256 INANITION AND MALNUTRITION 



in severe pellagra, with increase of polymorphonuclear eosinophiles during 

 convalescence. 



The effects of a dietetic deficiency of iron upon the blood structure have 

 attracted much attention, on account of the iron content of hemoglobin. Since 

 the loss of iron from the body is slight, however, but little is needed in the food 

 except during growth. Von Hosslin ('82) in young, growing dogs on diets very 

 deficient in iron found at first a decrease in hemoglobin with but slight loss in 

 the total mass of blood; but later a decrease also in the blood volume. Similar 

 experiments with variable success in the production of anemia in animals on iron- 

 poor diets were made by Hall ('94, '96); by Kunkel ('95), Tartakowsky ('04) 

 and Stoeltzner ('09a) in puppies; by Hausermann ('97), in man, rats, rabbits 

 and kittens; by Abderhalden ('00) in rats, rabbits and guinea pigs; by Schmidt 

 ('12) in white mice; and by Brinchmann ('21) in guinea pigs. Lazarus ('13) 

 opposed Immermann's doctrine that inanition causes the purest type of hypo- 

 plastic anemia. He concluded that the anemic appearance (pale skin and 

 mucosae) is often deceptive, and that a qualitative dietetic deficiency, espe- 

 cially of iron, is more important than a quantitative deficiency. Happ ('22) 

 found that well balanced diets, deficient in iron, do not produce anemia in the 

 rat in the first generation, although slight anemia may occur in the second 

 generation. 



In human rickets, Comby ('01) stated that the blood is usually found nor- 

 mal, though sometimes simple or splenic anemia occurs (with enlarged spleen). 

 According to Cheadle and Poynton ('07), there is usually a simple anemia, 

 proportionate in general to the severity of the rickets. The leukoctyes are 

 usually increased, and nucleated red corpuscles occur. The extreme anemia 

 associated with an enlarged spleen is probably due to a syphilitic complication. 

 Wohlauer ('11) reviewed the literature, indicating usually alteration of the blood 

 in rickets, but the data are variable. Heubner says the erythrocytes may sink 

 to 2 or 3 millions, with leukocytosis up to 20 or 30 thousand; the changes being 

 somewhat proportional to the severity of the rickets. Poikilocytosis, nucleated 

 red cells and megalocytes may occur. Kuttner's findings were similar. Schiff 

 and Widowitz, however, in rachitis with severe digestive disturbances 

 found a condition of chlorosis, with marked decrease of hemoglobin without 

 corresponding decrease in the red cell count. 



In adult osteoporosis, due to chronic dietetic deficiency in protein, calcium 

 and phosphorus, Alwens ('19) found the hemoglobin below 80 in 16 cases, with 

 the red and total white cell count within physiological limits. There was 

 lymphocytosis in 13 cases, and eosinophilia in 7. Happ ('22) concluded that 

 diets producing rachitoid changes in the rat may also produce anemia, if the 

 diet is prolonged, and also in the second generation. 



The effects of oxygen deficiency are of interest in this connection. Albitzki 

 ('84) reviewed the earlier work on thjs topic. The blood changes include 

 deformity and destruction of the erythrocytes, which are decreased in number. 

 Granules (probably from degenerated red cells) are found in the blood and urine; 

 hemoglobinuria, nasal hemorrhages and bloody diarrhea occur. Askanazy 

 ('13) mentioned blood stasis and ecchymoses as a result of oxygen-deficit, with 



