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Introduction
Introduction
Hyperthyroidism is a common thyroid disease, refers to increased synthesis and secretion of thyroid hormones by the thyroid gland.
The most common causes of hyperthyroidism:
Graves' disease (GD)
Toxic multinodular goiter (TMNG)
Toxic adenoma
There are three therapeutic treatments options for hyperthyroidism:
Thyroid surgery (the oldest option)
Radioactive iodine (RAI)
Antithyroid drugs (ATD) ←
Medications
Medications
The US FDA approval for thioureylene-containing antithyroid medications was issued for :
Propylthiouracil (PTU)
Methimazole (MMI)
Mechanism of action
Mechanism of action
The main mechanism of intrathyroidal action of ATD to inhibit thyroid hormone synthesis is competition with thyroglobulin tyrosine residues for iodination catalyzed by thyroid peroxidase (TPO).
What result is :
A Decrease in the number of monoiodotyrosines and diiodotyrosines.
An Interfere the TPO-catalyzed coupling of iodotyrosines to form the thyroid hormones: 3,5,3'-triiodothyronine (T3) and tetraiodothyronine (T4).
Propylthiouracil (PTU) is known to inhibit the conversion of T4 to T3 catalyzed by type 1 deiodinase in both thyroid and peripheral tissues.
This pathway contributes to nearly one-fifth of serum T3 in normal physiology and at least half in hyperthyroidism.
Pharmacokinetic Properties
Pharmacokinetic Properties
Based on in vitro results, there is no significant difference between the effectiveness (potency) of MMI and PTU in inhibiting TPO-catalyzed reactions. Therefore, the known up to 50 times stronger antithyroid effect of MMI compared to PTU is related to differences in intrathyroid metabolism. MMI has along serum and intrathyroidal half-life. Pharmacokinetic properities for methimazole and propylthiouracil summarized in the table below.
Execration
A significant portion of ATD and its metabolites are excreted into bile.
Due to enterohepatic circulation, the amount of fecal excretion is very small.
Small amounts of ATD and its metabolites are in urine.
Clinical use
Clinical use
Clinical conditions in which ATDs may be used as a temporary or long-term treatment option include:
Hyperthyroidism
Graves' disease (GD)
Toxic multinodular goiter (TMNG)
Radioactive iodine (RAI) in thyrotoxic patients who are elderly or have cardiovascular disease or severe hyperthyroidism
Compared with RAI therapy and surgery, ATD is the most advantageous treatment for GD but is usually the least chosen treatment for TMNG and especially toxic adenomas.
There are two strategies for ATD treatment:
1) The commonly recommended approach, titration regimens for ATD as monotherapy.
2) Block and replace regimen i.e. High-dose ATD in combination with levothyroxine and this increases the incidence of his ATD side effects.
Dose and adminstration
Dose and adminstration
Antithyroid medications are usually taken orally and can be taken rectally. The doses written in the table below are all taken orally.
Interactions
Interactions
Drug-Drug interaction of ATD
Drug-Drug interaction of ATD
Anticoagulant (Blood thinners)
Potential inhibition of vitamin K activity, resulting in increased activity of oral anticoagulants (e.g. warfarin, Coumadin, Jantoven); however, anticoagulant effect of warfarin also may be decreased.
β-Adrenergic blocking agents
Possible increased clearance of β-adrenergic blocking agents with a high extraction ratio during hyperthyroid state.
Digitalis glycosides
Possible increased serum digitalis concentrations when hyperthyroid patients receiving a stable digitalis glycoside regimen become euthyroid (e.g. Digoxin).
Theophylline
Possible decreased theophylline clearance when hyperthyroid patients on a stable theophylline regimen become euthyroid.
Drug-food interaction of ATD
Drug-food interaction of ATD
Ther is no drug-food interaction
Monographs
Monographs
For more information about anti-thyroid drugs see our monographs now by the buttons below:
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