No abstract

(1) Congenital syphilitic pancreatitis retards the development of the glandular acini but does not affect the islands of Langerhans. Embedded in the stroma, but not invaded by it, the latter maintain their continuity with the small ducts and acini with which they have a common origin. (2) Two types of chronic interstitial inflammation affecting the developed pancreas are distinguishable: (a) Interlobular Pancreatitis.—In the interlobular variety the inflammatory process is localized chiefly at the periphery of the lobule and implicates the islands of Langerhans only when the sclerotic process has reached a very advanced grade. When pancreatitis has followed obstruction of the ducts, the islands long remain unaltered though embedded in dense scar-like tissue. (b) Interacinar Pancreatitis.—In the interacinar type the process is diffuse, invading the lobules and separating individual acini. The inflammatory change invades the islands of Langerhans. (3) A relationship has been observed between lesions of the islands of Langerhans and the occurrence of diabetes mellitus. (a) In one of eleven cases of interlobular panereatitis diabetes of mild intensity occurred. The sclerosis, which in this case followed obstruction of the ducts by calculi, was far advanced and affected the islands of Langerhans. (b) In two of three cases of interacinar pancreatitis, diabetes was present. The third case was associated with a condition, hæmochromatosis, which at a later stage is associated with diabetes, the result of pancreatic lesion. (c) In a fourth case of diabetes, hyaline deposit between the capillaries and the parenchymatous cells had so completely altered the islands of Langerhans that they were no longer recognizable.

Necrosis of the skin was produced by the injection of measured quantities of electrolytes and of amino compounds into the dermis, and the relative ability of these substances to produce it was determined. Inflammation characterized by edema and accumulation of leucocytes accompanied necrosis. The ability of electrolytes to produce necrosis was found to increase with the valence of their basic ion, and in this respect was in accord with their ability to denature proteins. The quantity of different electrolytes needed to produce necrosis varied in the same order as the molar concentration of these electrolytes, that is isotonic with liver or kidney cells. Necrosis caused by amino compounds occurred with similar relation to the isotonicity of liver cells. In this as in other relations the cells acted as osmometers. The foregoing relations indicate that denaturation of proteins, necrosis of living tissue, and osmotic activity of liver or kidney cells are determined by molecular weight, valence, and ion-dissociation of electrolytes, that is, by the factors that determine the colligative properties of electrolytes. Agents such as turpentine, mustard, or croton oil and some halogen substitution compounds of methyl that are insoluble in water and soluble in lipoids have produced skin necrosis and inflammation.