ADDISON'S DISEASE 289 



the theory of chromaphil inadequacy as the cause of Addison's disease 

 w< ,11 Id serve to explain the frequent occurrence of status tliymicolym- 

 phatlcus in patients with the disease, since such individuals have probably 

 had from youth a condition of hypoplasia of the chromaphil tissue, render- 

 ing this tissue more vulnerable to the acquisition of secondary lesions of 

 tuberculosis, etc., which in turn produce sufficient destruction of the 

 suprarenal chromaphil tissue to give rise to the clinical symptoms of the 

 disease. Wiesel (d) has observed that subjects with status tliymicolym- 

 phaticus are especially prone to develop the disease. 



Our inadequate knowledge of the functions of the medulla and of the 

 cortex, or of any possible function of the gland as a whole, renders any 

 satisfactory explanation of the single symptoms of the disease impossible 

 at the present time. Some attempts at an explanation of these have, 

 however, been made. Wiesel (d) has divided the symptoms into two 

 groups: (1) those due to inadequacy of the chromaphil tissue (asthenia, 

 low blood pressure, stenocardia, mental depression, hypoglycemia, and 

 hypo-epinephrinemia) ; (2) those dependent upon a disturbance of the cor- 

 tical tissue (gastro-intestinal symptoms, severe nervous symptoms, 

 cachexia, exitus). The explanation of the pigmentation has proven espe- 

 cially difficult, the more so in view of the fact that the normal process of 

 pigmentation is yet unknown. Wiesel has suggested that it may arise 

 from a disturbance of the sympathetic innervation produced by an auto- 

 intoxication arising from inadequacy of the suprarenal cortex. The pig- 

 ment is generally regarded as belonging to the class of degenerative pig- 

 ments the melanins. Adami(a) has offered an hypothesis which attrib- 

 utes the pigmentation as due to chromaphil tissue inadequacy, assuming 

 that in epinephrin deficiency the tyrosin and other aromatic products of 

 protein decomposition, from which epinephrin may normally be manufac- 

 tured, remain in the tissues and become transformed into melanin by the 

 action of oxidases, Bittorf (fr), similarly, believes that the increase in pig- 

 ment formation is due to the presence in the epithelial cells of an oxidase 

 (tyrosinase) which acts upon the aromatic bodies to form a melanin. The 

 pigmentation has probably never been produced experimentally ( Vin- 

 cent (/)). 



The asthenia has commonly been explained on the basis of chromaphil 

 tissue inadequacy (Wiesel and others). Some writers (Paton(c)), how- 

 ever, attribute it to a loss of cortical function, basing such a view on the 

 results of Biedl's experiments on the skate. The muscular weakness has 

 been frequently produced experimentally by extirpation of the glands. 

 Gruber(d) believes, as a result, of animal experimentation, that epineph- 

 rin exerts some specific action upon fatigued muscle other than that due 

 to mere circulatory changes (vasodilatation of cardiac and skeletal 

 muscles), possibly in the nature of neutralization or destruction of fatigue 

 products. Cannon and Nice observed that epinephrin, injected in small 



