Abstract
Simple goitre is highly prevalent in New Zealand, and there is considerable incidence of toxic goitre. The ætiology of simple goitre seems fairly well established, and an attempt is being made to apply the data from simple goitre to the problems of toxic goitre.
Endemic goitre is of great antiquity among the Maoris, and has been described among Europeans for about fifty years. It occurs in both men and animals. At five years its incidence is similar in boys and girls, later it decreases in boys but increases greatly in girls. It is often hereditary, and many children are born goitrous. In children it is generally small, but may enlarge and cause pressure, myxœdema and toxicity. Its incidence varies greatly in different districts.
The only cause found consistent with this variation in distribution is lack of iodine in the soil. An inverse ratio has been demonstrated between the iodine content of the soil and the incidence of goitre in school children in thirty-three districts. The iodine content of the soil is reflected in the food raised upon it.
The daily iodine intake was estimated at 35 microgrammes in a non-goitrous, and at 20 microgrammes in a goitrous district.
The amount of iodine involved is infinitesimal, and its intake can be ensured by the use of salt for ordinary consumption, which contains four parts per million of potassium iodide.
Toxic goitre is also frequent: in this connexion, the influence of iodine on the thyroid has been investigated. If starved of iodine the thyroid adapts itself either by increasing its colloid or by a diffuse hyperplasia, both may occur in different parts of the same gland. Simple goitre is the response of the healthy thyroid to iodine deficiency, the responding areas may be diffuse or adenomatous, and degenerations may occur. Such goitres may be treated with iodine, in children re-adjustment to the increased intake is readily made, but in adults long accustomed to a low intake, excess often causes too great hormone production, with toxic symptoms, hence the minimal dose alone is permissible in iodized salt.
Goitre stored with iodine at low pressures may become toxic under stress, and this may be precipitated by iodine. The prevalence of toxic goitre may be partly due to the prescription of iodides in therapeutic doses for common ailments.
Diffuse colloid goitre may subside under physiological iodine, the adenomatous is more prone to toxic symptoms and may go on to secondary Graves' disease or to myxœdema. Diffuse hyperplasia is a possible manifestation of iodine deficiency as primary Graves' disease. Lugol's solution probably allows of a temporary storage in this condition. Iodine has certainly some bearing on the problems of toxic goitre.