THE CRETINIC DEGENERATION 459 



"Seventy-five per cent of all cretins have clinically enlarged thyroids, 

 and, if careful anatomical examinations could be made before the clinical 

 manifestations of cretinism supervened, there can be little doubt that a 

 well-marked active hyperplasia would be found in all cases in which thy- 

 roid tissue was present. It would thus seem that the same nutritional de- 

 ficiency or disturbance which causes the thyroid cells at first to grow and 

 divide, later causes their death when their work and growth energy is 

 exhausted. This process is more evident in myxedema in which the 

 age of the individual allows earlier detection through more careful ob- 

 servations during the early or developmental stage. The colloid is prac- 

 tically absent. The epithelial cells have lost their regular and uniform 

 columnar type characteristic of the early state of active hyperplasia and 

 are irregular in size and shape. There is perhaps some piling up of the 

 epithelial cells and desquamation of the partially degenerated cells. The 

 nuclei are in general large, often hyperchromatic and irregular in size 

 and outline. Nuclear figures are still observed, but the new formation 

 of cells is not, sufficient to offset the cell-death, and the follicles become 

 smaller, though still preserving the infoldings of well developed hyper- 

 plasia. The surrounding fibrous stroma is relatively, perhaps absolutely, 

 increased, and as the follicles become smaller from the death of their 

 secreting cells the fibrous bands appear wider, and finally give the appear- 

 ance of a generalized cirrhosis in which are nests of compressed epithelial 

 cells with or without the outlines of follicles. This interstitial cirrhosis 

 is secondary to and consequent on the death of the epithelial elements. 

 Lymphoid foci are scattered here and there throughout the stroma. This 

 is the simplest picture of the anatomical changes in the thyroid in myx- 

 edema, and those occurring in the cretin thyroid are similar. Most cases, 

 either of myxedema or cretinism, in man do not present so simple an ana- 

 tomical picture for the reason that other processes as cyst formation, hemor- 

 rhage, calcification, adenoma, groups of enlarged follicles filled with des- 

 iccated colloid, etc., may all be crowded into the same gland." 



"Summing up, then, the type of atrophy supervening on active hyper- 

 plasias and clinically associated with myxedema or cretinism is a cell- 

 death due to exhaustion from overwork and malnutrition. The process is 

 simple, -but the anatomical changes in such glands, especially in long-stand- 

 ing cases, are often highly complex." 



This standpoint is supported by a chain of evidence as follows : The 

 observation of Wilson and Kendall of the small amount of active iodin 

 in thyroid adenomata, the demonstration of Marine and Lenhart (c) of the 

 decrease in the amount of iodin in the gland immediately preceding the 

 hyperplastic changes, the parallelism of the degree of cellular increase with 

 the degree and duration of the iodin diminution, the inverse ratio existing 

 between the iodin content and amount of hyperplasia and finally the 



