2TO J. J. MACKENZIE 



striking abnormality that it is extremely likely that a correct interpreta- 

 tion would ^hrow a flood of light not only upon morbus Addisonii but also 

 upon the whole question of suprarenal function. There is evidence that 

 pigment production may be related to epinephrin. Melanin-like pigments 

 can be produced by the action of oxydase ferments (tyrosinase) upon 

 tyrosin and similar substances. Jaeger considered epinephrin to be the 

 source of melanin pigments. Roger (6) recently has demonstrated a chro- 

 mogen in horse suprarenals, which in the presence of oxygen gives a black 

 material insoluble in alcohol and nondialyzable. He suggests that this 

 black pigment is the cause of the pigmentation of Addison's disease and 

 that in normal subjects the gland abstracts the pigment and converts it 

 into its chromogen. This, however, is pure hypothesis and the difficulty 

 of correlating Addison pigmentation with epinephrin or similar substances 

 is that it is just in the cases in which we know there must be diminished 

 epinephrin secretion that the pigment appears. That it is due to local 

 cell metabolism, possibly of an oxidative character, upon substances in the 

 general circulation is indicated by the effect of pressure and irritation 

 upon the development of the pigmentation of the skin. The common cause 

 of Addison's disease is of course tuberculosis, but numerous cases are 

 reported in which the suprarenal destruction has been produced by other 

 pathological conditions, such as syphilis, hemorrhage or new growths. 



Tumors of the Suprarenals. From the cortex tumors arise which 

 more or less resemble normal cortical tissue depending upon the degree of 

 anaplastic alteration which has developed. There is possibly an unbroken 

 series between hyperplasia of the cortex through cortical adenomata (in 

 well marked examples Yirchow's(fr) struma suprarenalis) to the true su- 

 prarenal hypernephromata which are definitely malignant. 



Sarcomata, lymphosarcomata, alveolar sarcomata, endotheliomata of 

 the cortex have been described. In many instances the description of 

 these tumors leaves one in doubt as to whether they are to be regarded as 

 true sarcomata or as hypernephromata with an excessive degree of ana- 

 plastic change. Woolley(a) in 1902 described a malignant tumor originat- 

 ing from the suprarenal cortex which locally showed the characters of a true 

 hypernephroma but which in its distant metastases had the appearance 

 of a true sarcoma. He and Adami(&) would designate such tumors as 

 mesotheliomata and explain this extreme anaplasia as due to a reversion 

 of the colls to the original mesoblastic type. The hypernephromata are 

 well established. They usually show in the gross a strikingly variegated 

 appearance; the general tone is yellow but areas of hemorrhagic change 

 with various tints of brown and red are seen throughout it : microscopically 

 the tumor is made up of cells with a foamy protoplasm due to the presence 

 of lipoids and glycogen droplets. The cells more or less mimic the zona 

 glomerulosa or zona fasciculata of the normal gland with irregular 

 columns of cells resting upon sinusoidal blood vessels. There is a great 



