314 CLINICAL CONSIDERATIONS 



diagnosis of Addison's disease based solely on the occurrence 

 of pigmentation and asthenia, as frequently made, is open to 

 error. In the recent compilations only rare cases have been 

 reported of normal glands and the clinical history and autopsy 

 reports in these cases are not entirely convincing. 417 It is pos- 

 sible, of course, that disease of neighboring organs {e.g., malig- 

 nant involvement of the solar plexus 54 ) may lead to an acute 

 suppression of the secretion of the vital hormone without gross 

 anatomical evidence of disease of the adrenals. 



The adrenals of patients dying of the disease show almost 

 complete destruction of both cortex and medulla or cortex 

 alone, depending, as shall be described in subsequent sections, 

 on the type of lesion encountered. 417 



In Barker's 39 series of 73 cases of disease of the adrenals of 

 diverse etiology, in which the cortex remaining comprised ap- 

 proximately 10 to 50 per cent of the normal amount of tissue, 

 no clinical symptoms of Addison's disease were evident during 

 life. It was only when at least 90 per cent of the cortical tissue 

 had been destroyed that clinical symptoms became prominent. 

 Latent symptoms may possibly be present without such ex- 

 tensive destruction but have not been noted clinically. In 

 many cases of adrenal atrophy only the cortex is involved and 

 the medulla remains almost intact. 668 



Accessory interrenal tissue (cf. Chapter IV) is rarely en- 

 countered except in the intimate neighborhood of the main 

 glands. Hence pathological involvement of the adrenals usu- 

 ally involves these accessories and it is extremely rare for such 

 accessory tissue to prevent the appearance of symptoms of 

 Addison's disease. In the early stages of disease, particularly 

 in cases of so-called adrenal atrophy, the healthy tissue hyper- 

 trophies forming adenomatous nodules but these are ultimately 

 involved in the destructive process which caused the initial 

 lesion. 



In an analyses of 566 cases of Addison's disease collected 

 from the literature over the period 1900 to 1930, Guttman 260 



