PATHOLOGICAL ANATOMY 241 



mately the case. The symptoms which have been recognized as consequences 

 of diseases of the other blood-vessel glands are generally absent in the clinical 

 picture of acromegalia; or, if they do occur, they represent distinct compli- 

 cations, and the characteristic changes of acromegalia are not produced by 

 disease of any of them. Finally, the especial, peculiar, histological structure 

 of the hypophysial disease favors the opinion that this plays a role entirely 

 different from that of the other blood-vessel glands. 



In so far as we can arrive at logical conclusions by exclusion and without 

 experiment, we may maintain the view which was first expressed by Pierre 

 Marie that disease of the hypophysis is the etiologic factor in acromegalia. 



We will now consider in what manner the hypophysis causes the disease. 

 The original view of Pierre Marie that the changes are due to an absence 

 of function of the degenerated hypophysis — as in myxedema by an absence of 

 function of the thyreoid — is not substantiated by our more exact knowledge of 

 the character of the glandular proliferation. Somewhat more reasonable and 

 better founded are the hypotheses of Hansemann and UthofE, who hold that 

 the relation between the enlargement of the hypophysis and the affected parts 

 is an altruistic hyperplasia. In whatever way the progressive development of 

 the hypophysis is produced, in that way the progressive development of other 

 parts (extremities, bones of the face and internal organs) is also brought 

 about. According to Hansemann, altruistic hyperplasia may occur with organs 

 that have an embryologic connection, as between the anterior lobe of the hypoph- 

 ysis and the tongue, but we can hardly say that there is any such relation 

 between the gland and the extremities. This view becomes even less tenable 

 when it is clearly demonstrated that neither the changes of the hypophysis 

 nor those of the extremity represent simple progessive hyperplasia, and that 

 in both we are dealing with new tumor-like formations of entirely atypical 

 nature. 



In my previously published articles, I have accepted the view of Tamburini, 

 as do also Hanau and Woods Hutchinson, that the pathologic development of 

 the hypophysis is due to a hyperactivity and over-production of the secre- 

 tion which is to be utilized internally. Tamburini, at any rate, attributes 

 the phenomena of growth to these causes, while the cachexia observed in the 

 later stages of the disease is regarded as a consequence of the adenomatous 

 and cystic degeneration of the gland. For several reasons this theory must 

 now be somewhat modified. First, in its original form, the division of the 

 disease into two phases is impossible. On the contrary, in the purest type 

 of acromegalia, Sternberg's malignant form, the development of the tumor 

 of the hypophysis is unquestionably combined with symptoms of peripheral 

 hyperplasia and the injurious effects of this upon the entire organism. Tam- 

 burini's theory is also difficult of acceptance because its adherents, as well 

 as its opponents, have been forced to the conclusion that if his views are cor- 

 rect, the secretion of the hypophysis must also influence the normal growth 

 of the body; Woods Hutchinson has gone so far as to declare that the hypophy- 

 sis is the center for body growth. 



These difficulties lessen when the processes of peripheral growth are recog- 

 nized as constant but less important consequences of acromegalia (which is 

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