Cortisone-Ascorbic Acid Interaction and the Pathogenesis of Amyloidosis

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Abstract
The various methods of exptly. producing amyloidosis are reviewed. A scorbutogenic diet fed to guinea pigs produced amyloid in 8 weeks or longer. This amyloid is not a uniform chemical substance, but a series of closely-related protein compounds. The 2 processes that appear to be of importance in development of amyloids were: (a) the disturbance of the colloidal stability of the plasma and (b) formation of new plasma proteins of the alpha, beta and gamma types. In mice, previously treated for several weeks with injns. of casein, insufficient to produce amyloidosis, injns. of cortisone promptly resulted in the appearance of amyloid in the spleen. This same effect is produced in rabbits, hyperimmunized for many mos. with killed Pfeiffer bacillus culture. The antagonistic effects of cortisone on the mesenchymal tissue is also evidenced by vit. C deficiency. There is an inhibition of all connective tissue elements produced either by vit. C deficiency or by cortisone. The antagonistic effects of ascorbic acid and cortisone are also evidence of exptl. amyloidosis and ribonucleic acid synthesis. The established antagonistic effects of cortisone and ascorbic acid on mesenchymal tissue can be explained as an interaction of ascorbic acid and a hormone of the adrenal cortex of the cortisone type which control the accumulation of plasma cells in the reticulo-endothelial system, elevation of gamma globulin values in the serum by pyroninophilic (ribonucleic acid synthesis) mesenchymal cells in various organs and tissue, and in many cases by metachromatic extra-cellular material.

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