Thyroid hormone hyperthyroidism treatment

Hyperthyroidism, that is, the overproduction of thyroid hormones, is usually treated by surgical removal of the thyroid gland. Before such a procedure is undertaken, the hyperthyroidism is usually first brought under control by treatment with so-called antithyroid agents. 

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. 

Treatment of thyrotoxicosis due to hyperthyroidism is similar, regardless of the underlying cause. The goals of treating hyperthyroidism are to relieve symptoms, to reduce thyroid hormone production to normal levels and achieve biochemical euthyroidism, and to prevent long-term adverse sequelae. 

During treatment of hyperthyroidism, Lp(a), as well as LDL cholesterol and apolipoprotein B, increases, indicating an effect of thyroid hormone on receptor activity and on protein synthesis. The opposite effect is observed in treatment of hypothyroidism (B27, E9, K16). 

Hyperthyroidism results from excess production of thyroid hormones due to various reasons. Treatment of the resulting thyrotoxicosis (Basedow s disease) consists of using... 

In addition, the metabohsm of OCAs results in the release of large amounts of E into the circulation. As described for KI, I released from OCAs may have effects at the thyroid gland and if used alone to treat hyperthyroidism, OCAs carry the same potential to induce increased secretion of thyroid hormone and exacerbation of thyrotoxicosis. When an OCA is used in the treatment of hyperthyroidism, large doses of antithyroid agents are usually administered concomitantly. However, the combination of OCAs and antithyroid drugs may cause resistance to the antithyroid drugs with time, presumably because of the elevation in intrathyroidal 1 content. Thus, it is recommended that the use of OCAs be reserved for short-term treatment of patients with severe thyrotoxicosis and significant comorbidity (e.g., myocardial infarction, sepsis, stroke) for rapid control of plasma Tj concentrations. 

Subclinical hyperthyroidism is defined as a suppressed TSH level (below the normal range) in conjunction with normal thyroid hormone levels. Cardiac toxicity (eg, atrial fibrillation), especially in older persons, is of greatest concern. The consensus of thyroid experts concluded that hyperthyroidism treatment is appropriate in those with TSH less than 0.1 mlU/L, while close monitoring of the TSH level is appropriate for those with less TSH suppression. 

Several natural or synthetic substances interfere with the synthesis and/or secretion of the thyroid hormones. Two types of thionamides are used in the treatment of hyperthyroidism ... 

In a retrospective review of 497 patients taking propylthiouracil for hyperthyroidism, clinically overt hepatitis developed in six patients at 12-49 days after starting the drug (50). Jaundice and itching were present in five, fever in two, rash in two, and arthralgia in one. Serum bilirubin, alanine transaminase, and alkaline phosphatase were increased in five, four, and six patients respectively. The type of hepatic injury was cholestatic in three, hepatocellular in one, and mixed in two. There were no differences in age, sex, drug dose, or serum thyroid hormone concentrations at time of diagnosis in those with hepatic injury compared with those without. Liver function normalized in all patients at 16-145 days after withdrawal of propylthiouracil. In addition to these cases of overt liver injury, 14% of the cohort had mild asymptomatic liver enzyme rises at a mean of 75 days after the start of treatment. 

In 50 women taking levothyroxine either for primary thyroid failure or for hypothyroidism secondary to radioiodine treatment for hyperthyroidism, there was no difference between the two groups in terms of bone density at the hip or spine and no difference from the reference population (31). In addition, there was no correlation between bone density and circulating thyroid hormone concentrations or duration of levothyroxine replacement. These findings are reassuring, although large studies of fracture risk are required, in view of previous evidence of an adverse effect of levothyroxine on bone mineral density, especially in post-menopausal women (32). 

Inadvertent excessive use of thyroid hormones (for example, by eating ground beef contaminated with thyroid hormones (64), the incorrect use of these drugs for the treatment of obesity (65), excessive thyroid substitution therapy, and factitious use of thyroid hormones for psychiatric reasons (66)) result in mild hyperthyroidism, but serious short-term adverse effects are rare. 

It has been suggested that potassium perchlorate should be used in the treatment of type 1 hyperthyroidism and glucocorticoids in the treatment of type 2 (SEDA-21, 199). Since hypothyroidism due to amiodarone tends to occur in areas in which there is sufficient iodine in the diet, it has been hypothesized that an iodinated organic inhibitor of hormone synthesis is formed and that the formation of this inhibitor is inhibited by perchlorate to a greater extent than thyroid hormone iodination is inhibited, since the iodinated lipids that are thought to be inhibitors require about 10 times more iodide than the hormone. However, there is a high risk of recurrence after treatment with potassium perchlorate, and it can cause serious adverse effects (SED-13,1281). 

Lithium blocks the release of iodine and thyroid hormones from the thyroid and has been used to treat hyperthyroidism, as an adjunct to radioiodine therapy (602-605) and in metastatic thyroid carcinoma (606). However, it can also cause hyperthyroidism. Lithium enhanced the efficacy of radioiodine in 23 patients (607), but was ineffective in a larger comparison of lithium (n = 175) or radioiodine alone (n = 175) (608). In 24 patients with Graves disease, lithium attenuated or prevented increases in thyroid hormone concentration after methimazole withdrawal and radioiodine treatment (602,609). 

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. 

Thyroid Hormone. Treatment of rats with thyroxin increases hepatic microsomal NADPH oxidation in both male and female rats, with the increase being greater in females. Cytochrome P450 content decreases in the male but not in the female. Hyperthyroidism causes a decrease in gender-dependent monooxygenase reactions and appears to interfere with the ability of androgens to increase the activity of the enzymes responsible. Gender differences are not seen in the response of mice and rabbits to... 

Failure of the thyroid to produce sufficient thyroid hormone is the most common cause of hypothyroidism and is known as primary hypothyroidism. Secondary hypothyroidism occurs much less often and results from diminished release of TSH from the pituitary. Treatment of hypothyroidism is achieved by the replacement of thyroid hormone, primarily T4. A synthetic preparation of T4 is available, levothyroxine (Synthroid ), which has been a popular choice for hypothyroidism because of its consistent potency and prolonged duration of action. No toxicity occurs when given in physiological replacement doses. Desiccated animal thyroid is also available at a lesser cost. Overdoses cause symptoms of hyperthyroidism and can be used as a guide in clinical management. Hypothyroidism is not cured by the daily intake of thyroid hormone it is a life-long regimen. 

Thiourea derivatives are known for their anti-thyroid effects due to inhibition of thyroid peroxidase [1], Two thiourea compounds especially, have found wide application in the treatment of patients with hyperthyroidism, i.e., PTU and 2-mer-capto-l-methylimidazole (methimazole). It was soon recognized, however, that while methimazole only blocks thyroid hormone synthesis PTU has an additional effect on thyroid hormone metabolism [13]. These clinical findings have been confirmed in vitro showing that PTU, but not methimazole, is a potent inhibitor of the type I deiodinase [5-8]. Structure-activity studies of thiourea analogues [44,45] have... 

The TSH radioimmunoassays procedures have replaced other methods for the quantitative assessment of changes in pituitary responsiveness after repeated dose treatment, test compounds which enhance the secretion of thyroid hormones lead to a suppression of the serum TSH concentrations, a clinical example being hyperthyroidism (Connors et al. 1981, Pekary et al. 1980). On the other hand, a reduction in circulating concentrations of thyroid hormones (T3 and T4) will release the pituitary gland from feedback inhibition, and the serum concentration of TSH may arise in an exponential manner. 

Q8 The drug treatment of thyrotoxicosis involves using antithyroid drugs car-bimazole (which is converted to the active compound methimazole) and propylthiouracil inhibit the synthesis of thyroid hormone. Propylthiouracil also inhibits peripheral conversion of T4 to T3. Many of the symptoms of hyperthyroidism can also be alleviated by fl-adrenoceptor antagonists. Iodine... 

Treatment of thyroiditis (Hashimoto s thyroiditis, subacute thyroiditis of de Quervain). Where hyperthyroidism is a feature, treatment is by a P-adrenoceptor blocking drug. Antithyroid drugs should not be used. Where there is permanent hypothyroidism, the treatment is thyroid hormone replacement. 

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