302 C. P. HOWAED 



tion of the products of degeneration in the adenomata or in the thyroid 

 itself. Ligation of the vessels does not result in the marked improvement 

 that occurs in exophthalmic goiter from this procedure. However, in 

 Judd's opinion iodin seems to increase the symptoms of the thyrotoxic 

 patient. We believe that this group of thyrotoxicoses could also be covered 

 by the term dysthyroidism to distinguish it from the characteristic picture 

 of Graves' disease. 



As has been succinctly expressed in a recent editorial by Hoskins, 

 "The trend of literature of recent years is towards a conclusion that 

 Graves' disease is essentially a hyperthyroidism." Most writers use the 

 terms interchangeably. As has been said the most important justification 

 of the practice is the high protein metabolism in both the clinical syndrome 

 and the experimental hyperthyroidism in contrast to the greatly reduced 

 nitrogen metabolism of both the clinical and the experimental hypothyroid- 

 ism. Hoskins believes that the simplest explanation of these facts is 

 that the thyroid furnishes a hormone which serves as a general cell stim- 1 

 ulant ; in the event of a diminution of this stimulant the cell functions at a 

 reduced rate. 'But why should an organism or a cell be intrinsically 

 adjusted to a low level and be dependent upon a stimulant to keep it up 

 to normal ( The true explanation is not probably so simple. 



The crucial test as to whether or not Graves' disease is the result 

 of pure hyperthyroidism would be to reproduce the symptomatology of 

 hyperthyroidism by the administration of thyroid gland or its extract. 

 Crotti concludes that this has been satisfactorily done, though the majority 

 of the students of this subject are not yet convinced. 



The coexistence of Graves' disease simultaneously with hypothyroidism 

 which has been reported as occurring not infrequently by many authors, 

 renders untenable the theory that Graves' disease is a simple hyper- 

 thyroidism. Thyroid secretion cannot be both increased and decreased at 

 the same time. Xo explanation of this paradox as yet submitted suffices 

 to controvert this fact. 



Furthermore, eases in which thyroid medication has proved of benefit 

 in Graves' disease have been reported from time to time. Such in 

 substance is the presentation by Hoskins of this dilemma. 



Janney (b) offers an alternate theory a dysfunction of the thyroid 

 gland as the eause of Graves' disease. He believes, therefore, that there 

 is a toxic element in Graves' disease, the toxin being derived possibly from 

 the thyroid hormone which might be readily split into intermediate decom- 

 position products, one or more of which may be toxic. Ordinarily this 

 hypothetical toxic substance would be further acted on in the thyroid 

 gland itself and lie discharged thence only in some harmless or even 

 beneficial form. But, writes Janney, "it is possible that various factors 

 might disturb the normal synthesis of the hormone, the result being the 

 premature discharge of the toxic intermediary product into the circula- 



