Free triiodothyronine toxicosis: a distinct entity

Article Abstract:

The thyroid gland, located at the base of the neck, contains the iodine-containing protein thyroglobulin, which binds the thyroid hormones thyroxine (T4) and triiodothyronine (T3) until these hormones are released. When secreted into the bloodstream, thyroid hormones bind to blood proteins, such as thyroxine-binding globulin (TBG). Hyperthyroidism is increased activity of the thyroid glands leading to elevated levels of thyroid hormones, and can be diagnosed with the help of thyroid function tests. However, diagnosis of hyperthyroidism is difficult when TBG levels are low but T4 and T3 levels are normal, or during T3 toxicosis, when T3 levels are excessively high. Although TBG deficiency or T3 toxicosis can be detected by direct measurement of thyroid hormone levels, a patient may be diagnosed as having normal thyroid function when T3 toxicosis occurs in a patient with TBG deficiency, since free T4 and T3 levels may be normal. Three cases are described of patients with TBG deficiency associated with T3 toxicosis. One patient was thought to have hypothyroidism because levels of thyroid hormones were very low. However, the patients had no clinical signs of hypothyroidism but rather did have some evidence of hyperthyroidism. In addition, direct measurement of T3 levels showed that they were elevated. This form of hyperthyroidism, in which T3 levels are specifically elevated, has been termed T3 toxicosis. This abnormal thyroid condition can be diagnosed by a new test that can detect suppressed levels of thyroid-stimulating hormone associated with hyperthyroidism. (Consumer Summary produced by Reliance Medical Information, Inc.)

Thyroid diseases

---

Free triiodothyronine toxicosis in a patients with multinodular goiter

Article Abstract:

Thyrotoxicosis results from hyperactivity of the thyroid gland, and is characterized by rapid heart rate, tremors, elevated basal metabolism, enlarged thyroid gland, protrusion of the eyeballs, weight loss, and neurological symptoms. The diagnosis of thyrotoxicosis may be difficult, particularly in the elderly. A case is described of a 75-year-old man with symptoms of thyrotoxicosis, elevated levels of the thyroid hormone triiodothyronine (T3), and multinodular goiter (an enlarged thyroid containing several nodules or cell growths). This is the first reported case of thyrotoxicosis associated only with an increase in blood levels of T3. Radioactive iodine (131-I) and a saturated solution of potassium iodide (SSKI) were given to the patient to speed the recovery to a normal thyroid state. However, treatment with radioiodine and SSKI was associated with excessive iodine administration and radiation thyroiditis, or inflammation of the thyroid gland, which led to increased levels of another thyroid hormone, thyroxine (T4). SSKI given after 135-I therapy is not recommended for patients with multinodular goiter, unless large doses of antithyroid drug are given before and during iodine therapy. The cause of the prolonged and severe thyroiditis occurring after 131-I and SSKI therapy was not determined. The patient was maintained on the antithyroid agent propylthiouracil and was given the steroid dexamethasone, which improved the neck pain associated with his thyroiditis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Drug therapy, Thyroxine

---

Goiter and hypothyroidism during re-treatment with amiodarone in a patient who previously experienced amiodarone-induced thyrotoxicosis

Article Abstract:

Amiodarone is an iodine-containing drug used to treat heart abnormalities. Long-term use can result in thyroid problems, although the mechanism by which the drug affects the thyroid is not known. The case is presented of a patient retreated with the drug after initial treatment was withdrawn when thyroid abnormalities developed. The patient was treated for a heart condition with amiodarone in 1975 when she was 55 years old. Thyroid abnormalities appeared two and a half years later, and the drug was withdrawn. In 1979, alternative treatment for her heart condition began to fail, and amiodarone was again prescribed. Thyroid function was normal, although goiter was noted in 1982. In 1987, her thyroid function became severely depressed and treatment with L-thyroxin was begun. Amiodarone was not withdrawn. Treatment with the L-thyroxin has maintained thyroid functioning. These results indicate that the thyroid dysfunction caused by amiodarone is related to changes in the thyroid gland's sensitivity to iodine. The drug contains iodine, and this may decrease thyroid autoregulation of iodine. (Consumer Summary produced by Reliance Medical Information, Inc.)

Complications and side effects, Hypothyroidism, Amiodarone, Iodine compounds

Similar abstracts:

• Abstracts: Fluconazole therapy for chronic disseminated candidiasis in patients with leukemia and prior amphotericin B therapy
• Abstracts: Healing of erosive esophagitis with sucralfate and cimetidine: influence of pretreatment esophageal sphincter pressure and serum pepsinogen I levels
• Abstracts: HCFA's new take on physician incentives. Home (care) improvement: Medicare has fueled a boom in home health. But the president's reforms may change all that
• Abstracts: Aerosol pentamidine prophylaxis following Pneumocystis carinii pneumonia in AIDS patients: results of a blinded dose-comparison study using an ultrasonic nebulizer
• Abstracts: Cyclophosphamide: to pulse or not to pulse? Frequent occurrence of asplenism and cholelithiasis in patients with autoimmune polyglandular disease type I

This website is not affiliated with document authors or copyright owners. This page is provided for informational purposes only. Unintentional errors are possible.