Q:

What is amiodarone-induced thyrotoxicosis?

0

Mr BK, a 55-year-old male has presented with chief complaints of generalized weakness of 2 months duration, weight loss of two months duration and intermittent palpitation for last 15 days. He is a known case of hypertension on treatment. He had an acute anterior wall myocardial infarction one year ago for which he had to undergo percutaneous transluminal coronary angioplasty. Postcoronary intervention patient developed ventricular tachycardia on three occasions (one in ICU and two times in the ward). For which, he was electroverted and was put on amiodarone (200 mg tablets three times a day since then). Current clinical examination reveals sinus tachycardia with heart rate of 110 per minute, blood pressure is 126/80 mm Hg. He has a grade-1 soft diffuse goiter. On evaluation, his routine hemogram with renal function and liver function tests are normal. His thyroid function test reveals serum T3 of 190 ng/dL (normal range, 80–200 ng/dL), serum T4 of 22 mg/dL (normal range 5.1–14.1 mg/dL) and serum TSH of 0.01 mIU/mL (normal range, 0.27–4.20 mIU/ mL). Serum anti-TPO antibody is within normal range.

What is amiodarone-induced thyrotoxicosis?

All Answers

need an explanation for this answer? contact us directly to get an explanation for this answer

Amiodarone-induced thyrotoxicosis (AIT) occurs in 2–12% of patients on chronic amiodarone treatment depending on the dietary iodine intake of the population.

Type-I AIT: This occurs in patients with preexisting thyroid abnormalities and thyrotoxicosis is believed to result from iodine-induced excessive thyroid hormone synthesis. This is an example of the Jod-Basedow phenomenon. Type-II AIT: In patients with an apparently normal thyroid gland, thyrotoxicosis results from glandular damage with consequent release of preformed thyroid hormones into the circulation. Studies have shown amiodarone to be cytotoxic to FRTL-5 thyroid cells. On histopathology, moderate-to-severe follicular damage and disruption were demonstrated. The finding of markedly elevated serum levels of interleukin-6 (IL-6) in type II AIT patients further supports this destructive-cum-inflammatory process. Thyrotoxicosis in type II AIT patients is usually self-limiting, which may be due to dose-dependent cytotoxic effect of the drug (Table 11.1).

need an explanation for this answer? contact us directly to get an explanation for this answer

total answers (1)

Similar questions


need a help?


find thousands of online teachers now