Clinical meaning
The diagnostic approach to thyrotoxicosis (excess circulating thyroid hormone regardless of source) begins with a suppressed TSH (<0.4 mIU/L). Confirm with free T4 (elevated = overt hyperthyroidism; normal with low TSH = subclinical hyperthyroidism or isolated T3 thyrotoxicosis → check free T3). Subclinical hyperthyroidism: TSH 0.1-0.4 (grade I) or <0.1 (grade II) with normal FT4/FT3 — grade II is more clinically significant (AF risk, osteoporosis, progression to overt). Differentiating the cause is critical because treatment differs fundamentally: Graves disease (antibody testing: TSI positive, anti-TPO often positive; RAIU: high, diffuse, homogeneous; thyroid ultrasound: diffusely enlarged, hyperechoic, increased vascularity — 'thyroid inferno'), toxic multinodular goiter (RAIU: heterogeneous with hot and cold nodules; occurs in elderly with longstanding goiter; TSI negative), toxic adenoma (RAIU: single hot nodule with suppressed surrounding tissue; TSI negative), subacute thyroiditis/de Quervain (painful, tender thyroid; preceded by viral URI; elevated ESR; RAIU: very low/absent — thyroid is damaged and releasing stored hormone, not making new hormone), painless thyroiditis/postpartum (painless, small goiter; RAIU: low; often self-limited), and exogenous thyroid hormone (factitious or iatrogenic — thyroglobulin is LOW because exogenous hormone suppresses endogenous production; RAIU: low). The thyroglobulin level helps distinguish: elevated in all thyroid-source causes, LOW in exogenous intake (factitious thyrotoxicosis).