Abstract
The type 2 deiodinase (D2) has an important role in hypothyroidism, where its ability to activate thyroid hormone provides justification for levothyroxine "monotherapy." A prevalent polymorphism in D2, Thr92AlaD2, has been associated with improved well-being on "combination therapy" with T4+T3; the underlying mechanism is unclear as T4-to-T3 conversion appears normal. Novel studies indicate this might be a risk factor for neurodegenerative disease. If the relationship between Thr92AlaD2-expression and treatment preference is confirmed, personalized medicine may play a role in hypothyroidism.
Original language | English (US) |
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Pages (from-to) | 92-94 |
Number of pages | 3 |
Journal | US Endocrinology |
Volume | 11 |
Issue number | 2 |
DOIs | |
State | Published - 2015 |
Externally published | Yes |
Keywords
- Deiodinase
- Hypothyroidism
- Levothyroxine
- Polymorphism
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism