
TI - Dry eye disease in thyroid eye disease: A narrative review of pathogenic mechanisms and therapeutic implications
AU - Seyed Mohsen Rafizadeh
AU - Enes Eroglu
AU - Ali A. Haydar
AU - Haniyeh Zeidabadinejad
AU - Mostafa Heidari
AU - Mohammad Taher Rajabi
AU - Amirhossein Aghajani
AU - Ali Davarpanah
AU - Kamran Rezaei
AU - Mohammad Soleimani
PY - 2026
DA - 2026/09/19
JO - Therapeutic Advances in Ophthalmology
DO - 10.1177/25158414261491563
UR - https://doi.org/10.1177/25158414261491563
AB - Dry eye disease (DED) is a common and persistent manifestation of thyroid eye disease (TED), often remaining symptomatic despite apparent control of orbital inflammation or systemic thyroid dysfunction. This narrative review synthesizes current evidence within an integrated mechanistic framework relating the overlapping contributors to TED-associated DED to disease phenotype, therapeutic limitations, and opportunities for more targeted management. A literature review was conducted using PubMed and Scopus through March 2026, using broad MeSH and free-text terms related to TED, DED, ocular surface disease, and treatment, with manual screening of relevant references. Current evidence suggests that DED in TED reflects coordinated disruption of tear film homeostasis involving glandular, evaporative, inflammatory, epithelial/mucin, and neuro-sensory pathways rather than a single mechanism such as exposure or reduced tear production. The relative contribution of these pathways may vary according to disease activity and individual ocular surface phenotype. Recognition of the dominant contributors in individual patients may support a shift from uniform symptom-directed lubrication toward phenotype-directed ocular surface management. Emerging neuro-regenerative and regenerative therapies remain investigational because TED-specific evidence is limited.
SN - 2515-8414
ER -