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تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
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Causes of thyrotoxicosis in children and adolescents

Causes of thyrotoxicosis in children and adolescents
Name Synonyms Mechanism Antibody tests; thyroglobulin where indicated RAI Thyroid examination
Thyroid gland hyperfunction (increased synthesis of thyroid hormones)
Graves disease

Hyperthyroid goiter

von Basedow disease
TSHR-Ab

TSHR-Ab* positive (TSI positive and TBII positive in typical cases)

TPO-Ab positive or negative
High, diffuse Symmetric nontender goiter
Multinodular hyperthyroid goiter Toxic multinodular goiter Autonomous overproduction of thyroid hormone by nodules All negative Normal or high, multifocal Nodular
Autonomous nodule

Plummer disease

Toxic nodule
Autonomous overproduction of thyroid hormone by a single nodule All negative High, single focus; rest of gland suppressed Single nodule
TSH-producing pituitary adenoma   Autonomous overproduction of TSH All negative High, diffuse Normal or symmetric goiter
Pituitary resistance to thyroid hormone   Overproduction of TSH All negative High, diffuse Symmetric goiter
Thyrotoxic phase of thyroiditis (excess release of preformed thyroid hormones)
Thyrotoxic phase of autoimmune thyroiditis (Hashimoto disease)

Hashitoxicosis

Lymphadenoid goiter
Autoimmune; release of preformed hormone

TPO-Ab positive

Anti-thyroglobulin antibody positive

TSHR-Ab* usually negative (TSI is usually negative; TBII may be positive)
Low in majority; inhomogeneous pattern Firm goiter, sometimes tender
Subacute autoimmune thyroiditis

Painless sporadic thyroiditis

Silent thyroiditis

Autoimmune; release of preformed hormone

May also be associated with drugs (IFN-alpha, IL-2, checkpoint inhibitors, or lithium)
TPO-Ab positive Low (during thyrotoxic phase) Firm nontender, mildly enlarged thyroid
Subacute granulomatous thyroiditis

Subacute thyroiditis

Painful subacute thyroiditis

de Quervain thyroiditis

Granulomatous giant cell thyroiditis
Viral infection; release of preformed hormone

TPO-Ab negative

Elevated ESR
Low (during thyrotoxic phase) Painful goiter
Drug-induced thyrotoxicosis
Factitious thyrotoxicosis Thyrotoxicosis factitial Ingestion of exogenous thyroid medication Low serum thyroglobulin Low or absent No goiter
Iodine-induced hyperthyroidism   Underlying multinodular goiter; thyroid hormone release triggered by exposure to iodine (eg, contrast agents, amiodarone)   Usually decreased but may be normal or increased Often multinodular
RAI: radioactive iodine uptake; TSHR-Ab: thyrotropin receptor-stimulating antibodies; TSI: thyroid-stimulating immunoglobulin; TBII: thyrotropin-binding inhibitor immunoglobulin; TPO-Ab: thyroid peroxidase antibodies; TSH: thyroid-stimulating hormone (thyrotropin); IFN-alpha: interferon alfa; IL-2: interleukin-2; ESR: erythrocyte sedimentation rate.
* TSHR-Ab can be measured by either a TSI or TBII. In many laboratories, this is now ordered as "TSH receptor antibody" test (TSHR-Ab, or simply TRAb). A positive TSI confirms the presence of a stimulating antibody and a diagnosis of Graves disease. A positive TBII (or TSHR-Ab) confirms that there is an antibody that competes with TSH binding to its receptor, but does not provide information about whether it is a stimulating or blocking antibody. A positive TBII (or TSHR-Ab) in a patient with clinical thyrotoxicosis is most likely indicative of Graves disease.
Graphic 58890 Version 15.0

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