Urinary iodine and thyroid status of New Zealand residents.

OBJECTIVES: The aim of this project was to assess the clinical significance of our low iodine excretions in terms of thyroid hormone status and thyroid volume in an adult population in a low soil iodine area of the South Island of New Zealand. DESIGN AND SETTING: Two-hundred and thirty-three residents of Otago, New Zealand collected two 24 h urine samples for assessment of iodine status. Thyroid status was determined from serum total T(4), TSH and thyroglobulin, and thyroid volumes. Relationships between urinary iodide excretion and measures of thyroid status were determined and subjects were allocated to one of three groups according to low, medium and high iodide excretion, for comparison of thyroid hormones and thyroid volumes. RESULTS: Significant correlations were found for relationships between measures of urinary iodide excretion and thyroid volume and thyroglobulin. Multiple regression analysis of data for subjects divided into three groups according to 24 h urinary iodide excretion (<60, 60-90; >90 microg iodide/day) or iodide/creatinine ratio (<40; 40-60; >60 microg/g Cr) showed significant differences in thyroid volume (P=0.029; P=0.035, respectively) and thyroglobulin (P=0.019; P=0.005, respectively) among the groups. CONCLUSIONS: The results of this study confirm the low iodide excretions of Otago residents, and indicate that the fall in iodine status is being reflected in clinical measures of thyroid status, including enlarged thyroid glands and elevated thyroglobulin. Our observations suggest the possible re-emergence of mild iodine deficiency and goitres in New Zealand. This situation is likely to worsen should iodine intakes continue to fall and continued monitoring of the situation is imperative.

Iodine status of New Zealand residents as assessed by urinary iodide excretion and thyroid hormones.

The aims of this study were (1) to compare various measures of I status, and (2) to assess urinary I and thyroid hormone status of residents of two areas of New Zealand where, before the iodization of salt, goitre was endemic due to low soil I. A total of 189 subjects (102 males, eighty-seven females) were recruited from the Dunedin Blood Transfusion Centre, and 144 (sixty-seven males, seventy-seven females) from the Waikato Blood Transfusion Centre between November 1993 and June 1994. Blood was taken for thyroid hormone assays, and subjects collected a fasting overnight urine specimen, a double-voided fasting urine sample, and a complete 24 h specimen for iodide and creatinine analyses. Positive correlations (P < 0.0001) between daily iodide excretion and iodide concentrations in fasting and double-voided fasting urines, identical median values for iodide concentrations in the three samples, and similar numbers of subjects classified as at risk from I deficiency disorders according to the International Committee for the Control of Iodine Deficiency Disorders/World Health Organization categories (World Health Organization, 1994) confirmed indications from earlier studies that fasting urine samples were suitable for population studies. However 24 h urinary iodide excretion remains the recommended measure for individual I status. Waikato residents excreted more iodide in urine and all measures were significantly greater than for Otago residents. However median urinary iodide excretions for both areas (60 and 76 microgram/d for Otago and Waikato respectively) were considerably lower than those reported previously for New Zealand. Thyroid hormone concentrations were within normal ranges. Our findings suggest that I status of New Zealanders may no longer be considered adequate and may once again be approaching levels of intake associated with clinical I deficiency.