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) |
|---|---|
| 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
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