The thyroid in infections and toxemias: Pathological changes in the human gland

Abstract

We have observed that following infections and toxemias of a severe nature, the same changes take place in the human thyroid as occur in the thyroid gland of animals, but to a lesser extent. These changes are loss in colloid, hyperplasia, desquamation of acinous cells and decrease in iodine content. Administration of iodine by mouth is followed by an absorption of iodine by the thyroid glands of patients with exophthalmic goiter, adenomatous goiter (toxic or non-toxic) and normal glands. Injection of lipiodol into the lungs of 2 patients with lung abscesses and bronchiectasis produced a rise in the iodine content of the thyroid gland, to the extent of four or five times normal. This suggests that iodine can be absorbed from lipiodol, since the amount that escaped into the alimentary tract hardly seems sufficient to produce such a pronounced change in the iodine content of the thyroid. It seems probable that the tendency toward recurrence of exophthalmic goiter after operation can be predicted by the iodine content of the gland and its histological response to iodine. Hyperplasia of the type which can scarcely be differentiated from that seen in exophthalmic goiter is not uncommonly found in the thyroid glands of patients dying from acute infections.