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Obat antitiroid

Mekanisme kerja

Menghambat pembentukan hormon tiroid dengan cara :

• Menghambat pengikatan iodine pada residu tirosil pada tiroglobulin

• Manghambat coupling residu iodotyrosil untuk membentuk

• Menghambat enzim peroksidase shingga menghambat oksidasi iodide atau

grup iodotyrosyl yang dibutuhkan untuk mengubah hormon tiroid menjadi

bentuk aktifnya.

• Menghambat deiodinisasi T4-T3

efek samping

• Agranulositosis

• Granulositopenia

• Rash purpura, urtikaria

• pain and stiffness in the joints, paresthesias, headache, nausea, skin

pigmentation, and loss of hair

• Drug fever, hepatitis, and nephritis are rare

Indikasi :

Digunakan untuk pengobatan hyperthyroid dalam 3 cara :

1. Sebagai terapi definitif, untuk mengontrol penyakit dalam mengantisipasi

remisi spontan pada penyakit grave’s

2. Sebagai tambahan pada terapi radioactive iodine untuk mempercepat

penyembuhan sambil menunggu efek dari radiasi

3. Untuk mengontrol penyakit dalam persiapan pembedahan

Kontraindikasi

• Hipersensitif terhadap obat antitiroid

• Wanita menyusui

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Iodida

Mekanisme kerja

Iodida konsentrasi tinggi tampaknya mempenngaruhi aspek yang penting pada

metabolisme iodine oleh kelenjar tiroid. High concentrations of iodide appear to

influence almost all important aspects of iodine metabolism by the thyroid gland

(Roti and Vagenakis, 2005). The capacity of iodide to limit its own transport has

been mentioned above. Acute inhibition of the synthesis of iodotyrosines and

iodothyronines by iodide also is well known (the Wolff-Chaikoff effect ). This

transient, 2-day inhibition is observed only above critical concentrations of 

intracellular rather than extracellular concentrations of iodide. With time, "escape"

from this inhibition is associated with an adaptive decrease in iodide transport and a

lowered intracellular iodide concentration, most likely due to a decrease in NIS

mRNA and protein (Eng et al., 1999). The mechanism of the acute Wolff-Chaikoff 

effect remains elusive and has been postulated to be due to the generation of 

organic iodo-compounds within the thyroid (Pisarev and Gartner, 2000).

An important clinical effect of high [I-]plasma is inhibition of the release of thyroid

hormone. This action is rapid and efficacious in severe thyrotoxicosis. The effect is

exerted directly on the thyroid gland and can be demonstrated in the euthyroid

subject as well as in the hyperthyroid patient. Studies in a cultured thyroid cell line

suggest that some of the inhibitory effects of iodide on thyrocyte proliferation may

be mediated by actions of iodide on crucial regulatory points in the cell cycle

(Smerdely et al., 1993).

In euthyroid individuals, the administration of doses of iodide from 1.5 to 150 mg

daily results in small decreases in plasma thyroxine and triiodothyronine

concentrations and small compensatory increases in serum TSH values, with all

values remaining in the normal range. However, euthyroid patients with a history of 

a wide variety of underlying thyroid disorders may develop iodine-induced

hypothyroidism when exposed to large amounts of iodine present in many

commonly prescribed drugs ( Table 56-6), and these patients do not escape from the

acute Wolff-Chaikoff effect (Roti et al., 1997). Among the disorders that predispose

patients to iodine-induced hypothyroidism are treated Graves' disease, Hashimoto's

thyroiditis, postpartum lymphocytic thyroiditis, subacute painful thyroiditis, and

lobectomy for benign nodules. The most commonly prescribed iodine-containing

drugs are certain expectorants, topical antiseptics, and radiological contrast agents