ADDISON'S DISEASE. 349 



evidence that the sympathetic system is not responsible. He also refers to 6 

 eases of Addisson's disease reported by Siinmonds(l3) with adrenal destruction, 

 four of which had normal cceliac plexuses. 



Bittorf(6) in 1908 rejected Wiesel's theoiy and championed the pure adrenal 

 theory contending that disease of the sympathetic system can neither cause 

 Addison's disease nor essentially influence the symptoms. Those cases recorded 

 in the literature as clinically certain cases of Addison's disease without adrenal 

 disease he ascribed to inexact anatomical investigation, and those of adrenal 

 destruction without clinical symptoms he would not recognize. He draws at- 

 tention to the fact, as did v. Neusser, that lack of pigmentation of the skin does 

 not preclude the possibility of Addison's disease and thinks this may account 

 for the failure to make the diagnosis in some cases. According to Bittorf melano- 

 derma and sympathetic changes are the result of adrenal changes, and he mentions 

 the large and richly pigmented adrenals that occur in negros. 



VViesel considers the cortex and the medulla of the adrenal as two separate 

 organs related only topographically, and believes that the function of the cortex 

 is unknown. Bittorf, on the other hand, conceives the mutual physiological 

 interdependence of the two parts and the unity of the organ. According to 

 Bittorf, muscle poisons, and perhaps other similar metabolic products, reach 

 the cortex of the adrenal through its vessels, and there through simple splitting 

 are deprived of their poison ; through a further ^hemieal action in the medulla 

 they are converted into the active substance. 



So at the present day the two opposite views are held. The "adrenal- 

 ists" concede that the changes in the chromaffin system may he present 

 but regard them as secondary or accidental. Those who claim the causa- 

 tive lesions are in the chromaffin system admit that the adrenal medulla 

 may be the initial seat of the disease, but only in so far as it constitutes 

 a part of the system does it produce symptoms. 



Another factor, the importance of which is as yet unknown, is introduced in 

 the frequently noted association of Addison's disease with status lymphaticus. 

 Averbeck(29) noted the condition of lymphatic hyperplasia in his cases of Ad- 

 dison's disease and considered it an essential part of the disease. Star was the 

 first to note persistence of the thymus in Addison's disease, and since then the 

 association of the two diseases has been especially emphasized by Hart, (30) 

 Hedinger,(31) Wiesel,(20) Bittorf,(6) Kahn,(32) and Schridde.(33) Hedinger 

 found status lymphaticus in 7 out of 15 eases of Addison's disease. He con- 

 siders the possibility of their being due to a common cause which is to be found 

 in an imperfect Aniage or in an alteration of the chromaffin system, this latter 

 being suggested by Wiesel's observation of a ease of status lymphaticus with 

 marked hypoplasia of the chromaffin system. Kahn suggests the possibility of 

 the lymphoid hyperplasia being an evidence of reaction to the toxins of Addison's 

 disease. Wiesel in his ease just mentioned attributed the sudden death to the 

 hypoplasia of the chromaffin system rather than to the status lymphaticus. 

 It is now well known that sudden death is a frequent occurrence in status 

 lymphaticus and that many of these cases liave a large thymus gland. These 

 ideas are expressed in the terms "th^inus death" and "status thymo-lymphatieus." 



Schridde(34) has suggested that death may be due to a kind of endogenous 

 poisoning through excessive or disordered function of the thymus. Warthin(35) 

 especially has considered that the thymus causes death mechanically by tracheal 

 compression, particularly in children. That the thymus in status lymphaticus 

 presents no especial features other than that of delayed resolution or sometimes 



