mline 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 hyperthyroidism is present, or there is coincident disease that might be aggrevated by hyperthyroidism. SCH with TSH of 0.2-0.3.5 may not need treatment. Individuals with TSH at or below 0.1uU/ml most likely will require treatment by one of the methods described b elow.
Apathetic hyperthyroidism designates a thyrotoxic condition characterized by fatigue, apathy, listlessness, dull eyes, extreme weakness, often congestive heart failure, and low-grade fever.[ 34, 35] Often such patients have small goiters, modest tachycardia, occasionally cool and even dry skin, and few eye signs. The syndrome may, in some patients, represent an extreme degree of fatigue induced by long-standing thyrotoxicosis. Once the diagnosis is considered, standard laboratory tests should confirm or deny the presence of thyrotoxicosis even in the absence of classical symptoms and signs.
Other diagnostic problems Two common diagnostic problems involve (1) the question of hyperthyroidism in patients with goiter of another cause, and (2) mild neuroses such as anxiety, fatigue states, and neurasthenia. Most patients with goiter receive a battery of examinations to survey their thyroid function at some time. Usually these tests are done more for routine assessment than because there is serious concern over the possibility of thyrotoxicosis. In the absence of significant symptoms or signs of hyperthyroidism and ophthalmologic problems, a normal FTI or TSH determination is sufficiently reassuring to the physician and the patient. Of course, the most satisfactory conclusion of such a study is the positive identification of an alternate cause for enlargement of the thyroid. Some patients complain of fatigue and palpitations, weight loss, nervousness, irritability, and insomnia. These patients may demonstrate brisk reflex activity, tachycardia (especially during examinations), perspiration, and tremulousness. In the abscence of thyrotoxicosis, the hands are more often cool and damp rather than warm and erythematous. Serum TSH assay should be diagnostic.
Mild and tem