286 THE INTERNAL SECRETIONS—1920 
acute adrenal irritation; and the adrenal irritation in 
angioneurotic edema appears never to be of a type 
severe enough to overcome local vasodilation until the 
local vasodilators are paralyzed through fatigue. Yet, 
once local vasodilator paralysis has occurred, adrenal 
‘ support of the unopposed vasoconstriction results in a 
severe and long-continued angiospasm and interruption 
of the circulation in the involved area, the end product 
of which is a large, persistent wheal—the true lesion of 
angioneurotic edema. All evidence, therefore, points to 
a primarily predominating vasodilator irritability 
(hyperthyroid phenomenon) to which has been added a 
powerful continuing constricting impulse (hyperadre- 
nal phenomenon) as being the direct causes of angio- 
neurotic edema. 
These facts and circumstances show conclusively the 
endocrine factor in angioneurotic edema, and appear to 
the author to reveal thyro-adrenal irritation as the real 
cause thereof. Neuromuscular fatigue of the vessel 
walls appears to be merely an incidental circumstance 
which makes possible localized vessel-wall permeability 
and the resultant serum oozing. The cause of aug- 
mented vasodilation and reénforced vasoconstriction 
logically must be the real cause of this disorder, which 
might better be known as “Thyro-Adrenal Urticaria,” 
a pluriglandular hypersecretory syndrome. 
An added evidence of the predominance of adrenal 
hypersecretion in this condition lies in the uniform ex- 
istence in angioneurotic edema of a lowered sugar toler- 
ance and a glycosuria of small degree. Animal experi- 
mentation has shown (8) that extreme glycosuria may 
be produced by adrenin injections. 
Treatment: The treatment should be that of mild 
hyperthyroidism and lowered sugar tolerance, plus free 
elimination, alkalies to restore the normal alkali re- 
serve, a large fluid intake, local sedation, and physical 
and mental rest. Many patients are particularly sen- 
