THE PANCKEAS AS AN ENDOCRIN GLAND 723 



cells in diabetes mellitus may be an expression of an automatic regulative 

 diminution of function of these especial cells to relieve the insufficient 

 islet apparatus. It is evident that the pathology of diabetes must be 

 extended to a fuller comprehension of the changes in the endocrinal glands 

 and in the sympathetic, and a much broader view than that of "pancreatic 

 disease" be taken. 



Herxheimer (1920) reviews the history of pancreatic diabetes, and 

 concludes that, in opposition to Weichselbaum, Fischer, etc., he must 

 reject the pure islet theory for the explanation of diabetes. He places 

 himself en the side of Lombroso, Koch, Fahr, Frankel, etc., who hold that 

 the internal secretion of the pancreatic acini and that of the closely re- 

 lated islet epithelium are both concerned in carbohydrate metabolism. 

 The latter, which has no connection with the external secretion, plays the 

 chief role. All disturbances affecting both elements of the pancreas, par- 

 ticularly the islets, leading to a marked change in this hormone will cause 

 diabetes. Herxheimer mentions the frequent occurrence of adenomas of 

 the acinar tissue in diabetes, and interprets them as compensatory hyper- 

 plasias for the preservation of the internal secretion. The fact that hyper- 

 trophy and proliferation of the acinar tissue, leading to the formation of 

 atypical lobules of acini, often adenomatous in character, are very fre- 

 quently found in the diabetic pancreas gives color to these views. The 

 writer has found them in all of his autopsy cases of diabetes in which 

 there is a chronic pancreatitis. These formations are undoubtedly those 

 so often interpreted as newly formed islands. In fact, the illustrations 

 given by Opie and others of regenerated islands are nothing more than 

 proliferations of the ducts leading to the new-formation of acinar tissue. 

 Their general appearances often closely resemble superficially the ap- 

 pearances of an islet, but they all contain a lumen and develop centro- 

 acinar cells, and arise from a proliferation of duct epithelium. That new 

 islets develop is not yet positively shown; and the writer has never seen 

 anything in pancreatic pathology to convince him that such a new-forma- 

 tion does occur. 



Etiology of Disturbances of Pancreatic Endocrinal Secretion. Sys- 

 tematic pathologic studies of the pancreas show that morbid changes are 

 of frequent occurrence in this organ. Atrophy, chronic interstitial 

 inflammation, islet degeneration and fibrosis, regeneration and hyper- 

 trophic conditions of the acini, occur in varying degrees of severity in 

 a large number of cases, both in diabetics and non-diabetics. The same 

 pathologic lesions may exist under the two conditions ; there is no qualita- 

 tive specific pathology for diabetes; and a quantitative criterion, while 

 holding for the great majority of diabetic cases, does not hold for all. In 

 some non-diabetic cases the pancreatic changes, including those in the 

 islands, are just as marked as in diabetic cases, while in some cases of 

 diabetes there may be no apparent changes in the pancreas at all, or the 



