Euthyroid state

Once a euthyroid state is achieved, tlie primary health care provider may add a thyroid hormone to tlie therapeutic regimen to prevent or treat hypothyroidism, which may develop slowly during long-term antithyroid drug therapy or after administration of 131I. 

There are three major goals in the treatment of hypothyroidism replace the missing hormones, relieve symptoms, and achieve a stable biochemical euthyroid state. 

Patients receiving LT4 therapy who are not maintained in a euthyroid state are at risk for long-term adverse sequelae. In general, overtreatment and a suppressed TSH is more common than undertreatment27 with an elevated TSH. Patients with long-term overtreatment may be at higher risk for atrial fibrillation and other cardiovascular morbidities, depression, and post-menopausal osteoporosis. Patients who are undertreated are at higher risk for hypercholesterolemia and other cardiovascular problems, depression, and obstetric complications. 

Desired outcomes include relieving signs and symptoms and achieving a euthyroid state. 

Success of therapy for thyroid disorders must be based not only on short-term improvement of the patient s clinical status and abnormal laboratory values but also on achievement of a long-term euthyroid state. Maintaining the TSH level in the normal range improves symptoms and reduces the risk of long-term complications. 

In the hyperthyroid patient, relieving signs and symptoms and achieving a euthyroid state are the desired outcomes. The method of achieving these outcomes may change over time with the use of antithyroid drugs versus radioactive iodine. 

Euthyroid State of normal thyroid function or hormone activity. 

If thyroidectomy is planned, propylthiouracil (PTU) or methimazole (MMI) is usually given until the patient is biochemically euthyroid (usually 6 to 8 weeks), followed by the addition of iodides (500 mg/day) for 10 to 14 days before surgery to decrease the vascularity of the gland. Levothy-roxine may be added to maintain the euthyroid state while the thiona-mides are continued. 

Iodides are often used as adjunctive therapy to prepare a patient with Graves disease for surgery, to acutely inhibit thyroid hormone release and quickly attain the euthyroid state in severely thyrotoxic patients with cardiac decompensation, or to inhibit thyroid hormone release after RAI therapy. 

The goal of therapy is to destroy overactive thyroid cells, and a single dose of 4,000 to 8,000 rad results in a euthyroid state in 60% of patients at 6 months or less. A second dose of RAI should be given 6 months after the first RAI treatment if the patient remains hyperthyroid. 

TSH and T4 concentrations should both be checked every 6 weeks until a euthyroid state is achieved. An elevated TSH level indicates insufficient replacement. Serum T4 concentrations can be useful in detecting noncompliance, malabsorption, or changes in levothyroxine product bioequivalence. TSH may also be used to help identify noncompliance. 

Replacement therapy of hypothyroidism. Whether primary, i.e caused by thyroid disease, or secondary, i.e resulting from TSH deficiency, hypothyroidism is treated by oral administration of T4. Since too rapid activation of metabolism entails the hazard of cardiac overload (angina pectoris, myocardial infarction), therapy is usually started with low doses and gradually increased. The final maintenance dose required to restore a euthyroid state depends on individual needs (approx. 

IV or IM IV or IM injection can be substituted for the oral dosage form when oral ingestion is precluded for long periods of time. The initial parenteral dosage should be approximately one-half of the previously established oral dosage. A daily maintenance dose of 50 to 100 meg parenterally should suffice to maintain the euthyroid state once established. Close observation of the patient, with individual adjustment of the dosage as needed, is recommended. 

The initial dose for carbimazole or methimazole is 20-60 mg/day until the patient is rendered euthyroid with maintenance therapy of 5-15 mg/day. For propylthiouracil the initial dose is 300 50 mg/day with maintenance doses of 50-150 mg/day. Higher doses are sometimes used in severe disease. Two different treatment regimens may be used (1) titration regimen, to try to achieve a euthyroid state by dose tritation and (2) block-replacement regimen, with... 

Amiodarone inhibits the peripheral and possibly in-trapituitary conversion of thyroxine (T4) to triiodothyronine (Tj) by inhibiting 5 -deiodination. The serum concentration of T4 is increased by a decrease in its clearance, and thyroid synthesis is increased by a reduced suppression of the pituitary thyrotropin T3. The concentration of T3 in the serum decreases, and reverse T3 appears in increased amounts. Despite these changes, most patients appear to be maintained in an euthyroid state. Manifestations of both hypothyroidism and hyperthyroidism have been reported. 

Hypothyroid women frequently have anovulatory cycles and are therefore relatively infertile until restoration of the euthyroid state. This has led to the widespread use of thyroid hormone for infertility, although there is no evidence for its usefulness in infertile euthyroid patients. In a pregnant hypothyroid patient receiving thyroxine, it is extremely important that the daily dose of thyroxine be adequate because early development of the fetal brain depends on maternal thyroxine. In many hypothyroid patients, an increase in the thyroxine dose (about 30-50%) is required to normalize the serum TSH level during pregnancy. Because of the elevated maternal TBG levels and, therefore, elevated total T4 levels, adequate maternal thyroxine dosages warrant maintenance of TSH between 0.5 and 3.0 mll/L and the total T4 at or above the upper range of normal. 

Both the thiouracils and thioimidazoles readily cross the placenta and can cause fetal hypothyroidism, resulting in a slight delay in neurological or bone maturation. Various degrees of goiter have also been observed, even to the extent of severe tracheal compression and death. Antithyroid drug dosage should therefore be reduced to the minimum required to maintain a euthyroid state without supplementation of levothyroxine (93). 

Antithyroid drugs for long-term therapy (C). Thiourea-derivatives (thioamides) inhibit peroxidase and, hence, hormone synthesis. To restore a euthyroid state, two therapeutic principles can be applied in Graves disease (a) monotherapy with a thioamide, with gradual dose reduction as the disease abates (b) administration of high doses of a thioamide, with concurrent administration of thyroxine to offset diminished hormone synthesis. Adverse effects of thioamides are rare, but the possibility of agranulocytosis has to be kept in mind. 

Iodine is are primarily used to induce a euthyroid state before surgery. It increases vascularity and increase the density of the thyroid gland, which decreases postoperative complications. 

Assays of thyroid function Advances in thyroid function tests (TFTs), including the development of sensitive assays for TSH and the use of analog assays that provide a reasonable estimate of the free level, have markedly improved the diagnosis and treatment of thyroid disorders. These assays nonetheless can be misleading, as the TSH level can remain low for weeks to months after a hyperthyroid patient is restored to a euthyroid state and the analog assays of free T can provide misleading results in certain settings such as critical iUness. 

Notes In a comparison of the clinical characteristics at baseline in the patients with iodine restriction, the pretreatment iodine intake in the recovery group (patients who recovered from hypothyroidism to the euthyroid state spontaneously after 12-week iodine restriction) tended to be higher than that of the nonrecovery group (patients who did not recover from hypothyroidism to the euthyroid state after 12-week iodine restriction), but the difference was not statistically significant. ... 

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