Kapronczay Károly szerk.: Orvostörténeti Közlemények 194-195. (Budapest, 2006)

TANULMÁNYOK — ARTICLES - ELEK, Gábor - MÜLLER, Miklós: Ervin Bauer as pathologist

Table 1. Views on the adrenal gland around 1910. It was known that but not yet known that therefore it was assumed that adrenaline is a product of the adrenal gland adrenaline is formed in the medulla of the adrenal gland the precursors of adrenaline are located in the adrenal cortex Addison's disease is caused by pathological processes in the adrenal gland Addison's disease is due to the loss of the function of cortical tissue, its damage or hypoplasy Addison's disease originates in the medulla and its essence is the lack of adrenaline

4 pigment is formed from tyrosine of the proteins under the influence of oxygen the pigment in the reticulate zone of the adrenal cortex is not related to this process the adrenal gland regulates the pigment formation tyrosine is the precursor of adrenaline that is converted to adrenaline by the adrenal gland the pigment formation in Addison's disease is connected with hypophyseal hyperfunction adrenal cortex has a detoxifying function and pigment deposition in Addison's disease is due to the lack of this function silver impregnation is suitable for the detection of nerve fibres

5 argirophilia and argentafllnity are separate phenomena argirophil reactions are as specific as chemical detection In post mortem material Bauer evaluated the weight of adrenal glands, the thickness of adrenal cortex and pigment depositions in the skin and adrenal gland in control subjects and patients with Addison's disease and uremia (Bauer 1918). He was the first to note that in patients with kidney diseases the weight of the adrenal gland increases and the adrenal cortex becomes thicker and more pigmented. In his days the term ^parenchymal nephritis" was used for chronic and terminal kidney diseases (Kaufmann 1922, 1050). Today these changes are explained by the release of renin and angiotensin by the kidney, which can induce directly the production of aldosterone in the reticular zone of the adrenal cortex (and its pigmentation - secondary aldosteronism, DeLellis 1989, 1249, 1259; Nemes 2004, 922; Iványi, 2004, 966, 989; McCance and Huether 1990, 631-632). In addition, adaptive mechanisms elicit increased hypophyseal ACTH production leading to cortical hypertrophy. This understanding has been developed only in the 1940s (Sayers and Sayers 1948). In Addison's disease no cortical hypertrophy can develop, and a thickening of the cortex is due to an independent pathological process (eg. tuberculosis, Kaufmann 1922, 1004). Bauer indeed mentions the presence of tuberculi in the cortex in one patient. In Bauer's summary table some patients are diagnosed as having Addison's disease, while others are listed having „bronzed disease," in fact a synonym for Addison's disease. Bauer arrived at this 3 e.g. Kaufmann 1922, 1000-1005. 4 Gierke 1919, 1070-1071. 5 Bielschowsky 1904, 1905 - see Romeis, 1948, 569.