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Forty-three patients treated with amiodarone hydrochloride with an average daily dose of 204.7 +/- 79.4 mg/day for a mean period of 37.1 +/- 25.3 months, were studied by clinical examination, chest roentgenograms, pulmonary function tests and blood gas analyses. The habits of cigarette smoking were also recorded and expressed as cigarette pack/years. Pulmonary function tests did not show any differences from control subjects and no correlation was found between exposure to drug and lung function. However, one patient developed abnormalities in the chest X-ray (interstitial type) and a reduction of carbon monoxide diffusion capacity as a possible manifestation of amiodarone lung toxicity. Nine patients (22%) had a 20% decrease from normal in carbon monoxide diffusion capacity and three (7%) had a 15% decrease in total lung capacity. More treated patients had interstitial abnormalities in the chest X-ray (14%) than controls (5.5%). Although pulmonary function test abnormalities could be detected in patients taking amiodarone, they were not usually severe enough to interfere with gas exchange. Our results confirm the rarity of amiodarone lung toxicity when a low dosage is used, and suggest the advisability of periodical monitoring, including clinical examination, chest X-ray and pulmonary function tests in order to detect the earliest signs of amiodarone lung toxicity.

Forty-six patients treated with amiodarone hydrochloride for a mean period of 41 +/- 3.5 months, with an average daily dose of 240 +/- 57 mg/day, have been studied. Thyroid function was assessed clinically and by laboratory tests, which included free-triiodothyronine (free-T3), free-thyroxine (free-T4) and thyrotropin. Antimicrosomal and antithyroglobulin antibodies were also looked for. Three patients (6.5%) were found to be hyperthyroid and two (4.3%) hypothyroid. Of the 41 clinically euthyroid patients, 19 (46.3%) showed one or more abnormalities in the thyroid function tests. In this group, only free-T4 was found significantly increased (p less than 0.05) as compared to both control populations. Antimicrosomal antibodies (titre greater than or equal to 1:1600) were present in 4 of 41 (9.7%) euthyroid patients, but not in hyper- or hypothyroid patients. There were no antithyroglobulin antibodies in any patients. Free hormone measurements have proved to significantly correlate with the clinical picture. Increases in free-T3 and free-T4 are the main features of hyperthyroidism, while a reduction in free-T4 serum level was specific for hypothyroidism. There are probably several mechanisms responsible for hyperthyroidism and some genetically controlled defects in synthesis and release of thyroid hormones might be among these. The presence of antithyroid antibodies could be due to deposits of amiodarone in the thyroid gland, with a consequent release of antigen from the follicle cell, but only in those patients with genetically determined defects in immunological surveillance could an autoimmune thyroiditis, with consequent hypothyroidism, develop.