ADDISON'S DISEASE 287 



search at the present time, it would seem, do not appear to justify clin- 

 icians in ascribing the clinical symptoms of Addison's disease, in any gen- 

 eral sense, to a diminished epinephrin secretion. 



Concerning the function of the cortex (interrenal system) there is 

 still less exact information. Three important hypotheses have been formu- 

 lated, viz., that the function of the cortex is concerned with (1) the growth 

 and development of the reproductive organs; (2) the neutralization of 

 toxic substances; (3) the internal secretion of the medulla. The view 

 is rather generally held that it is the cortex, and not the medulla, which 

 is essential to life. It is known to be especially rich in lipoids and 

 cholesterin esters, and Elliott has shown that these lipoids are stored and 

 lost under conditions entirely different from those which govern the other 

 fats in the body. There is some reason for suggesting ( Vincent (#)) that 

 these lipoid granules may yield a hormone possibly of the nature of a 

 complex lecithalbumin, which influences the growth and nutrition of cer- 

 tain tissues, especially the organs of reproduction. A pressor substance, 

 not epinephrin, but a cholesterin-like body, has been isolated from the 

 cortical tissue by Voegtlin and Macht. It has also been assumed that the 

 cortex possesses a detoxicating action, to the absence of which many writers 

 have attributed the toxic symptoms frequently noted in the terminal stages 

 of Addison's disease. No experimental evidence has been found^ however, 

 in proof of this detoxicating function of the cortical tissue. 



The composite morphological structure of the suprarenal gland, and 

 the presumably separate functions of the two constituents of the gland 

 substance, have given rise to much speculation as to whether the Addiso- 

 nian syndrome is caused by a destructive lesion primarily of the medullary, 

 or of the cortical tissue, or whether an involvement of both tissues is neces- 

 sary for the production of the symptom-complex. A final conclusion in 

 regard to this question has not been reached, but the work of Wiesel(J) in 

 this connection has proven most significant, and has served to establish the 

 present trend of opinion. This author, in a careful histochemical study 

 of six cases of Addison's disease, observed destruction of the chromaphil 

 tissue in the medulla of the suprarenal and in the sympathetic system* 

 No alterations, or at the most only slight, were found in the cortical tissue. 

 In one case of clinical Addison's disease, in which no lesion of the supra- 

 renal gland was detected at autopsy, he found a complete absence of certain 

 other parts of the chromaphil system (the paraganglionic nodules), and 

 in yet another case of tuberculosis of both suptrarenals, in which the 

 Addisonian syndrome had been absent clinically, he was able to demon- 

 strate hypertrophy of the chromaphil tissue in the sympathetic system. 

 In his opinion, the destructive lesion begins primarily in the chroma- 

 phil tissue, involving the cortex only secondarily. Nor is it necessary, 

 he maintains, that the suprarenal chromaphil tissue (medulla) be dis- 

 eased, since a lesion in the chromaphil tissue outside of the suprarenal 



