No abstract

Iodine kinetic studies were performed serially in 15 patients taking 300 mg amiodarone/day for 6 months to assess the biological significance of the high iodine content of the drug. Urinary inorganic iodide excretion increased from 0.25 +/- 0.03 (+/- SE) mumol/mmol creatinine before treatment to over 7 mumol/mmol during therapy. Thyroid iodide clearance fell from 5.93 +/- 0.82 ml/min to less than 0.5 ml/min, while plasma inorganic iodide rose from 0.05 +/- 0.01 mumol/liter to approximately 2.2 mumol/liter during treatment. Thyroid absolute iodide uptake rose from 16.3 +/- 2.7 to 54.6 +/- 5.7 nmol/h after 6 weeks of therapy (P less than 0.001). Thereafter, it progressively declined, but it was still significantly elevated (32.0 +/- 4.3 nmol/h) after 24 weeks (P less than 0.01). The calculated daily excretion of inorganic iodide rose to over 80 mumol during the study, accounting for about 10% of amiodarone iodine. During this time, the patients all had the characteristic plasma thyroid hormone changes associated with amiodarone therapy, i.e. increased T4, free T4, and rT3 and decreased T3, while remaining clinically euthyroid. The massive increase in available inorganic iodide during amiodarone treatment is probably responsible for the induction of both the hypothyroidism and the thyrotoxicosis that can occur in patients receiving the drug.

SUMMARY The response to the subcutaneous injection of glucagon (1 mg) has been studied as a test of the ability of the pituitary to secrete ACTH and growth hormone (GH). Tests have been performed on fifteen normal subjects or patients with unrelated conditions, nine patients with pituitary tumours and seventeen with acromegaly. It is suggested that a normal response is a peak level of 5 ng/ml or more of GH (standard NIH GH 1216C) and either a rise of plasma cortisol measured by competitive protein binding of at least 4 μg/100 ml or a peak level of 7 μg/100 ml. In seventeen patients the responses were compared with those obtained in the insulin hypoglycaemia test and there was good agreement. Measurement of plasma ACTH showed that the response is at pituitary and not adrenal cortical level. Peak responses of ACTH and GH were obtrained at 150 min and of cortisol at 180 min. Plasma glucagon concentrations were falling steadily by this time although still above the control level. The mechanism of action of glucagon is not clear but does not appear to be related to fall of blood sugar. The subcutaneous injection of glucagon is not without side effects; about half the patients were nauseated and nine vomited. Nevertheless we believe that a subcutaneous glucagon test is of value for testing the pituitary reserve of ACTH and GH in situations where insulin hypoglycaemia cannot be used.