PROGRESSIVE PERNICIOUS ANEMIA 311 



in arriving at our present standpoint. To-day we know that progressive per- 

 nicious anemia may undoubtedly often follow other diseases, and not as an 

 independent disease, but only as a symptom ; as, for instance, in the case of 

 diabetes. We shall now briefly describe what has been demonstrated with 

 certainty. 



The best illustration of severe anemia which we possess is the case of 

 individuals who" harbor the bothriocephalus latus in their intestines. Not- 

 withstanding all the controversies on this subject, there can be no doubt that 

 this worm, living or dead, may produce the most severe anemic conditions, and 

 that this bothriocephalus anemia is a true progressive pernicious anemia. We 

 understand fully the mode of action of this parasite, and may regard it as 

 proven that the disease is due to toxic substances that have a hemolytic effect, 

 and thus cause anemia. Further it may also be assumed as likely that the 

 parasite changes the activity of the bone-marrow in a peculiar way. The in- 

 contestable fact that a very large number of people are afflicted with bothrio- 

 cephalidae without becoming anemic may be explained in different ways. In the 

 first place, there may be a difference in the degree of virulence of the toxins ; 

 or, again, a difference in the susceptibility of the host. For there is no doubt 

 that individuals of one species may possess a very different susceptibility to 

 the same poison; for example, the susceptibility of rabbits to crotin has lately 

 been proven to show enormous variations. Finally, the explanation of a grad- 

 ual autoimmunization to the toxin is quite reasonable. 



Leaving now the consideration of bothriocephalus anemia, which is at pres- 

 ent understood, we may say that all that is known of the presumable causes 

 of progressive pernicious anemia may thus be summarized : " The same dele- 

 terious agents which are capable of producing a ' simple ' anemia may also 

 develop the progressive pernicious form." Why apparently identical causes 

 may in some instances produce the common simple anemia and in others the 

 comparatively rare progressive pernicious anemia we do not as yet know. 



In considering the symptoms of progressive pernicious anemia, changes 

 OF THE B'LOOD, especially morphological alterations, claim our closest at- 

 tention. 



In a typical, well-defined case of progressive pernicious anemia, the first 

 glance at a good stained preparation is sufficient to distinguish it from simple 

 anemia. We find that the majority of erythrocytes, or at least a large number 

 of them, have a diameter largely above the normal, 15 to 18 /x (megalocytes) 

 and, by their stain, these cells disclose to us a great richness in hemoglobin. 



On repeated examination, we almost always find some megaloUasts, i. e., 

 erythrocytes with nuclei, the predecessors of the megalocytes. Except in the 

 worst stages of the disease, the number of megaloblasts is always very scant. 

 [The number of megaloblasts usually exceeds the number of other erythroblasts, 

 but presents no close parallelism with the severity of the clinical manifesta- 

 tions or with the intensity of the anemia. It is true that in most cases the 

 number of megaloblasts increases as the symptoms are aggravated, and dimin- 

 ishes in the remissions of the disease. But to this rule there are many excep- 

 tions. Ed.] Besides megaloblasts, normoblasts and microblasts are also to 



be found. Ot non-nucleated red corpuscles, besides megalocytes, we also see 



