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Thyroiditis painless

A low RAIU indicates the excess thyroid hormone is not a consequence of thyroid gland hyperfunction. This may be seen in painful subacute thyroiditis, painless thyroiditis, struma ovarii, follicular cancer, and factitious ingestion of exogenous thyroid hormone. [Pg.243]

Iodine excess (including radiocontrast, amiodarone) Thyrotoxicosis without hyperthyroidism Subacute thyroiditis Silent (painless) thyroiditis... [Pg.676]

Painless (silent, lymphocytic, postpartum) thyroiditis is a common cause of thyrotoxicosis its etiology is not fully understood and may be heterogeneous autoimmunity may underlie most cases. [Pg.241]

Painless thyroiditis has a triphasic course that mimics that of painful subacute thyroiditis. Most patients present with mild thyrotoxic symptoms lid retraction and lid lag are present but exophthalmos is absent. The thyroid gland may be diffusely enlarged, but thyroid tenderness is absent. [Pg.242]

During the thyrotoxic phase of painless thyroiditis, the 24-hour RAIU is suppressed to less than 2%. Antithyroglobulin and antimicrosomal antibody levels are elevated in more than 50% of patients. [Pg.243]

Cytokines Interferon- and interleukin-2 - Therapy with interferon- has been associated with the development of antithyroid microsomal antibodies in 20% of patients and some have transient hypothyroidism, hyperthyroidism, or both. Patients who have antithyroid antibodies before treatment are at higher risk of thyroid dysfunction during treatment. Interleukin-2 has been associated with transient painless thyroiditis in 20% of patients. [Pg.351]

III.b.1.6. Radioactive iodine. Radioactive iodine (Iodine-131) is a radioactive isotope of iodine, usually taken in an oral solution formulation as sodium 1. Given orally as sodium I, radioactive iodine is rapidly absorbed, concentrated and stored in the thyroid follicles. The therapeutic effect depends on beta-ray emission and destruction of thyroid parenchyma manifests some weeks after treatment. It is relatively safe, cheap, painless and avoids side effects associated with surgery. It is widely regarded as the treatment of choice in adults with toxic multinodular goiter, toxic nodule and people who relapse after a course of antithyroid medication. [Pg.761]

A 41-year-old woman developed painless thyroiditis after receiving leuprolide acetate for 4 months. [Pg.488]

Amino N, Hidaka Y, Takano T, Tatsumi K, Izumi Y, Nakata Y. Possible induction of Graves disease and painless thyroiditis by gonadotrophin-releasing hormone analogues. Thyroid 2003 8 815-8. [Pg.492]

The incidence of optic neuropathy in thyroid eye disease is 5% to 10%. The class 6 patient usually has mild to moderate proptosis and relatively shallow orbits. Thyroid optic neuropathy may be evidenced by papilledema, papillitis, or retrobulbar neuritis and usually is characterized by a painless and gradual loss of visual acuity. Common visual field defects include central scotomas, arcuate or altitudinal defects, paracentral scotomas, or generalized depressions. Thus visual field and optic disc examinations are the best diagnostic tools for early optic neuropathy. Occasionally, vision loss can occur precipitously over 1 or 2 weeks. Other features of optic nerve dysfunction frequently associated with the decreased visual acuity are color vision disturbances, afferent pupillary defects in the less proptotic eye in patients with asymmetric involvement, and prolongation of the pupil cycle time. [Pg.650]

Since its description in 1975, painless (sUent, lymphocytic, postpartum) thyroiditis has been recognized as a common cause of thyrotoxicosis and may represent up to 15% of cases of thyrotoxicosis in North America. The etiology is not fully understood and may be heterogeneous. The triphasic course of this illness mimics that of painful thyroiditis. Most patients present with mild thyrotoxic symptoms. Lid retraction and lid lag are present but exophthalmos is absent. The thyroid gland may be diffusely enlarged but thyroid tenderness is absent. [Pg.1375]

The 24-hour RAIU wiU be suppressed to less than 2% during the thyrotoxic phase of painless thyroiditis. Antithyroglobuhn and antimicrosomal antibody levels are elevated in more than 50% of patients. Painless thyroiditis frequently occurs during the immediate postpartum period, and individual patients may experience recurrence of the disease with subsequent pregnancies. Patients with mild hyperthyroidism and painless thyroiditis should be reassured that they have a self-hmited disease. Adrenergic symptoms may be ameliorated with propranolol. Antithyroid drugs are not indicated because they do not decrease the release of preformed thyroid hormone. [Pg.1375]

Subacute thyroiditis exhibits easily recognizable clinical features. It is not a common cause of hypothyroidism in the elderly. Painless thyroiditis is also infrequent in aged people. These conditions may cause transient hyperthyroidism followed by a transient permanent thyroid hypofunction phase. Infiltrative diseases affecting the thyroid gland (Riedel s thyroiditis, hemochromatosis, scleroderma, leukemia, amyloidosis) and infections are rare causes of hypothyroidism at all ages. Toxic injury to the thyroid gland has been reported after exposure to polybrominated biphenyls and polychlorinated biphenyls (Roberts and Ladenson, 2004). [Pg.1035]

Previous total or subtotal thyroidectomy for nodular goiter and the presence of an increase in serum TSH level indicate the diagnosis of post-operative hypothyroidism. Loss of thyroid function may also occur after definitive therapy for previous thyrotoxicosis, either with radioiodine or thyroidectomy. Some patients may exhibit a transient phase of thyroid hypofunction after partial thyroidectomy or radioiodine therapy with recovery of function. Other causes of hypothyroidism, such as thyroid dysgenesis, infiltrative diseases, iodine deficiency, iodine excess, painless thyroiditis and subacute thyroiditis are less common in the elderly and are usually easily recognizable by their clinical and analytical features. [Pg.1037]

From a practical standpoint, serial determinations of iodine content may be helpful in the differential diagnosis between Graves disease and painless thyroiditis (23). In Graves disease, no change in iodine content is observed without treatment while in painless thyroiditis a decrease of the iodine content is observed. [Pg.154]

Woolf PD. 1978. Painless thyroiditis as a cause of hyperthyroidism. Subacute or chronic lymphocytic. Arch Intern Med 138, 26-27. [Pg.161]

Fig. 1. Relative contribution of different types of thyroid disease to the incidence of hyperthyroidism in East-Jutland, Denmark, and in Iceland. Onfy the contr ution of the four major forms is shown. GD = Graves disease, MNG = multinodular toxic goitre, STA = solitary toxic adenoma, SAT = subacute and painless thyroiditis. The numbers represent the percentage of all cases. Fig. 1. Relative contribution of different types of thyroid disease to the incidence of hyperthyroidism in East-Jutland, Denmark, and in Iceland. Onfy the contr ution of the four major forms is shown. GD = Graves disease, MNG = multinodular toxic goitre, STA = solitary toxic adenoma, SAT = subacute and painless thyroiditis. The numbers represent the percentage of all cases.

See other pages where Thyroiditis painless is mentioned: [Pg.2059]    [Pg.2059]    [Pg.370]    [Pg.229]    [Pg.1372]    [Pg.1375]    [Pg.84]    [Pg.118]    [Pg.1033]   
See also in sourсe #XX -- [ Pg.228 , Pg.229 , Pg.230 ]

See also in sourсe #XX -- [ Pg.228 , Pg.229 , Pg.230 ]

See also in sourсe #XX -- [ Pg.1375 ]




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