Showing papers by "Garth J. S. Cooper published in 1984"

Iodine intake in an urban environment: a study of urine iodide excretion in Auckland.

Abstract: Dietary iodine intake was estimated by measurement of iodide in random overnight 12 hr and 24 hr urine samples. Urinary iodide excretion was measured in 231 healthy females comprising 127 female secondary students (ages 16-19), 27 female tertiary students (17-23 yr), 42 female laundry workers (18-52 yr) and 26 pregnant women in the third trimester (18-40 yr). Urine iodide excretion was also examined in a group of 28 patients attending a thyroid clinic, with thyroid disease of diverse aetiology and in 34 patients taking the antiarrhythmic drug amiodarone for control of cardiac arrhythmias. The mean daily urine iodide excretion was 2.4 mumol/day (0.9-5.8 mumol/day) and iodide to creatinine ratio 0.21 mumol/mmol (0.09-0.29). Iodine deficiency (less than 0.4 mumol/day) was not observed in any subject. Excessive iodine (greater than 8 mumol/day) was found only in patients known to be taking iodine-containing drugs and in one normal individual. The urine iodide was normal in 154 female students, 14 of whom had a trivial thyroid enlargement. The study suggests that dietary sources other than iodised salt contribute significantly to dietary iodine intake and that residual goitre in the community is not secondary to deficiency or excess of dietary iodine.

Iodide excretion in a salt-restriction trial.

Abstract: Twenty-four hour urinary iodide excretion was measured twice, with a four month interval, in 133 individuals who were in a 12-month salt-restriction study in an area where iodine-deficiency goitre was once common and where most household salt is iodised. Half the subjects were salt restricted; their mean 24 h sodium excretion after eight months was 89 mmol for men and 73 mmol for women. Iodide excretion correlated with sodium excretion in the whole group on each occasion. After eight months mean 24 h iodide excretion in the salt-restricted group (men 1.3 SD 0.6 mumol, women 1.1 SD 0.4 mumol) was lower (p less than 0.01) than that in the control group (men 1.8 SD 0.8 mumol, women 1.7 SD 0.8 mumol), but was reasonable in terms of recommended dietary allowances (1.2 mumol, 150 mg). Mean iodide content of local milk was 1.3 mumol/l. Any salt that is used in the home should continue to be iodised. However, it has become unnecessary in this population to use salt (ie, iodised salt) simply in order to avoid iodine deficiency, so long as other foodstuffs continue to contain iodine as at present. As the other sources of iodine may be subject to change, the adequacy of intake of iodine from these sources should be monitored from time to time in samples of the population.

Goitre and thyroid dysfunction during chronic amiodarone treatment

Abstract: We measured thyroid function in a cross-sectional survey of 37 unselected patients receiving chronic amiodarone treatment. Palpable goitre was presented in 17 patients and was a new finding in ten. Despite frequent elevations of serum free T4 (67%) or free T4 index (43%), all 37 patients were clinically euthyroid with a normal or decreased serum free T3 or free T3 index. Mean urine iodide/creatinine excretion was increased 13-fold. Three patterns of thyroid function were seen; in 21 patients with normal TRH responses, the mean basal serum TSH was significantly elevated. Five patients had biochemical hypothyroidism which did not require treatment. Eleven patients had evidence of thyroid autonomy and the three patients with absent TRH responses each gave a past history of goitre or thyrotoxicosis; a trial of carbimazole treatment in these three was without clinical benefit. The observed spectrum of subclinical goitre and thyroid dysfunction may result from an unpredictable thyroid response to excessive free iodide combined with a weak goitrogenic effect of amiodarone mediated by increased TSH secretion.