1 62 INTERNAL SECRETION 



organ, whether the destructive process is partial or entire, which 

 produces the typical symptom-complex of Addison's disease. 



Bittorf, like Neusser, adopted the view that derangement of 

 suprarenal function may be caused, not only by disease of the 

 organ itself, but also by a pathological condition of the secretory 

 nerves which regulate its function. Those cases of Addison's 

 disease in which the suprarenals were apparently sound, are 

 readily explicable by the assumption of a primary affection of the 

 secretory nerves. Moreover, as Bittorf points out, and his view- 

 is confirmed by Beitzke, the recent literature of the subject con- 

 tains no conclusive accounts of cases such as these, and he believes 

 that the frequency of the findings is in an inverse ratio to the 

 accuracy with which the cases were observed. 



Cases of one-sided partial destruction of the suprarenals 

 unaccompanied by Addisonian symptoms, are readily explained 

 by the presence, either of functionally active suprarenal tissue in 

 larger or smaller quantities, or of accessory suprarenals. It is 

 a more difficult matter to account for those cases where one-sided 

 suprarenal disease is accompanied by symptoms of Addison's 

 disease. Neusser believes this to be due to the transmitted 

 influence of the diseased organ upon the sound one, but Bittorf 

 believes that the influence is rather chemical. He regards as 

 analogous the "transmitted " anuria which, with other symptoms 

 characteristic of total suprarenal suppression, is seen in one-sided 

 suppression ; and he points moreover to those cases of one- 

 sided suprarenal tuberculosis, where the removal of the diseased 

 capsule is followed by complete cessation of all symptoms of 

 Addison's disease. 



This theory derives no support, however, from the results of- 

 experimental pathology. One-sided suprarenal suppression is 

 not attended here by symptoms of a deranged organic function, 

 and there is no insufficiency of the half of the pair which 

 remains intact. On the contrary, there is rather a functional 

 hyperactivity, which may ultimately be expressed by anatomical 

 hypertrophy, of the sound capsule. It is evident from this that 

 the pathogenesis of Addison's disease, where associated with the 

 destruction of one suprarenal capsule, is in need of further 

 investigation. 



We are in a more favourable situation in regard to those 

 cases, formerly so much discussed, in which, though the clinical 

 signs of Addison's disease are absent, post-mortem examination 

 shows a more or less complete destruction of both suprarenals. 

 As Bittorf with justice points out, these are usually cases where 

 the clinical observation has been faulty, the absence of the 

 pigmentation of the skin in many instances being regarded as 

 sufficient ground for the exclusion of Addison's disease, other 

 clinical signs passing unnoticed. The clinical observation of 

 these cases, if it is to be of value, requires to be scrupulously exact. 



