Thyroid-Stimulating Hormone (TSH)


Send Email

Recipient(s) will receive an email with a link to 'Thyroid-Stimulating Hormone (TSH)' and will have access to the topic for 7 days.

Subject: Thyroid-Stimulating Hormone (TSH)

(Optional message may have a maximum of 1000 characters.)



  • This glycoprotein hormone of 28–30 kDa is composed of alpha and beta subunits. It is secreted by the anterior pituitary. TSH controls the biosynthesis and release of thyroid hormones T4 and T3.

  • Normal range: 0.5–6.3 μIU/mL, depending on age and sex (Table 16.78).

TABLE 16–78
Normal Ranges of TSH According to Age and Sex


  • Sensitive measure of thyroid function. First line of test for suspected thyroid disorders

  • Assessing true metabolic status

  • Screening for euthyroidism

    • Normal level in stable ambulatory patient not on interfering drugs excludes thyroid hormone excess or deficiency.

    • TSH is recommended as the initial test rather than T4.

    • Screening is not recommended for asymptomatic persons without suspicion of thyroid disease or for hospital patients with acute medical or psychiatric illness.

  • Initial screening and diagnosis for hyperthyroidism (decreased to undetectable levels except in rare TSH-secreting pituitary adenoma) and hypothyroidism

  • Especially useful in early or subclinical hypothyroidism before the patient develops clinical findings, goiter, or abnormalities of other thyroid tests

    • Differentiation of primary (increased levels) from central (pituitary or hypothalamic) hypothyroidism (decreased levels)

    • Monitoring of adequate thyroid hormone replacement therapy in primary hypothyroidism, although T4 may be mildly increased (up to 6–8 weeks before TSH becomes normal). Serum TSH suppressed to the normal level is the best monitor of dosage of thyroid hormone for treatment of hypothyroidism

    • Monitoring adequate thyroid hormone therapy in the suppression of thyroid carcinoma (should suppress to <0.1 μIU/mL) or goiter or nodules (should suppress to subnormal levels) with third- or fourth-generation assays

  • Replacement of TRH stimulation test in hyperthyroidism, because most patients with euthyroid TSH level have a normal TSH response and patients with undetectable TSH level almost never respond to TRH stimulation


Increased In

  • Primary untreated hypothyroidism. The increase is proportionate to the degree of hypofunction, varying from 3 times normal in mild cases to 100 times normal in severe myxedema. A single determination is usually sufficient to establish the diagnosis.

  • Patients with hypothyroidism receiving insufficient thyroid hormone replacement therapy.

  • Patients with Hashimoto thyroiditis, including those with clinical hypothyroidism and about one third of those patients who are clinically euthyroid.

  • Use of various drugs: amphetamines (abuse), iodine-containing agents (e.g., iopanoic acid, ipodate, amiodarone), and dopamine antagonists (e.g., metoclopramide, domperidone, chlorpromazine, haloperidol).

  • Other conditions (test is not clinically useful).

    • Iodide deficiency goiter or iodide-induced goiter or lithium treatment

    • External neck irradiation

    • Postsubtotal thyroidectomy

    • Neonatal period; increased in first 2–3 days of life due to postnatal TSH surge

    • Thyrotoxicosis due to pituitary thyrotroph adenoma or pituitary resistance to thyroid hormone

    • Euthyroid sick syndrome, recovery phase

    • TSH antibodies

Decreased In

  • Toxic multinodular goiter

  • Autonomously functioning thyroid adenoma

  • Ophthalmopathy of euthyroid Graves disease; treated Graves disease

  • Thyroiditis

  • Extrathyroidal thyroid hormone source

  • Factitious

  • Overreplacement of thyroid hormone in treatment of hypothyroidism

  • Secondary pituitary or hypothalamic hypothyroidism (e.g., tumor, infiltrates)

  • Euthyroid sick patients (some patients)

  • Acute psychiatric illness

  • Severe dehydration

  • Drug effect, especially large doses (use FT4 for evaluation)

  • Assay interference (e.g., antibodies to mouse IgG, autoimmune disease)

  • First trimester of pregnancy

  • Isolated deficiency (very rare)


  • TSH may be normal in

    • Central hypothyroidism: In the absence of hypothalamic or pituitary disease, normal TSH excludes primary hypothyroidism.

    • Recent rapid correction of hyperthyroidism or hypothyroidism

    • Pregnancy

    • Phenytoin therapy

  • TSH may not be useful to evaluate thyroid status of hospitalized ill patients.

    • Approximately 3 months of treatment of hypo- or hyperthyroidism; FT4 is test of choice.

    • Lag time of 6–8 weeks is required for normalization of TSH after initiation of thyroid hormone replacement therapy.

  • Dopamine or high doses of glucocorticoids may cause false normal values in primary hypothyroidism and may suppress TSH in nonthyroid illness.

  • Rheumatoid factor, human antimouse antibodies, heterophile antibodies, and thyroid hormone autoantibodies may produce spurious results, especially in patients with autoimmune disorders (≤10%).

  • Amiodarone may interfere with TSH.

  • TSH is not affected by variation in thyroid-binding proteins.

  • TSH has a diurnal rhythm, with peaks at 2:00–4:00 am and troughs at 5:00–6:00 pm with ultradian variations. TSH levels vary diurnally by up to 50% and up to 40% variations on specimens performed serially during the same time of the day.

  • Serum levels typically falls below 0.1 mIU/L during first trimester of pregnancy due to thyroid stimulatory effects of HCG and returns to normal in the second trimester.