To the Editor: I wish to add another cause of exogenous hyperthyroidism to those mentioned in the comprehensive review on hyper- and hypothyroidism by Topliss and Eastman.1 Inadvertent ingestion of animal thyroid (“hamburger” thyrotoxicosis), although rare, is worth mentioning. Meat may be inadvertently contaminated with thyroid tissue through the process of “gullet trimming” during butchering. While this process has been prohibited in most countries since the recognition of outbreaks of hamburger thyrotoxicosis,2,3 it may still occur when farm animals or wild game are prepared for consumption by farmers, hunters or local butchers unaware of the prohibition.

I recently reported a case of a woman living on a farm in Canada who had five episodes of transient hyperthyroidism over a decade.4 These were initially diagnosed as episodes of “silent thyroiditis”, but were later attributed to consumption of meat patties contaminated with thyroid tissue, as the local butcher was not aware of the prohibition on gullet trimming. A history of eating wild game or locally prepared meat should be considered before a diagnosis of silent thyroiditis is made. Thyroid uptake of radioiodine is low in both conditions, but serum thyroglobulin level is raised in thyroiditis and decreased during the hyperthyroid phase of exogenous hyperthyroidism.

To the Editor: The recent article on thyroid disorders by Topliss and Eastman notes that “around the world, iodine deficiency still remains the predominant cause of hypothyroidism” and furthermore that “mild iodine deficiency is re-emerging in Australia”.1 Indeed, the Journal has recently published at least two articles suggesting that the iodine status of the Australian population needs to be further explored.2,3

My question therefore is: when treating a patient who has results indicating clinical or subclinical hypothyroidism, would it be relevant and important to test for iodine deficiency (by 24-hour urine collection)? This seems analogous to undertaking iron studies in a patient with a falling haemoglobin level. In the same way that iron deficiency can exist and produce symptoms, even in the absence of anaemia, may not iodine deficiency affect health and well-being? Without the elemental “building blocks” of iron and iodine, the relevant systems are put into overdrive to no avail.

It seems simple to test routinely for this possibility, correct any deficiency and then recheck thyroid function. There may be more “clinically significant iodine deficiency” than we realise.

As it will no doubt be some time until further studies in the Australian population shed more light on this, is it not relevant meanwhile to at least check for this possibility in individual patients?

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.