Note: TSH interpretation is affected by many factors. Results may be unreliable in patients taking biotin supplements (hold 2 days before testing), amiodarone, lithium, or dopamine agonists. TSH is naturally higher in older adults. For pregnant patients, use trimester-specific reference ranges. This tool supports clinical decision-making — always interpret in the full clinical context.
TSH Result
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Enter TSH value to interpret
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mIU/L
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Free T4: ng/dL
📊 TSH Reference Ranges
TSH Range (mIU/L)
Classification
Clinical Significance
< 0.4
Low / Suppressed TSH
Hyperthyroidism or non-thyroidal illness. Requires FT4/FT3 to distinguish.
0.4 – 4.0
Normal / Euthyroid
Reference range for most adults. May still miss early/mild thyroid dysfunction.
4.0 – 10.0
Subclinical Hypothyroidism
Elevated TSH with normal T4. May cause vague symptoms. ~1–5% per year progress to overt.
> 10.0
Overt Hypothyroidism
Markedly elevated TSH with low T4. Causes full symptom complex. Levothyroxine usually indicated.
Age-specific note: TSH rises naturally with age. A TSH of 4.5 in a 75-year-old may represent normal aging rather than hypothyroidism. The ATA recommends against treating subclinical hypothyroidism (TSH 4–10) in patients aged >80 years given lack of proven benefit and potential cardiovascular risk.
🩺 Clinical Context
Primary hypothyroidism is the most common form (~95% of cases), caused by Hashimoto's thyroiditis, post-thyroidectomy, radioactive iodine therapy, or medications (amiodarone, lithium, immune checkpoint inhibitors).
Key next steps by TSH level:
TSH 4.0–10.0, normal FT4: Confirm with repeat TSH in 3–6 months before initiating treatment. Check TPO antibodies (anti-TPO) — positive in ~80% of Hashimoto's. If symptomatic, trial levothyroxine with goal TSH 2.5–4.5. In patients >80, ATA advises against treatment.
TSH >10.0, low FT4: Overt hypothyroidism — initiate levothyroxine. Start low (25–50 mcg/day) in older patients or those with cardiovascular disease; full replacement ~1.6 mcg/kg/day. Recheck TSH 6–8 weeks after dose change.
TSH elevated, normal FT4, TPO negative: Consider physiological adaptation, recovery phase of non-thyroidal illness, or assay variability. Repeat test in 4–6 weeks before acting.
Primary hyperthyroidism most commonly caused by Graves' disease, toxic multinodular goiter (TMNG), or toxic adenoma. Low TSH requires full thyroid panel (FT4 + FT3) to confirm true hyperthyroidism vs suppressed TSH from medication or illness.
Key next steps by TSH level:
TSH 0.1–0.4, normal FT4: Subclinical hyperthyroidism — confirm with repeat test. Assess for osteoporosis risk, atrial fibrillation (annual ECG), and cardiovascular disease. Consider treatment if TSH persistently <0.1 or symptomatic.
TSH <0.1, elevated FT4: Overt hyperthyroidism — check FT3 for T3 toxicosis. Order TRAb (TSH receptor antibodies) for Graves' vs other causes. Urgent cardiology review if atrial fibrillation present. Treat with antithyroid drugs (methimazole first-line; PTU in first trimester or thyroid storm), radioactive iodine ablation, or surgery.
TSH low, normal FT4: Could be subclinical hyperthyroidism, recovery from non-thyroidal illness, medications (glucocorticoids, dopamine), or early pregnancy (hCG-mediated). Repeat in 4–6 weeks.
Graves' workup: TRAb (TSI), thyroid ultrasound (nodular vs diffuse), radioiodine uptake scan if etiology unclear. Watch for thyroid eye disease (orbitopathy) and pretibial myxedema.
Preconception and pregnancy impose strict TSH targets because thyroid hormone is critical for fetal neurodevelopment, especially in the first trimester before the fetal thyroid is functional.
Preconception: Target TSH <2.5 mIU/L (some guidelines say <1.5) before attempting conception. If on levothyroxine, titrate to goal before stopping contraception. Check FT4 — TSH alone may miss overt hypothyroidism.
First trimester: TSH reference range is narrower — <2.5 (some assays use <4.0, but <2.5 is the evidence-based target for pregnancy). hCG cross-reacts with TSH receptor, causing physiological TSH suppression in normal pregnancy.
Second and third trimester: TSH upper limit rises slightly (approximately +0.5 mIU/L per trimester) due to rising TBG and declining hCG. Use trimester-specific reference ranges from the laboratory where available.
Pregnancy with hypothyroidism: Levothyroxine dose typically increases 20–30% after conception (often self-prescribed by many women based on a well-known pregnancy protocol). Endocrine follow-up monthly.
Central (secondary) hypothyroidism results from pituitary or hypothalamic disease — TSH may be normal, low, or even mildly elevated despite low FT4, because the pituitary is damaged and cannot mount an appropriate TSH response. Never use TSH alone in patients with known or suspected pituitary disease.
Low or normal TSH + low FT4: Raises concern for central hypothyroidism. Check cortisol (清晨) — pituitary patients often have concurrent ACTH deficiency (secondary adrenal insufficiency) which is life-threatening if untreated. Do not start levothyroxine until cortisol is assessed (thyroid hormone accelerates cortisol clearance, precipitating adrenal crisis).
Elevated TSH + low FT4: Can rarely occur in central hypothyroidism when there is a TSH-secreting pituitary adenoma, or in the rare syndrome of thyroid hormone resistance (RTH). MRI of the pituitary is indicated.
Workup: MRI brain with pituitary protocol, full pituitary hormone panel (ACTH/cortisol, LH/FSH, estradiol/testosterone, IGF-1, prolactin), visual fields if mass effect suspected.
⚕️ Clinical Disclaimer: This calculator is for educational and clinical decision-support purposes only. TSH interpretation requires the full clinical context including free T4, thyroid antibodies, patient age, pregnancy status, medications, and clinical symptoms. TSH-based monitoring of levothyroxine therapy should target age-appropriate goals. This tool does not replace clinical judgment. Non-thyroidal illness, medications, and assay variability can all affect TSH results.
About TSH
Thyroid Stimulating Hormone (TSH) is the single most useful initial test for assessing thyroid function. Produced by the anterior pituitary, TSH regulates the thyroid gland's production of T4 (thyroxine, the main circulating hormone) and T3 (triiodothyronine, the active form). Under normal physiology, the hypothalamic-pituitary-thyroid (HPT) axis maintains a log-linear relationship: small changes in circulating T4 produce large changes in TSH, making TSH the most sensitive marker of thyroid dysfunction.
TSH Reference Ranges
Standard reference range: 0.4–4.0 mIU/L (third-generation immunoassay)
Age-adjusted: TSH rises ~0.1 mIU/L per decade of aging
Pregnancy (1st trimester): <2.5 mIU/L (or <4.0 with trimester-specific range)
Levothyroxine therapy target: 0.5–2.5 mIU/L (age-dependent)
The HPT axis has a logarithmic sensitivity: a 50% change in T4 produces a 10-fold change in TSH. This makes TSH the earliest detectable marker of thyroid dysfunction — it becomes abnormal before FT4 falls outside the normal range. In primary hypothyroidism, TSH rises while FT4 is still normal (subclinical hypothyroidism). In primary hyperthyroidism, TSH falls before FT4 rises (subclinical hyperthyroidism). This is why TSH is the preferred initial test for both screening and monitoring.
Causes of Hypothyroidism
The differential for hypothyroidism differs by TSH level and FT4 status:
Clinical context; repeat when acute illness resolves
Medications That Affect TSH
Several common medications interfere with TSH measurement and interpretation:
Biotin (vitamin B7): High-dose biotin (>5 mg/day, used for hair/nail/skin) causes falsely low TSH on streptavidin-based immunoassays. Hold biotin for 2 days before thyroid testing.
Amiodarone: High iodine load causes hypothyroidism (20–30% of patients) or hyperthyroidism (10–15%). Monitor TSH q6months. Both require separate treatment protocols.
Lithium: Inhibits thyroid hormone secretion and causes goiter. Causes clinical hypothyroidism in 20–30% of chronic users. Monitor TSH q6–12 months.
Glucocorticoids / Dopamine: Suppress TSH secretion — a low TSH in an ICU patient may not reflect true hyperthyroidism.
Estrogen / OCP: Increase TBG (thyroid-binding globulin), raising total T4 but leaving TSH and FT4 unaffected.
Checkpoint inhibitors (nivolumab, pembrolizumab): Can induce thyroiditis causing transient hyper- or hypothyroidism.
References
Garber JR, Cobin RH, Gharib H, et al. Clinical practice guidelines for hypothyroidism in adults. Thyroid. 2012;22(12):1200–1235. (ATA/AACE Guidelines)
Ross DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism. Thyroid. 2016;26(10):1343–1421.
Alexander EK, et al. 2017 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum. Thyroid. 2017;27(3):315–389.
Biondi B, Cooper DS. The clinical significance of subclinical thyroid dysfunction. Endocr Rev. 2008;29(1):76–131.