THE THYROID APPARATUS IOI 



assumption that the toxins pass into the milk (Lanz), was pre- 

 pared from the milk of thyroidectomized goats, were at one 

 time very widely employed, and, it is said, with good result. 

 But the earlier enthusiasm for this method appears to have some- 

 what abated; at least, very little has latterly been heard of it. 



Isolated attempts have also been made to treat Graves's 

 disease by means of thyrotoxic immune serum (Thompson, 

 Stradiotti). 



From the nature of the evidence before us, the etiological 

 relationship between Graves's disease and the thyroid gland cannot 

 any longer be doubted. The further question, as to whether the 

 etiological factor is to be found in a quantitatively increased 

 secretion, a hyperthyrosis, or in a qualitatively altered secre- 

 tion, a dysthyrosis, is not so easily answered. Although the 

 greater number of facts appear to be in favour of hyperfunction, 

 yet the absence of any histological signs of an increased secretion, 

 the failure of all attempts to produce a complete clinical picture of 

 Graves's disease by means of experimental hyperthyroidization, 

 and more particularly, the not infrequent occurrence of symptoms 

 of thyroid insufficiency in Graves's disease, are factors not readily 

 explained by a theory of hyperfunction. According to Moebius's 

 theory, the thyroid secretion of Graves's disease is not only 

 increased, but it is also perverted. 



Nevertheless, an increased knowledge of the nature of thyroid 

 secretion and, more particularly, of its chemical composition 

 and physiological activity, together with a more accurate analysis 

 of the clinical symptoms and of their significance, renders the 

 probability of a dysthyroidism in Graves's disease more and more 

 remote. As Kraus points out, this is a problem which, for the 

 present at any rate, cannot be explained beyond a certain point. 



The evidence in favour of a qualitative change in the nature 

 of the thyroid secretion is becoming gradually less significant. 

 The absence of any signs of hypersecretion, more particularly 

 the small amount of iodine present in the goitres of Graves's 

 disease, is sufficiently explained by the assumption of an 

 abnormally small capacity on the part of the gland for the fixation 

 of iodine, and by the over-rapidity with which the active substance 

 is expended (Kocher, Kraus). The failure of hyperthyroidization 

 to produce the entire symptom-complex of Graves's disease in 

 animals, can scarcely be regarded as unequivocal evidence, when 

 we remember that by the methods employed, only very imperfect 

 imitations of the clinical conditions as seen in man were repro- 

 duced. The positive results of experiments with animals have a 

 much greater value in their relation to individual cardinal 

 symptoms. With regard to the symptoms of thyroid insufficiency 

 sometimes encountered in Graves's disease, it must be remembered 

 that similar phenomena are seen in pathological affections of other 

 internal secretory organs as, for instance, the hypophysis and the 



