THYROID FUNCTION TESTS

✓ Medically ReviewedINVESTIGATIONID: MDBT0303🚨 TRIAGE: ROUTINE

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Definition

CLINICAL DEFINITION

Thyroid function tests (TFTs) are a group of laboratory blood assays used to assess the functional status of the thyroid gland and the hypothalamic–pituitary–thyroid axis. They most commonly comprise serum thyroid-stimulating hormone (TSH), free thyroxine (FT4), and free triiodothyronine (FT3), and are used to diagnose, classify, and monitor hypothyroidism, hyperthyroidism, and related disorders. Results must be interpreted in the context of clinical findings, medications, non-thyroidal illness, and, where relevant, thyroid autoantibodies.

IN PLAIN ENGLISH

Thyroid function tests are blood tests that check how well your thyroid gland is working. They measure hormones that control your body's energy use and help doctors find out if your thyroid is underactive or overactive.

COMMON MISCONCEPTION / WHAT IT DOES NOT MEAN

Thyroid function tests are NOT a single measurement and do NOT assess thyroid structure or nodular disease. They must not be interpreted in isolation without accounting for non-thyroidal illness, medication effects, assay interference, and pregnancy-related reference range changes.

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Word Breakdown

thyr-

=shield-shaped (from Greek 'thyreos', referring to the thyroid cartilage)

Literal Meaning: Tests of the function of the shield-shaped gland in the neck

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Abbreviations

TFTs=Thyroid Function Tests — the collective term for the panel of thyroid blood tests.

TSH=Thyroid-Stimulating Hormone — the first-line test of thyroid function.

FT4=Free Thyroxine — the unbound, metabolically active fraction of T4.

FT3=Free Triiodothyronine — the unbound, metabolically active fraction of T3.

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Synonyms & Variants

Thyroid Function Test›Thyroid Panel›Thyroid Profile›

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Category-Specific Context

As an investigation, thyroid function tests are laboratory assays that quantify circulating thyroid hormones and TSH. They are used to classify thyroid status into euthyroid, primary hypothyroidism (overt or subclinical), primary hyperthyroidism (overt or subclinical), central hypothyroidism, and non-thyroidal illness patterns, based on the relationship between TSH and free hormone concentrations.

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Clinical Context & Usage

CLINICAL SETTINGS

Endocrinology Outpatient ClinicGeneral PracticeGeneral Medicine WardAntenatal ClinicPaediatric ClinicIntensive Care Unit

USAGE & DOCUMENTATION NOTES

TFTs are documented as, for example, 'TFTs: TSH 2.1 mU/L, FT4 14 pmol/L' or 'thyroid function tests pending'. In ward rounds the pattern is often summarised as 'biochemical hypothyroidism', 'suppressed TSH', or 'subclinical hyperthyroidism'. Referral letters typically include the trend of TSH and FT4, the current levothyroxine dose, and any interfering medication. When monitoring levothyroxine replacement, TSH is usually rechecked 6–8 weeks after a dose change.

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Primary Causes & Pathophysiology

PATHOPHYSIOLOGY

Thyroid function is regulated by the hypothalamic–pituitary–thyroid axis. The hypothalamus secretes thyrotropin-releasing hormone (TRH), which stimulates the anterior pituitary to release TSH. TSH stimulates the thyroid gland to synthesise and secrete thyroxine (T4) and triiodothyronine (T3). Most circulating T3 is derived from peripheral deiodination of T4. T4 and T3 exert negative feedback on TRH and TSH secretion. TFTs measure circulating hormones and TSH to infer the functional state of the axis. In primary thyroid failure, loss of negative feedback causes TSH to rise; in primary hyperthyroidism, excess hormone suppresses TSH. In central hypothyroidism, pituitary or hypothalamic dysfunction produces low or inappropriately normal TSH with low FT4.

PRIMARY CAUSES

Primary hypothyroidism

Thyroid gland failure reduces T4 and T3 production; loss of negative feedback causes an elevated TSH. FT4 is low in overt disease and normal in subclinical disease.

Subclinical hypothyroidism

Mild thyroid failure raises TSH while FT4 remains within the reference range; progression to overt hypothyroidism is possible.

Primary hyperthyroidism (thyrotoxicosis)

Excess thyroid hormone production suppresses TSH; FT4 and/or FT3 are elevated.

Subclinical hyperthyroidism

Autonomous thyroid hormone excess suppresses TSH while FT4 and FT3 remain within reference limits.

Central hypothyroidism

Pituitary or hypothalamic disease reduces TSH secretion; TSH is low or inappropriately normal, and FT4 is low.

Non-thyroidal illness

Acute or chronic illness alters deiodinase activity and binding proteins; T3 is often low, TSH may be low, normal, or transiently elevated, and FT4 may be low.

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Drug-Induced Causes

💊 Amiodarone ↗

Mechanism: Rich in iodine; can cause hypothyroidism or hyperthyroidism and inhibits T4-to-T3 conversion, raising FT4 and lowering FT3.

→ Check TSH before starting and every 6 months; interpret TSH as the most reliable marker; investigate abnormal results.

💊 Lithium ↗

Mechanism: Inhibits thyroid hormone release and can cause goitre and hypothyroidism.

→ Monitor TSH periodically; investigate abnormal results.

💊 Biotin (vitamin B7) at doses ≥1 mg/day ↗

Mechanism: Interferes with streptavidin–biotin immunoassays, causing falsely low TSH and falsely high FT4/FT3 in some assays.

→ Ask about biotin supplements; stop for at least 3 days before repeat testing if safe to do so.

💊 Glucocorticoids (e.g., prednisone ≥20 mg/day) ↗

Mechanism: Suppress TSH secretion and reduce T4-to-T3 conversion.

→ Interpret TFTs with caution; repeat after glucocorticoid dose reduction if clinically appropriate.

💊 Dopamine and dopamine agonists ↗

Mechanism: Suppress TSH secretion.

→ Interpret TSH in the context of dopamine therapy; repeat testing when clinically feasible.

💊 Heparin ↗

Mechanism: Can alter free hormone assays via in-vitro effects on binding proteins.

→ Interpret with caution; repeat if results are discordant with the clinical picture.

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Epidemiology

Prevalence:Thyroid dysfunction is common worldwide. Overt hypothyroidism affects approximately 3–20 per 1000 females and 1–7 per 1000 males; hyperthyroidism affects approximately 2–19 per 1000 females and 1–2 per 1000 males. Subclinical thyroid dysfunction is more prevalent than overt disease. Prevalence varies with iodine intake, age, and screening practices.

Age Group:All ages. Hypothyroidism prevalence increases with age. Congenital hypothyroidism is detected by newborn screening. Graves' disease and hyperthyroidism are most common in adults aged 20–50 years, particularly reproductive-age women.

Sex Predilection:Female

Geographic Distribution:Iodine deficiency remains a major determinant of thyroid dysfunction globally. Autoimmune thyroid disease is more common in iodine-sufficient regions. Prevalence and the relative frequency of hypothyroidism versus hyperthyroidism vary with iodine intake and population screening practices.

Red Flags & Triage ★

TRIAGE LEVEL

🚨 ROUTINE

DO NOT MISS — LIFE-THREATENING PRESENTATIONS

Suppressed TSH with normal FT4/FT3 — consider assay interference (e.g., biotin) or subclinical hyperthyroidism; repeat testing and review medications before labelling as thyroid disease.
Low FT4 with low or inappropriately normal TSH — consider central hypothyroidism and evaluate the pituitary axis.
Altered mental status, hypothermia, bradycardia, or hypotension in a patient with severe hypothyroidism — consider myxedema coma and initiate emergency assessment and treatment.

URGENT EVALUATION TRIGGERS

Suppressed TSH with markedly elevated FT4 and/or FT3 (suspected thyrotoxicosis)
TSH >10 mU/L with low FT4 (severe hypothyroidism)
Altered mental status, hypothermia, or hypotension in a patient with known hypothyroidism (possible myxedema coma)
Thyroid function abnormalities in pregnancy

Contraindications & Precautions

CONTRAINDICATIONS

No absolute contraindication to venepuncture for TFTs.
Relative: avoid routine TFTs during acute severe illness unless thyroid dysfunction is strongly suspected
because non-thyroidal illness can distort results.

SPECIAL PRECAUTIONS

Ask about biotin supplements and stop for at least 3 days before repeat testing if safe.
Interpret results in the context of acute illness
pregnancy
and medications.
Repeat abnormal results before committing to lifelong treatment when the clinical picture is uncertain.
Use trimester-specific reference ranges in pregnancy.
Consider assay interference when TFT results are discordant with the clinical picture.

Complications

DOWNSTREAM CLINICAL COMPLICATIONS

Missed severe hypothyroidism — risk of myxedema coma
an endocrine emergency with high mortality
Unrecognised thyrotoxicosis — risk of atrial fibrillation
osteoporosis
and thyroid storm
Iatrogenic thyrotoxicosis from over-replacement with levothyroxine — risk of atrial fibrillation and bone loss

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Reference Ranges

NORMAL RANGETypical adult reference ranges: TSH 0.4–4.0 mU/L; FT4 9.0–25.0 pmol/L; FT3 3.5–7.8 pmol/L. Total T4 approximately 60–160 nmol/L; total T3 approximately 1.2–2.6 nmol/L. Ranges vary by laboratory, assay method, and population (including pregnancy and age).

UNIT OF MEASUREMENTTSH: mU/L (or mIU/L); FT4: pmol/L; FT3: pmol/L; total T4: nmol/L; total T3: nmol/L. Conventional units: FT4 ng/dL, FT3 pg/mL, total T4 mcg/dL, total T3 ng/dL.

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Confused With (LASA & DDx) ★

LEXICAL (LASA) — SIMILAR NAMES

Free T4 (FT4)

May be confused with total T4; FT4 is the unbound, active fraction, whereas total T4 includes protein-bound hormone and is affected by binding-protein changes.

Total T3

May be confused with free T3; total T3 includes bound hormone and is influenced by binding-protein abnormalities, whereas free T3 reflects the active fraction.

CLINICAL DIFFERENTIAL DIAGNOSES (DDx)

Non-thyroidal illness

Key Distinguishing Feature: Low T3 with variable TSH and FT4; abnormal results are transient and improve with recovery from the acute illness.

Assay interference (e.g., biotin, heterophile antibodies)

Key Distinguishing Feature: Discordant TFTs that do not fit the clinical picture; results normalise after stopping the interfering substance or using an alternative assay.

Central hypothyroidism

Key Distinguishing Feature: Low or inappropriately normal TSH with low FT4; other pituitary hormone deficits may be present.

Resistance to thyroid hormone

Key Distinguishing Feature: Elevated FT4 and/or FT3 with non-suppressed TSH; often familial and may have variable clinical features.

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Clinical Pearls

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Biotin at doses of 1 mg/day or higher can cause falsely low TSH and falsely high FT4/FT3 on many immunoassays. Ask about supplements and stop biotin for at least 3 days before repeat testing.

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Amiodarone can cause both hypothyroidism and hyperthyroidism and inhibits T4-to-T3 conversion, so FT4 may be high and FT3 low; TSH remains the most reliable marker of thyroid status.

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In non-thyroidal illness, TSH may be low, normal, or transiently elevated, and T3 is often low. Do not diagnose thyroid disease during acute illness unless clinical suspicion is strong; repeat testing after recovery.

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TSH alone is sufficient for screening most adults when pituitary disease is not suspected; add FT4 when TSH is abnormal, in pregnancy, in children, or when central hypothyroidism is a concern.

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Pregnancy requires trimester-specific reference ranges; the upper limit of TSH is lower in the first trimester than in non-pregnant adults.

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Example Usage & SOAP

CLINICAL SENTENCE

"Bloods showed TSH 8.2 mU/L (0.4–4.0) and FT4 11.5 pmol/L (9.0–25.0), consistent with primary hypothyroidism; levothyroxine 50 mcg once daily was started with repeat TFTs in 6–8 weeks."

IN A SOAP NOTE

S: 52-year-old woman reports fatigue, cold intolerance, and weight gain. O: TSH 9.1 mU/L, FT4 10.2 pmol/L; TPO antibodies positive. A: Primary hypothyroidism, likely Hashimoto's thyroiditis. P: Start levothyroxine at approximately 1.6 mcg/kg/day; repeat TSH in 6–8 weeks; patient education.

DIFFERENTIAL DIAGNOSIS CONTEXT

Differential for abnormal TFTs: (1) Primary hypothyroidism — high TSH, low FT4; (2) Subclinical hypothyroidism — high TSH, normal FT4; (3) Central hypothyroidism — low or inappropriately normal TSH, low FT4; (4) Non-thyroidal illness — low T3 with variable TSH; (5) Assay interference — discordant results not fitting the clinical picture.

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Prognosis

SHORT-TERM OUTCOME

Short-term prognosis depends on the underlying disorder. Treated primary hypothyroidism usually improves within weeks. Untreated myxedema coma has high short-term mortality (approximately 30–40% even with treatment).

LONG-TERM PROGNOSIS

Long-term prognosis is generally good with appropriate treatment and monitoring. Untreated hyperthyroidism is associated with increased risk of atrial fibrillation, osteoporosis, and mortality. Severe hypothyroidism and myxedema coma carry substantial long-term risk if unrecognised.

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References & Coding

LITERATURE CITATIONS & GUIDELINES

[1]British Thyroid Foundation. Thyroid function testing. BTF. 2021.

[2]NICE. Thyroid disease: assessment and management. NICE guideline NG145. 2019, updated 2023.

[3]American Thyroid Association. Medications that affect thyroid function test results: what you need to know. ATA. 2026.

[4]Buschur E. An Update on Thyroid Disease. Ohio State University Wexner Medical Center. 2015.

[5]GPnotebook. TFTs. GPnotebook. 2025.

MEDICAL DISCLAIMER — This content is intended for educational purposes and qualified healthcare professionals only. Always refer to current clinical diagnostic criteria, institutional protocols, and official guidelines. Medobo is not responsible for clinical decisions made based on this content.