ents with HIV(33.2), has occurred during recovery of low lymphocyte levels induced by therapy with CAMPATH in patients with Multiple sclerosis, has occurred after cessation of immune-suppressive treatment in patients with T1DM, and has developed during thyroid invasion by lymphoma(18).
|Table 4. Causes of Thyrotoxicosis|
Course of disease
|Graves’ disease||Familial, prolonged||Goiter||+ Ab, + RAIU, eye signs||Antithyroids, RAI, Surgery|
|Transient thyrotoxicosis||Brief||Small goiter||Low Ab, no eye signs, RAIU=0||Time, beta blocker, ? steroids|
|Subacute thyroiditis||Brief||Tender goiter||RAIU=0, elevated ESR, recent URI||Nothing, NSAID, steroids|
|Toxic multinodular goiter||Prolonged, mild||Nodular goiter||Typical scan||Antithyroids, RAI, surgery|
|Iodide induced||Recent, mild||Nodular goiter, occ.normal||Low RAIU, abnormal scan||Antithyroids, KClO4, time, stop I source|
|Toxic adenoma||Prolonged, mild||One nodule||“Hot” nodule on scan||Surgery, RAI, ? Sclerosis|
|Thyroid carcinoma||Recent||Variable, metastases||Functioning metastases||Surgery + RAI|
|Exogenous hormone||Variable||Small thyroid||RAIU and TG low, psychiatric illness||Withdrawal, counseling|
|Hydatiform mole||Recent, mild||Goiter||Pregnancy, bleeding,HCG||Surgery, chemotherapy|
|Choriocarcinoma||Recent, mild||Goiter||Increased HCG||Surgery, chemotherapy|
|Excess TRH||Goiter||Poor response to TRH||Not known||?|
|TSH-oma||Prolonged||Goiter||Excess alpha, TSH, adenoma||Op, somatostatin, thyroid ablation|
|Pituitary T3 resistance||Prolonged||Goiter||Elevated or normal TSH, no tumor, mod. thyrotox, no excess alpha||? Triac, somatostatin, thyroid ablation, beta blocker|
|Struma ovarii||Variable||+ / – goiter||Positive scan or US||Surgery|
|Hamburger toxicosis||Recent, self-limited||Small gland, no eye signs||Suppressed TSH and TG and RAIU||Avoid neck meat trimmings|
|Hyperemesis||Onset first trimester||Pregnancy, variably toxic||UP FTI, Low TSH, High HCG||ATD if severe, pregnancy termination|
|TSH-R mutation||Congenital||Typical thyrotoxicosis||+ FH, germline mutation||Thyroid ablation|
|Familial gestational hyperthyroidism||Onset first trimester||Severe hyperthyroidism||+ FH, TSH-R mutation sensitizing to hCG||ATD, Surgery|
|Amiodarone||Prolonged||Thyroid usually enlarged. Often heart disease.||Suppressed RAIU, nl or increased FTI, elevated T3||ATD + KClO4,Prednisone, Surgery,iopanoic acid|
|Interferon-alpha induced||Induced by INF treatment of hepatitis C||Clinically significant||Often remits if IFN stopped.|
|Treatment of HIV||During T cell recovery||Clinically significant||With or without prior thyroid autoimmunity||May need treatment|
|Administration of CAMPATH||During recovery of T cells||Clinically significant||With or without prior thyroid autoimmunity||May need treatment|
|Sunitinib therapy||During tyrosine kinase therapy for cancer||Clinically significant||Usually induces hypothyroidism, rarely hyper||May need treatment|
Subclinical hyperthyroidism It should be remembered that thyrotoxicosis is today not only a clinical but also a laboratory diagnosis. Consistent elevation of the fT4 , and the T3 level, and suppressed TSH, or only suppression of TSH, can indicate that thyrotoxicosis is present even in the absence of clear-cut signs or symptoms These elevations themselves may be a sufficient indication for therapy, especially in elderly patients with coincident cardiac disease(33a,b). Antithyroid drug treatment of patients with subclinical hyperthyroidism was found to result in a decrease in heart rate, decrease in number of atrial and ventricular premature beats, a reduction of the left ventricular mass index, and left ventricular posterior wall thickness, as well as a reduction in diastolic peak flow velocity. These changes are considered an argument for early treatment of subclinical hypothyroidism. Subclinical hyperthyroidism may disappear, evolve into Graves hyperthyroidism., or, with MNG, persist for long periods unchanged. Individuals of any age with consistent suppression of TSH should be fully evaluated to determine if evidence of hyperthyroidi