THE PATHOGENESIS OF BRONZING; ADDISON'S DISEASE. 



81 



viously stated tends to show that one-twentieth of both glands 

 suffices for the continuation of those functions for a given time. 



In the light of all that has been incorporated in this work 

 so far, these cases suggest an explanation of the causes of 

 bronzing which it might be well to outline before going any 

 farther. Collectively considered, the data alluded to suggest 

 that any case of suprarenal disease may proceed to death without 

 reaching the stage of bronzing, for, in all instances in which this 

 symptom occurs, the suprarenal insufficiency, whether due to 

 intrinsic or extrinsic disease, must have reached a correspond- 

 ingly advanced stage. Disease of any structure which directly 

 or indirectly nourishes or innervates the adrenals, or any or- 

 ganic lesion of the organs themselves, can thus inaugurate a 

 condition that will lead to their physiological insufficiency both 

 quantitative and qualitative. But, and this is the important 

 feature: the integrity of the organs must be greatly compromised 

 before their all-important functions become implicated in the mor- 

 bid process so great is the supply of cellular reserve which 

 Nature has granted them, or so small perhaps, in proportion 

 to its potency, is the amount of secretion required to satisfy 

 the needs of the systemic functions which they normally sup- 

 ply. It is only when this minimum limit of normal activity is 

 passed that the stage of bronzing begins, preceded or soon fol- 

 lowed by the earlier symptoms of Addison's disease. The latter 

 would thus represent but an advanced stage of slowly pro- 

 gressive suprarenal insufficiency brought on by a pathogenic 

 cause of any kind. 



The application of this conception to the many paradoxical 

 phases which Addison's disease presents in respect to its main 

 symptom, bronzing, singularly clears the field, besides afford- 

 ing a basis for all the theories, based on careful study, which 

 have been advanced so far concerning the origin of this 

 symptom. 



If Lewin's proportion of caseous glands in Addison's dis- 

 ease, 74 per cent., and Oilman's, 80 per cent., are considered 

 collectively, i.e., 77 per cent., we are only obliged to account 

 for 23 out of 100 cases which do not present tuberculous 

 lesions of the adrenals. For this purpose we have at our dis- 

 posal all the diseases to which the nervous, vascular, and lym- 



