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Published on: July 21, 2023
Hyperthyroidism induced by Graves' disease reversibly affects skin microvascular reactivity
Nataša Bedernjak Bajuk1, Katja Zaletel1, Simona Gaberšček1
1Department of Nuclear Medicine, University Medical Centre Ljubljana, Ljubljana, Slovenia.
Graves' disease (GD) hyperthyroidism alters skin microcirculation, increasing blood flow and vasodilator capacity. These changes are reversible with treatment, suggesting a potential role for TSH receptor stimulating antibodies (TSAb).
Area of Science:
- Endocrinology
- Vascular Biology
- Dermatology
Background:
- The effect of Graves' disease (GD) induced hyperthyroidism on skin microcirculation remains unclear.
- Assessing vascular reactivity in hyperthyroid patients before and after treatment is crucial.
Purpose of the Study:
- To investigate the impact of hyperthyroidism from Graves' disease on skin microcirculation.
- To evaluate vascular reactivity changes during hyperthyroid treatment.
Main Methods:
- Laser Doppler flux (LDF) measured in 31 untreated hyperthyroid GD patients, 30 healthy controls, and 30 treated GD patients.
- Postocclusive reactive hyperemia (PRH) assessed via brachial artery occlusion.
- TSH receptor stimulating antibody (TSAb) levels monitored.
Main Results:
- Untreated GD patients showed higher baseline LDF in finger pulp and forearm compared to controls and treated patients.
- Finger pulp PRH time to maximal LDF was shorter in untreated GD patients.
- Forearm PRH duration was longer in untreated GD patients compared to controls.
- Triiodothyronine and TSAb correlated with PRH indices in treated GD patients.
Conclusions:
- Hyperthyroidism in Graves' disease reversibly impacts skin microcirculation.
- Increased vasodilator capacity is presumed to cause these microcirculatory changes.
- TSH receptor stimulating antibodies may play a role in these vascular alterations.
Related Concept Videos
Graves' Disease I: Introduction
Graves Disease II: Pathophysiology
Hyperthyroidism II: Pathophysiology
Hyperthyroidism I: Introduction
Hypothyroidism II: Pathophysiology
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