Medical biology - Endocrinology and thyroid pathology
Thyroid Profile | Clinique Omicron Quebec
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The thyroid work-up is a series of blood tests designed to assess the functioning of the thyroid gland, an endocrine organ located at the base of the neck, which regulates the metabolism of the entire body through the secretion of thyroid hormones. This assessment is based primarily on the measurement of thyroid stimulating hormone (TSH), the pituitary hormone that constitutes the central regulatory signal for thyroid production, supplemented, depending on the context, by the measurement of free thyroxine (free T4) and free triiodothyronine (free T3). Additional markers, notably anti-thyroid antibodies and thyroglobulin, are added according to specific clinical indications. Thyroid tests are among the most frequently prescribed biological examinations in primary care medicine in Quebec. It is indicated in cases of unexplained fatigue, unjustified weight gain or loss, heart rhythm disorders, menstrual cycle abnormalities, resistant depression, or as part of the follow-up of known thyroid disease and its treatment. Rigorous interpretation of the thyroid work-up requires simultaneous consideration of all results, the clinical context and potential interfering factors.
Thyrotoxic crisis and myxedematous coma: endocrine emergencies
Thyrotoxic crisis (acute decompensation of hyperthyroidism) and myxedematous coma (severe decompensation of profound hypothyroidism) are two potentially fatal endocrine emergencies. The former presents with high fever, extreme tachycardia, agitation and confusion. The second presents with hypothermia, bradycardia, altered consciousness and hypoventilation. Both conditions require immediate intensive care hospitalization.
Call 911 immediately.
Thyroid workup components
Thyroid workup is modular: TSH is the universal first-line screening test, supplemented by other assays depending on initial results and clinical context.
| Marker | Abbreviation | Usual values | Role and origin |
|---|---|---|---|
| Thyroid stimulating hormone | TSH | 0.4 to 4.0 mIU/L | Thyroid-regulating pituitary hormone; first-line screening test; inverse of thyroid function: rises in hypothyroidism, falls in hyperthyroidism |
| Free thyroxine | Free T4 (FT4) | 10 to 25 pmol/L | Main hormone secreted by the thyroid; biologically active free fraction; more reliable measurement than total T4, independent of carrier proteins |
| Free triiodothyronine | Free T3 (FT3) | 3.5 to 6.5 pmol/L | Most biologically active thyroid hormone; produced partly by the thyroid gland and largely by peripheral conversion of T4; useful in hyperthyroidism with predominant T3 |
| Anti-thyroperoxidase antibodies | Anti-TPO | Less than 34 IU/mL (variable according to laboratory) | Marker of thyroid autoimmunity; positive in Hashimoto's thyroiditis and Graves' disease; present in 10 to 15 % of the general population without thyroid dysfunction |
| Anti-thyroglobulin antibodies | Anti-TG | Less than 115 IU/mL (variable according to laboratory) | Complementary marker of thyroid autoimmunity; useful when anti-TPO is negative and clinical suspicion persists; interferes with thyroglobulin assay |
| Anti-TSH receptor antibodies | TRAK (TRAb) | Less than 1.75 IU/L (variable according to laboratory) | Specific marker for Graves' disease; autonomously stimulates TSH receptor, causing autoimmune hyperthyroidism |
| Thyroglobulin | Tg | 1.6 to 59.9 ng/mL (varies with thyroid status) | Thyroid hormone storage protein; used as a tumor marker in the follow-up of differentiated thyroid cancer after total thyroidectomy and radioactive iodine treatment |
| Calcitonin | CT | Less than 5 to 10 pg/mL depending on sex | Secreted by parafollicular C cells; tumor marker for medullary thyroid carcinoma; measured in cases of suspected thyroid nodule or family history of NEM2 |
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TSH is the first-line thyroid screening test recommended by all endocrine societies. Due to the log-linear relationship between TSH and free thyroid hormones, small variations in T4 or T3 levels result in large variations in TSH, making it a much more sensitive indicator of incipient thyroid dysfunction than the peripheral hormones themselves.
Indications for thyroid assessment
| Clinical context | Markers recommended for first-line use |
|---|---|
| Screening for thyroid dysfunction (suggestive symptoms) | TSH alone as first-line treatment; free T4 if TSH abnormal |
| Chronic unexplained fatigue, resistant depression | TSH, free T4, anti-TPO |
| Unexplained weight gain, chilliness, constipation, bradycardia | TSH, free T4 (suspected hypothyroidism) |
| Weight loss, palpitations, trembling, thermophobia, nervousness | TSH, free T4, free T3, TRAK (suspected hyperthyroidism) |
| Thyroid goiter or nodule | TSH, free T4, anti-TPO, calcitonin according to context |
| Menstrual disorders, infertility, recurrent miscarriage | TSH, free T4, anti-TPO |
| Pregnancy (screening or follow-up) | TSH, free T4, anti-TPO; trimester-specific reference values |
| Monitoring of treated hypothyroidism (levothyroxine) | TSH alone in stable regime; free T4 if recent adjustment |
| Monitoring of treated hyperthyroidism (antithyroid drugs, radioactive iodine) | TSH, free T4, free T3 |
| Post-thyroidectomy follow-up for differentiated cancer | TSH, thyroglobulin, anti-TG (to detect interference with Tg) |
| Initiation of potentially thyrotoxic treatment (amiodarone, lithium, interferon, immunotherapy) | TSH, free T4 as baseline, then regular monitoring |
| De novo atrial fibrillation or unexplained tachycardia | TSH, free T4, free T3 |
Interpretation of thyroid biology profiles
Interpretation of the thyroid work-up is based on the combination of markers measured and their correlation with the clinical picture. TSH is at the heart of any interpretation.
| TSH / T4L profile | Interpretation | Common causes |
|---|---|---|
| TSH normal / T4L normal | Euthyroid thyroid function | No biological thyroid dysfunction |
| TSH high / T4L normal | Subclinical hypothyroidism | Early Hashimoto's thyroiditis, mild iodine deficiency, recovery phase after thyroiditis, medications (lithium, amiodarone) |
| TSH high / T4L low | Frank hypothyroidism (clinical) | Advanced Hashimoto's thyroiditis, post-thyroidectomy hypothyroidism, post-radioiodine, severe iodine deficiency, thyrotoxic drugs |
| TSH low / T4L normal | Subclinical hyperthyroidism | Early Graves' disease, toxic adenoma, early toxic multinodular goiter, levothyroxine excess, low physiological TSH in early pregnancy |
| TSH low / T4L high | Frank hyperthyroidism (clinical) | Graves' disease, toxic adenoma, toxic multinodular goiter, subacute thyroiditis in hyperthyroid phase, iodine overload (amiodarone, contrast media) |
| TSH low / T4L low | Central hypothyroidism (pituitary or hypothalamic) | Pituitary insufficiency, Sheehan's syndrome, pituitary tumor, craniopharyngioma, autoimmune hypophysitis |
| TSH normal or elevated / T3L elevated | Predominantly T3 hyperthyroidism | Early-stage Graves' disease, T3-secreting toxic adenoma, thyroid hormone resistance |
| TSH normal / T4L low (T3 low syndrome) | Non-thyroidal illness syndrome | Severe systemic diseases, malnutrition, major surgery, sepsis: reduction of peripheral T4 to T3 conversion; does not require thyroid treatment |
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During pregnancy, normal TSH values differ from those of the general population and vary according to the trimester. In the first trimester, TSH is physiologically lower due to the thyroid-stimulating effect of beta-HCG, dropping as low as 0.1 mIU/L without pathological significance. When interpreting thyroid tests in pregnant women, it is essential to use the reference ranges specific to pregnancy.
Factors that may affect results
Numerous factors external to thyroid pathology can influence workup values, leading to falsely abnormal or falsely normal results. Their identification is essential before any therapeutic decision is taken.
| Interfering factor | Balance sheet impact |
|---|---|
| Amiodarone | Raises free T4 and lowers free T3 through desiodase inhibition; can cause hypothyroidism or true hyperthyroidism depending on context |
| Lithium | Inhibits thyroid secretion and can induce frank hypothyroidism, particularly in the presence of pre-existing anti-TPO agents |
| High-dose glucocorticoids | Transiently lowers TSH and inhibits peripheral conversion of T4 to T3; may mimic central hypothyroidism |
| High-dose Biotin (vitamin B7) | Interferes with immunoassays using biotin-streptavidin technology, which can simulate hyperthyroidism (falsely low TSH, falsely high T4 and T3); stop supplementation 48 to 72 hours before sampling. |
| Pregnancy | Physiological modification of reference intervals depending on the trimester; increase in carrier proteins (TBG) under estrogen, physiological lowering of TSH in the first trimester. |
| Oral contraceptives and estrogens | Increases TBG, raises total T4 without altering free T4; justifies measuring free T4 rather than total T4 |
| Severe systemic diseases (sick euthyroid syndrome) | Lowered free T3, sometimes free T4, with normal or slightly lowered TSH; does not reflect primary thyroid pathology |
| Heterophilic antibodies | Rare immunological interferences that can generate discordant results (high TSH with high T4, or vice versa); to be suspected in the event of any clinico-biological discordance. |
| Levothyroxine (Synthroid) | Ideally, the sample should be taken in the morning before taking the tablet, for a representative measurement of the therapeutic balance; a recent dose may transiently elevate free T4. |
Recommended frequency of check-ups depending on the context
- First-line screening in symptomatic adults: TSH alone; check at 6 weeks if slightly abnormal before treating.
- Initiation of levothyroxine therapy: TSH checked 6-8 weeks after each dosage adjustment, then annually during stable therapy
- Treatment with synthetic antithyroid drugs (Tapazole, PTU): TSH and free T4 every 4 to 6 weeks at the start of treatment, then every 3 months in the stabilization phase
- Pregnancy with known hypothyroidism: TSH and free T4 every trimester, or every 4 weeks in the first trimester in the event of recent dosage adjustment
- Post-thyroidectomy follow-up for differentiated cancer: TSH, thyroglobulin and anti-TG according to oncology protocol (frequency varies from 3 to 12 months depending on risk level)
- Amiodarone treatment: thyroid check-up before initiation, then every 6 months for the duration of treatment and up to 12 months after discontinuation.
- Systematic screening of at-risk individuals without symptoms (family history, known positive anti-TPO, Down syndrome, Turner syndrome): Annual TSH
Conditions requiring a full thyroid workup with antibodies
- Confirmed hypothyroidism: anti-TPO assay to identify autoimmune origin (Hashimoto's thyroiditis) and stratify risk of progression to frank hypothyroidism
- Confirmed hyperthyroidism: TRAK assay to distinguish Graves' disease from other causes (toxic adenoma, thyroiditis) and guide the choice of treatment.
- Pregnancy with abnormal TSH or personal or family history of autoimmune thyroid disease
- Recurrent miscarriages or unexplained infertility: anti-TPO positives are associated with an increased risk of obstetrical complications even in euthyroidism
- Diffuse goiter or thyroid nodule in a clinical setting suggestive of autoimmunity
- Initiation of immunotherapy with immune checkpoint inhibitors (pembrolizumab, nivolumab): risk of immune thyroiditis and autoimmune thyroid dysfunction
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The isolated presence of positive anti-TPO antibodies with normal TSH does not, in the absence of symptoms, justify the initiation of treatment. It does, however, indicate the need for annual TSH monitoring, as the risk of progression to clinical hypothyroidism is of the order of 2 to 4 % per year in this situation.
Particularities of thyroid assessment in specific populations
| Population | Specific features of interpretation and monitoring |
|---|---|
| Newborn | Systematic neonatal screening for congenital hypothyroidism in Quebec using TSH measurement on blotting paper at D3 to D5 of life; TSH values are physiologically very high in the first few hours of life (physiological peak). |
| Children and teenagers | Reference values differ from adults according to age; Hashimoto's thyroiditis is the main cause of acquired hypothyroidism in schoolchildren |
| Pregnant woman | Specific quarterly reference intervals; untreated hypothyroidism associated with risks of miscarriage, prematurity and impaired fetal neurological development; screening recommended in the first trimester in the presence of risk factors |
| Elderly (over 70) | The upper limit of normal TSH increases physiologically with age (some experts tolerate TSH up to 6-7 mIU/L without treatment in asymptomatic octogenarians); symptoms of hypothyroidism are often atypical or attributed to normal aging |
| Patient on levothyroxine | The TSH target varies according to the indication: 0.5 to 2.5 mIU/L in simple hypothyroidism; 0.1 to 0.5 mIU/L in post-thyroidectomy for intermediate- or high-risk cancer; lower TSH values tolerated in pregnancy. |
| Patients undergoing immunotherapy | Thyroid monitoring mandatory before each cycle; immune thyroiditis may initially present as a transient hyperthyroid phase followed by permanent hypothyroidism |
Consult at Clinique Omicron
Un bilan thyroïdien complet peut être prescrit et interprété par les médecins et infirmières praticiennes spécialisées (IPS) de Clinique Omicron dans le cadre d'un bilan de santé préventif, d'une investigation de symptômes évocateurs de dysfonction thyroïdienne ou du suivi d'une maladie thyroïdienne connue et de son traitement. Les résultats sont analysés en tenant compte du contexte clinique global, des médicaments en cours et des facteurs interférents potentiels. En présence d'anomalies nécessitant une investigation complémentaire, notamment une échographie thyroïdienne ou une consultation en endocrinologie, une orientation est assurée depuis les points de service de Clinique Omicron au Québec. Prenez rendez-vous en ligne ou par téléphone à l'un des points de service au Québec.
The content of this page is provided for informational purposes only and is not intended to replace the advice of a qualified healthcare professional. Consult a physician for any symptoms, questions or decisions you may have regarding your health.
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