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    Home > Active Ingredient News > Endocrine System > One table summary: the main points of the differential diagnosis of Graves hyperthyroidism | clinical practice

    One table summary: the main points of the differential diagnosis of Graves hyperthyroidism | clinical practice

    • Last Update: 2021-05-10
    • Source: Internet
    • Author: User
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    Introduction: Graves’ hyperthyroidism (GH) is the most common cause of hyperthyroidism, but it is easily associated with non-hyperthyroid thyrotoxicosis, autonomous high-functioning thyroid adenoma, toxic multinodular goiter, central hypothyroidism, and pituitary gland TSH adenomas are confused, and attention should be paid to distinguish them.

    So, regarding the differential diagnosis of GH, what are the main points that need to be paid attention to? GH-the most common type of hyperthyroidism GH is an organ-specific autoimmune disease that often occurs in people who are genetically susceptible (especially women).
    Smoking, high iodine diet, stress, infection, and pregnancy can promote the disease.
    Both cellular immunity and humoral immunity are involved in the pathogenesis.

     TSAb is the main pathogenic antibody that induces GH.
    It activates TSH receptors to promote thyroid synthesis and excessive secretion of thyroid hormones, leading to GH.

    The latest data show that the prevalence rate of adult clinical hyperthyroidism in my country is 0.
    78%, the prevalence rate of subclinical hyperthyroidism is 0.
    44%, and the prevalence rate of GH is 0.

     Diagnosis of GH 1.
    Preliminary diagnosis of GH can be made based on the following characteristics: ➤ Palpitations, hyperhidrosis and irritability, and other symptoms and signs of high metabolism caused by increased sympathetic nerve excitability; ➤ Diffuse thyroid enlargement (a few cases may not have goiter); ➤TSH level decreased, FT4 level increased; ➤serum TRAb positive.

    The following features are helpful in assisting the diagnosis of GH: ➤Invasive exophthalmos; ➤Mixed edema of the anterior tibia; ➤Increase in 131I iodine uptake (RAIU) or thyroid radionuclide imaging suggests increased thyroid uptake.

    A small number of patients with atypical clinical manifestations should be noted.
    In actual clinical practice, a small number of patients with GH may have atypical clinical manifestations, and may have atrial fibrillation, periodic muscle paralysis, diarrhea or paroxysmal hypertension as the first manifestation.
    , There is a possibility of misdiagnosis, and it is necessary to combine serum FT4, TSH determination and other tests to confirm the diagnosis.

     Key points of differential diagnosis of GH In clinical, diseases that are easily confused with GH include non-hyperthyroid thyrotoxicosis, autonomous high-functioning thyroid adenoma and toxic multinodular goiter, central hypothyroidism and pituitary TSH adenoma, etc.
    Pay attention to differential diagnosis.

    Table 1 Key points for differential diagnosis of GH 1.
    Non-hyperthyroid thyrotoxicosis As the most common cause of hyperthyroidism, GH needs to be differentiated from non-hyperthyroid thyrotoxicosis caused by excessive intake of exogenous thyroid hormones or thyroiditis destroying thyroid follicles.

    Thyroiditis is the main cause of thyrotoxicosis, including chronic lymphocytic thyroiditis, subacute thyroiditis, painless thyroiditis and postpartum thyroiditis.

     Compared with GH, this disease is characterized by a transient increase in FT4, a decrease in RAIU, TRAb-negative, and no infiltrating exophthalmos and pretibial mucinous edema.

    Patients with subacute thyroiditis are characterized by elevated serum FT4 levels, decreased RAIU, or diffusely decreased uptake of the thyroid radionuclide imaging tracer "separation phenomenon".

    Autonomous high-functioning thyroid adenoma and toxic multinodular goiter without GH autoimmune disease characteristics, such as TRAb positive and autoantibody attack caused by pretibial mucinous edema, infiltrating exophthalmos, etc.

    Thyroid radionuclide imaging is helpful in distinguishing from GH.
    Autonomous high-functioning thyroid adenomas are "hot nodules", and the surrounding thyroid tissue is partially visible or not, while multinodular toxic goiters are multiple "hot nodules".
    Or "cold and hot nodules".

    Central hypothyroidism and pituitary TSH adenoma Central hypothyroidism refers to the compression of pituitary thyrotropin cells and hypothalamic-pituitary portal blood flow due to diseases of the pituitary, hypothalamus, or hypothalamic-pituitary portal circulation Discontinuation and other reasons cause abnormal thyroid function caused by TSH deficiency.
    Some patients may show the false appearance of "subclinical hyperthyroidism" with low serum TSH levels and normal FT4 levels.
    Pituitary adenomas are the most common cause.

    Some pituitary adenomas increase the secretion of TSH leading to hyperthyroidism, which is usually accompanied by symptoms of pituitary tumor compression such as visual field defects and abnormal secretion of pituitary hormones such as galactorrhea.

    Iodine-induced hyperthyroidism Iodine-induced hyperthyroidism is common in patients with existing nodular goiter or occult GH who have had a recent history of iodine exposure (such as examination of iodine-containing contrast agents, taking iodine-rich drugs such as amiodarone).
    It often occurs several weeks to several months after iodine is used.

    Amiodarone-induced thyrotoxicosis (AIT) is divided into AIT type I and AIT type II.

    AIT type I is hyperthyroidism induced by high iodine content of amiodarone.
    It has the characteristics of increased blood flow in the thyroid gland, reduced, normal or increased RAIU intake, and short onset time (average 3 months) after taking amiodarone.

    AIT type II is a destructive thyroiditis caused by the direct toxic effect of amiodarone on thyroid follicular epithelial cells, which is characterized by reduced RAIU and a long onset time (average 30 months) after taking amiodarone.

    Other reasons Artificial intake of thyroid hormone, ovarian goiter and metastasis of functionally differentiated thyroid cancer can lead to excessive exogenous or endogenous thyroid hormone.

    In addition, thyroid hormone resistance syndrome, severe systemic diseases, pregnancy and the use of estrogen or glucocorticoids can cause changes in FT4 and (or) TSH levels.

     Reference materials: Nuclear Medicine Branch of Chinese Medical Association.
    131I Treatment of Graves' Hyperthyroidism Guidelines (2021 Edition) [J].
    Chinese Journal of Nuclear Medicine and Molecular Imaging.
    2021, 41 (4): 242-253.
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