Although Hashimoto first described struma lymphomatosa of the thyroid gland nearly 50 years ago,1 the nomenclature, etiology, and classification of this disease are still not clear. It is usually considered a form of thyroiditis, but is not truly inflammatory, since there is a notable absence of acute inflammation, necrosis, and abscess formation. It is characterized by diffuse infiltration of the thyroid gland with lymphoid cells, associated atrophy of the parenchyma, and varying degrees of interstitial fibrosis.2 When not treated it is a progressive disease, occurring almost entirely in females, predominantly in the middle-aged.3
Recent investigations have implicated an autoimmunity type of reaction to be related to the etiology. Raitt and Doniach reported that sera from patients with Hashimoto's disease were high in gamma globulin and caused abnormalities in liver flocculation tests.4 These sera reacted with saline extracts of normal human thyroid tissue to produce a precipitate,