Last reviewed: 6 Nov 2021
Last updated: 05 Oct 2018



If screening for thyroid dysfunction in the absence of hypothalamic or pituitary pathology is undertaken, serum thyroid-stimulating hormone (TSH) assay is usually the initial laboratory test. Suppressed or elevated TSH confirms presence of thyroid dysfunction but not its cause. Diagnosis of hyperthyroidism is usually confirmed with suppressed TSH and high serum levels of free thyroxine (T4) and/or free triiodothyronine (T3). If screening for hypothyroidism (primary) is undertaken, this is generally done with detection of an elevated TSH. Further testing (e.g, radioactive iodine uptake) may be used subsequently to clarify aetiologies in some cases.

Graves' disease is an autoimmune thyroid disease and is the most common form of hyperthyroidism in most areas of the world. Hyperthyroidism is caused by stimulatory TSH receptor antibodies (TRAb). The combination of a diffuse goitre, recent onset of orbitopathy, and symptoms of hyperthyroidism is diagnostic of Graves' disease.[1] In questionable cases, measurement of TRAb is used as a diagnostic test.

A toxic multinodular goitre (MNG) contains multiple autonomously functioning nodules, resulting in hyperthyroidism that generally does not remit spontaneously. Nodules function independently of TSH and are almost always benign. However, non-functioning thyroid nodules in the same goitre may be malignant. Worldwide, iodine deficiency is the most common cause of nodular goitre.[2]

An autonomously functioning thyroid nodule that causes hyperthyroidism and, generally, does not remit spontaneously.[1] Typically presents as a single large nodule and is almost always benign.[3] Worldwide, iodine deficiency is the most common cause of nodular goitre.[2]

Autoimmune-mediated inflammation of the thyroid gland with release of thyroid hormone (destructive thyroiditis), resulting in transient hyperthyroidism, frequently followed by a hypothyroid phase before recovery of normal thyroid function.[4][5] Permanent hypothyroidism may occur. Considered by many to be a variant of chronic lymphocytic (Hashimoto's) thyroiditis.[6]

Inflammation of the thyroid characterised by a triphasic course of transient thyrotoxicosis, followed by hypothyroidism, followed by return to euthyroidism.[7][8] The initial thyrotoxic phase is associated with thyroid pain, high serum thyroid hormone levels with a low radioiodine uptake, elevated erythrocyte sedimentation rate, elevated C-reactive protein, and a systemic illness similar to influenza, with fever, myalgia, and malaise.[9][10]

Clinical state resulting from underproduction of T4 and T3. Low free T4 with an elevated TSH is diagnostic of primary hypothyroidism. Autoimmune thyroiditis (Hashimoto's disease) is the most common cause of primary hypothyroidism.[11] Secondary/central hypothyroidism is caused by pituitary or hypothalamic dysfunction.

The result of anterior pituitary or hypothalamic dysfunction. Aetiology may be congenital, neoplastic, inflammatory, infiltrative (e.g., tuberculosis, syphilis, fungal infections, toxoplasmosis, sarcoidosis, haemochromatosis, histiocytosis[12][13][14]), traumatic, or iatrogenic. Pituitary mass lesions, especially pituitary adenomas, are the most common cause.[15]

Most commonly presents as an asymptomatic thyroid nodule in a woman in her 30s or 40s. Detection might follow physical examination or be an incidental finding on neck ultrasound or computed tomography. Treatment of the most common types (papillary or follicular) generally involves surgery, followed by radioactive iodine ablation and TSH suppression.

Thyroid parenchymal expansion can result from diffuse enlargement or infiltration of the thyroid gland, or from the presence of one or more thyroid nodules.

Ultrasonography is the initial test of choice for evaluating the structure and anatomical location of a neck mass. If the mass or nodule arises from the thyroid gland, clinical evaluation and biochemical tests will determine whether the mass is hormonally active.



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