Goiter treatment

Myxedema and goiter are the main conditions for which thyroid preparations are indicated. The treatment of cretinism is difficult because it is recognized only at or after birth. Even if this disease could be diagnosed m utero, thyroid hormones do not readily cross the placental barrier. In addition, the fetus, as does a premature infant, rapidly deactivates the thyroid hormones. The halogen-free analogue DlMlT [26384-44-7] (3), which is resistant to fetal deiodinases, may prove useful for fetal hypothyroidism (cretinism). 

Lithium. In the lithium carbonate treatment of certain psychotic states, a low incidence (3.6%) of hypothyroidism and goiter production have been observed as side effects (6,36) (see Psychopharmacologicalagents). It has been proposed that the mechanism of this action is the inhibition of adenyl cyclase. Lithium salts have not found general acceptance in the treatment of hyperthyroidism (see Lithiumand lithium compounds). 

Hyperthyroidism (thyrotoxicosis), defined as excessive thyroid activity, causes a state of thyroid hormone excess (thyrotoxicosis) characterized by an increased metabolic rate, increase in body temperature, sweating, tachycardia, tremor, nervousness, increased appetite and loss of weight. Common causes of hyperthyroidism are toxic multinodular goiter, toxic adenoma or diffuse toxic goitre ( Graves disease). Antithyroid diugs (methimazol, carbimazole, propylthiouracil) block thyroid hormone production and are hence suitable for the treatment of hyperthyroidism. 

Levothyronine has properties of levothyroxine however, it acts faster and binds less with blood proteins. Indications for using levothyronine are the same as with levothyroxine -hypothyroidism, euthyroid goiters, thyroiditis however, its use is considered more appropriate in the first stage of treatment. Synonyms of this drug are tibon, cinomel, tertroxin, and others. 

Pituitary TSH suppressants In the treatment or prevention of various types of euthyroid goiters, including thyroid nodules, subacute, or chronic lymphocytic thyroiditis (Hashimoto), multinodular goiter, and in the management of thyroid cancer (except liothyronine). 

In the treatment of benign nodules and nontoxic multinodular goiter, TSH generally is suppressed to a higher target (eg, 0.1 to 0.5 or 1 milliunits/L). 

Autoimmune polyglandular syndrome-Chron c autoimmune thyroiditis may occur in association with other autoimmune disorders. Treat patients with concomitant adrenal insufficiency with replacement glucocorticoids prior to initiation of treatment. Failure to do so may precipitate an acute adrenal crisis when thyroid hormone therapy is initiated. Patients with diabetes mellitus may require upward adjustments of their antidiabetic therapeutic regimens. Nontoxic diffuse goiter or nodular thyroid disease Use caution when administering levothyroxine to patients with nontoxic diffuse goiter or nodular thyroid disease in order to prevent precipitation of thyrotoxicosis. If the serum TSH is already suppressed, do not administer levothyroxine. 

Iodine is an essential nutrient element required for thyroid gland. It is added to salt and to animal feeds for the prevention of goiter. In medicine it is used as a therapeutic reagent for the treatment of various thyroid-related diseases. It also is used as an antiseptic. Radioactive isotopes of iodine are used for treating thyroid cancer, heart diseases including tachycardia, and as a tracer for diagnosing certain diseases. 

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. 

Surgery is usually a near-total thyroidectomy, with main indications being suspected coexistent thyroid carcinoma, solitary toxic nodule, large goiter, failed medical treatment, patient preference and occasionally in pregnancy if adverse effects from antithyroid dmgs occur. 

York City, 1928, pp. 272-96. Article by Dr. David Marine on Iodine in the prevention and treatment of goiter. ... 

TSH, T3, T, T3-resin uptake, free thyroxin index), but careful attention to early signs and symptoms of hypofunction (e.g., weight gain, cold intolerance, hair loss) may be more productive. Thyroid-stimulating hormone is sensitive to early thyroid changes and, if elevated, should prompt treatment with thyroid supplements to avoid goiter or hypothyroidism. 

Beebe RT, Propp S, McClintock JC, Versaci A. Fatal agranulocytosis during treatment of toxic goiter with propylthiouracil. Ann Intern Med 1951 34(4) 1035-40. 

Appetecchia M. Effects on bone mineral density by treatment of benign nodular goiter with mildly suppressive doses of L-thyroxine in a cohort women study. Horm Res 2005 64(6) 293-8. 

Thyroid function tests were measured before and after treatment of amiodarone-induced hyperthyroidism (n = 12) and the response to combined antithyroid and glucocorticoid treatment (n = 11) was recorded (61). One patient had type 1 hyperthyroidism, nine had type 2, and two probably had a mixed form. Six patients had diffuse hypoechoic goiters. The median time to euthyroidism (defined as a normal free T3 concentration) with a thionamide + prednisolone (starting dose 20-75 mg/day) was... 

The clinical, biochemical, and thyroid imaging characteristics of thyrotoxicosis resulting from interferon alfa treatment have been retrospectively analysed from data on 10 of 321 patients with chronic hepatitis (75 with chronic hepatitis B and 246 with chronic hepatitis C) who developed biochemical thyrotoxicosis (505). Seven patients had symptomatic disorders, but none had ocular symptoms or a palpable goiter. Six had features of Graves disease that required interferon alfa withdrawal in four and prolonged treatment with antithyroid drugs in all six. Three presented with transient thyrotoxicosis that... 

Mild hypothyroidism with a goiter developed in a 15-year-old boy 6 weeks after lymphangiography with Lipiodol ultrafluid the goiter disappeared after 3 months treatment with levothyroxine (SEDA-7, 454). 

The many effects of lithium on thyroid physiology and on the hypothalamic-pituitary axis and their clinical impact (goiter, hypothyroidism, and hyperthyroidism) have been reviewed (620). Lithium has a variety of effects on the hypothalamic-pituitary-thyroid axis, but it predominantly inhibits the release of thyroid hormone. It can also block the action of thyroid stimulating hormone (TSH) and enhance the peripheral degradation of thyroxine (620). Most patients have enough thyroid reserve to remain euthyroid during treatment, although some initially have modest rises in serum TSH that normalize over time. 

Despite the predominantly antithyroid effects of lithium, thyrotoxicosis continues to be described during treatment and after withdrawal (642-644). In a retrospective review of 201 patients taking lithium (mean duration 6.4 years), hypothyroidism requiring supplemental thyroxine developed in 10% (3.4% of men, 15% of women) after a mean duration of 56 months. Women over 50 years of age tended to have an earlier onset. Two patients developed goiter requiring surgery and two others developed thyrotoxicosis (631). 

Euthyroid or hypothyroid goiter can also complicate lithium therapy, although the goiter is seldom of clinical importance and tends to resolve on withdrawal or with thyroxine treatment. In one ultrasound study, there was a... 

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