Volume 180 - Issue 10
Diagnosis and management of hyperthyroidism and hypothyroidism
Authors: Duncan J Topliss and Creswell J Eastman
Med J Aust 2004; 180 (10): 541-542. || doi: 10.5694/j.1326-5377.2004.tb06068.x
Published online: 17 May 2004
Published online: 17 May 2004
Duncan J Topliss,* Creswell J Eastman†
* Director, Endocrinology and Diabetes, Alfred Hospital, Commercial Road, Melbourne, VIC 3004; † Director, Institute of Clinical Pathology and Medical Research, Westmead Hospital, Sydney, NSW. Duncan.toplissATmed.monash.edu.au
In reply: Jones asks if iodine excretion should be measured routinely in all patients with hypothyroidism in Australia as part of the initial assessment. We do not advocate this for the following reasons.
Urinary iodine estimations are unreliable for assessing individual patients, as urinary iodine levels can vary considerably from day to day with iodine intake. These measurements should be reserved for population studies to provide an overall assessment of iodine nutrition in that population.
In Australia, it is probable that virtually all cases of primary hypothyroidism are caused by chronic autoimmune lymphocytic thyroiditis, ablative therapy for Graves’ disease, or inadequate thyroxine replacement therapy in these conditions, as is the case in the United States and the United Kingdom.1-3 This contention is supported by data from the Busselton (Western Australia) survey on thyroid peroxidase antibody levels,4 which suggest that these antibodies will be of great diagnostic assistance, in contrast to the dubious clinical value of individual measurement of iodine excretion. In support of this view, in a large survey of the US population, where iodine intake has probably fallen similarly but not to the same degree as in Australia, there was no association between low urinary iodine levels and increased serum levels of thyroid stimulating hormone (TSH).5 In that study, the significant association between raised TSH and female sex disappeared after controlling for the presence of thyroid peroxidase antibodies, while the prevalence of clinical hypothyroidism was strongly correlated with positive results for these antibodies.
In Australia, current information indicates that iodine deficiency, where it exists, is mild. The prevalence and regional variation are currently the subject of the National Iodine Nutrition Survey, which is surveying iodine excretion and thyroid size in primary school children. There is no evidence that this mild deficiency is associated with an increased prevalence of hypothyroidism. Jones’s suggestion that iodine deficiency impairs health by a mechanism other than impairment of thyroid function is not supported by any scientific evidence.
Any consideration of advocating routine assessment of iodine status should await the results of the ongoing national study. However, iodine nutrition would appear to be best addressed as a public health issue, by promoting use of iodised salt and ensuring adequate iodine nutrition in pregnant and breastfeeding women and their infants.
References
- Hamburger JI. Factitious elevation of thyrotropin in euthyroid patients. N Engl J Med 1985; 313: 267-268. CHDFIDJF
- Tunbridge WM, Evered DC, Hall R, et al. The spectrum of thyroid disease in a community: the Whickham survey. Clin Endocrinol 1977; 7: 481-493.
- Sawin CT, Geller A, Hershman JM, et al. The aging thyroid. The use of thyroid hormone in older persons. JAMA 1989; 261: 2653-2656. i1083055
- Hawkins BR, Cheah PS, Dawkins RL, et al. Diagnostic significance of thyroid microsomal antibodies in randomly selected population. Lancet 1980; 2: 1057-1059. CHDEJIIC
- Hollowell JG, Staehling NW, Flanders WD, et al. Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). J Clin Endocrinol Metab 2002; 87: 489-499. i1083059