460 NELSON W. JANNEY 



absolute chemical identification of the iodin as a large part (over '60 

 per cent) o^the molecule of the thyroid hormone (Kendall (i) ). It may 

 therefore be regarded as probable almost to the point of actual demon*- 

 stration that thyroid hyperplasia and hypertrophy is a compensatory and 

 not an idiopathic process requiring highly theoretical hypotheses for its 

 explanation. According to Marine and Lenhart's important investigations 

 there may ensue during the early phases of hyperplasia a quantitative 

 increase of thyroid hormone secretion into the blood stream which, how- 

 ever, merely compensates for the decreased qualitative efficiency of the 

 same. From this new viewpoint, all thyroid hyperplasias except the physi- 

 ological (goiter of pregnancy, etc.), indicate decreased thyroid function 

 per integral unit of the thyroid gland. 



Thus we are faced with a new conception of thyroid pathology which 

 is diametrically opposed to Mobius and Kocher's original conception of 

 hyperthyroidism as the antithesis of hypothyroidism. A discussion of the 

 hyperfunctional theory of exophthalmic goiter lies beyond the limits of 

 the present treatise. It may suffice to state that there are grave ob- 

 jections to this viewpoint, also that the hypertrophy of the gland in thyro- 

 toxicosis may with propriety be accounted for by a subfunctional or dys- 

 functional hypothesis. (See the excellent discussion of the pathogenic 

 theories of Graves' disease by C. P. Howard in a chapter of the present 

 work.) 



Hypertrophy and hyperplasia of the gland is, as stated, the primary 

 reaction to the toxic agent. According to McCarrison (a), the first changes 

 include an increase in height of the vesicular epithelium, increase in the 

 number of vesicular and parenchyma cells, formation of new vesicles. 

 The vessels become enlarged and congested, the colloid is absorbed, the 

 multiplying cells show unusual variations in size and shape, also mitotic 

 figures. The- vesicles become irregular in outline. An increase in fibrous 

 stronia and lymphoid cells ensues. This process is both compensatory and 

 of a chronic inflammatory nature. If now the toxic causative agent abates, 

 the colloid goiter develops. Growth ceases and colloid is again stored up. 

 True colloid glands are "physiologically normal and anatomically abnor- 

 mal" (Marine and Lenhart). They are distinguished from normal glands 

 only by their size and their showing signs of previous hypertrophy. In- 

 dividuals with such thyroids do not develop hypothyroid signs and symp- 

 toms, but such may have appeared previously. 



If, however, the original toxic agent continues its action, the harm- 

 less colloid goiter just mentioned may fail to develop and the hyperplastic 

 processes Income overshadowed by the atrophic. A colloid goiter at first 

 fully compensated as to function may on further toxic or infectious insult, 

 .secondarily, lose much of its functionating tissue and hypothyroidism 

 result (goitrously degenerated thyroids of cretins). Goiters are subject 

 to various retrogressive processes, including cloudy swelling, hyaline, cal- 



