DISTURBANCES OF PANCREATIC METABOLISM 673 



broso(&)). The same holds good for human cases in instances of patho- 

 logical duct obstruction (Orlowski, Gross (c), Pratt (6), Tileston, Crohn 

 (6), Matko and others). 



Three main conclusions may be drawn from the reports in the litera- 

 ture regarding the metabolism of digestion and absorption in pancreatic 

 disease. 



1. The nature of the disease does not determine the degree of 

 fat and nitrogen disturbance. 



2. The amount of food absorption is independent of the patency 

 of the duct, or the activity of the external secretion of the gland. 



3. The degree of interference with intestinal absorption is de- 

 pendent upon the extent of destruction of the parenchyma of the 

 gland. 



4. That by means of an internal secretion the pancreas controls 

 absorption or at least complements the digestion and absorption 

 capacity of its external secretion. 



Conclusions 1 and 2 are based upon experimental as well as clinical 

 evidence. The most difficult obstacle to overcome to its acceptance is 

 the work of Pratt, Lamson and Marks and also Hess(&). Yet the former 

 assert that a rapid and complete atrophy of the gland followed its separa- 

 tion from the intestine, and it is therefore more logical to attribute to 

 this atrophy the disturbances that follow. 



As regards conclusions 3 and 4, could one demonstrate a direct 

 proportion between parenchyma disorganization and interference with 

 absorption, the solution of the problem would be materially advanced. 

 Such exceptions as could or would be advanced against this conclusion 

 would be in the nature of citation of cases wherein normal or good ab- 

 sorption was maintained in the face of the destruction of almost all the 

 gland. Such exceptional instances can be explained only on one basis, 

 namely, that small remnants of parenchyma can and often do succeed in 

 preventing metabolism imbalance. Not the amount alone, nor the size, 

 of the surviving fraction of tissue, but its functional activity is the de- 

 ciding factor, a point which is amply verified by the experiments of Lom- 

 broso(a), Fleckseder, Niemann and others, and clinically by the cases of 

 Walker, Keuthe, O. Gross (a) and others. 



Conversely, the phenomenon of emaciation and fatty and nitrogenous 

 stools when a large amount of pancreatic tissue survives the disease, is 

 again explainable only upon the functional inactivity of the surviving gland 

 tissue. Thus to the above conclusion should be added a fifth, namely, 

 that the degree of disturbance is proportional not alone to the extent of the 

 damages to the parenchyma but also to the functional ability of the sw- 

 viving fragment to compensate for the loss. 



