Amiodarone thyroid-stimulating hormone

Of 26 fetuses with hydrops fetalis and supraventricular tachycardias, 25 received transplacental drug therapy prenatal conversion occurred in 15 (82). Nine fetuses were converted to sinus rhythm using either flecainide (n = 7) or amiodarone (n = 2) as first-line therapy, while digoxin either alone or in association with sotalol failed to restore sinus rhythm in all cases. After first-line therapy, supraventricular tachycardia persisted in 10 fetuses, nine of whom received amiodarone alone or in association with digoxin as second-line therapy, and five of whom converted to sinus rhythm. Of 11 neonates who received amiodarone in utero, two developed raised thyroid stimulating hormone concentrations on postnatal days 3-4 they received thyroid hormone and had normal outcomes. 

A patient with a mechanical prosthetic mitral valve is seen in the clinic. He has been stable on 5 mg of warfarin taken every evening. His INRs have been ranging from 2.5 to 2.7 for the past 6 months. He was started on amiodarone 2 weeks ago for an arrhythmia. Today his INR is 5.1 and thyroid-stimulating hormone (TSH) level is 2.1 mlU/L. How does amiodarone play a part in this patient s anticoagulation therapy ... 

Notes. rTs, reverse triiodothyronine T3, triiodothyronine T4, thyroxine TSH, thyroid-stimulating hormone (thyrotropin). Amiodarone has intrinsic effects on the thyroid and thyroid hormone production besides those related to excessive iodine intake, and this means that it induces thyroid dysfunction more frequently than any other iodine-containing pharmaceutical. 

However, these same characteristics make lithium a useful adjunct in the treatment of hyperthyroidism with i l. A 39-year-old woman with Graves disease who may have developed thyrotoxicosis secondary to treatment with amiodarone, an iodine-rich medication [92 ]. She was administered lithium 900mg/day for 12 days to increase uptake. When this was combined with two doses of 0.9 mg of recombinant human thyroid stimulating hormone (rhTSH), there was a fivefold increase in uptake [92 ]. In a retrospective study of 204 hyperthyroid patients (n = 163 Graves disease, n = 26 toxic multinodular goiter, and n=15 solitary toxic thyroid adenoma), 103 patients received alone (median dose 558 MBq) and 101 received 1 with lithium (median... 

Endocrine In patients receiving the minimum dose of amiodarone, thyroid abnormalities were observed at a rate between 14% and 18%. The effects on the thyroid gland are variable. Amiodarone may cause abnormal thyroid function detected only by laboratory test as well as clinically manifested thyroid dysfunction. The mechanism of this adverse effect is complex. Amiodarone inhibits the action of deiodinase and decreases peripheral conversion of thyroid hormones. Moreover, it decreases their renal elimination and inhibits their entry to peripheral tissues. The level of T4 increases by 40% within 1-4 months of amiodarone therapy. The deiodinase activity inhibition can be noticed after 3 months of treatment. It leads to an increase in the level of thyroid stimulating hormones. Amiodarone and its metabolite have a direct cytotoxic effect on thyroid follicular cells, which results in destructive thyroiditis. Amiodarone-induced thyroid damage can lead either to hypo- or hyperthyroidism. The latter can be of two types. Type 1 usually occurs in patients with prior thyroid damage. In this type, iodine excess causes excessive synthesis of thyroid hormones whereas in type 2 the inflammatory process is followed by destruction. A destructive thyroiditis leads to the release of hormones from damaged thyroid follicular cells. This mechanism occurs in patients with no history of thyroid disorders [15]. 

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