Overview
Clinical Meaning
Thyroid hormone therapy centers on replacing or supplementing endogenous T4 (thyroxine) and T3 (triiodothyronine) to restore euthyroid status.
PNP-PC
PNP-PC
Thyroid hormone therapy centers on replacing or supplementing endogenous T4 (thyroxine) and T3 (triiodothyronine) to restore euthyroid status. Levothyroxine (synthetic T4) is the mainstay of therapy because T4 serves as a prohormone that is peripherally converted to active T3 by type 1 and type 2 deiodinase enzymes in target tissues (liver, kidney, skeletal muscle, brain), providing a stable and physiologic T3 supply. The hypothalamic-pituitary-thyroid axis regulates this process: TRH from the hypothalamus stimulates TSH release from the anterior pituitary, which stimulates the thyroid. Exogenous T4 suppresses TSH through negative feedback, making TSH the primary monitoring parameter. Levothyroxine has a long half-life of 6-7 days, allowing once-daily dosing and stable serum levels. Bioavailability is approximately 70-80% when taken fasting, but decreases significantly with concurrent food, calcium, iron, aluminum-containing antacids, proton pump inhibitors, and soy products. Dose requirements are influenced by body weight (1.6 mcg/kg/day for full replacement), age, pregnancy (30-50% dose increase needed), and concurrent medications affecting thyroid hormone metabolism (phenytoin, carbamazepine, rifampin increase hepatic clearance; estrogen increases TBG requiring dose adjustment). In hypothyroid patients with coexisting adrenal insufficiency, glucocorticoid replacement...
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