588 SAMUEL H. HURWITZ 



iron in the liver and 23 milligrams in the spleen in three instances of 

 posthemorrhagic anemia, as contrasted with 290 milligrams of iron in 

 the liver, and 113 milligrams in the spleen in a case of hemolytic anemia. 

 It has been suggested that the decreased elimination and the lessened 

 iron storage noted after hemorrhage is probably due to the rapid utiliza- 

 tion of iron for the rebuilding of the lost hemoglobin. 



Studies of iron metabolism in chlorosis have been largely concerned 

 with the factors of iron deficiency in the food and of faulty iron assimila- 

 tion as possible causes of this disease, as well as with the efficacy and 

 mode of action of organic and of inorganic salts of iron in the treatment 

 of this condition. 



The question raised by Bunge(a) concerning the absorption of inor- 

 ganic iron in anemia and its value in chlorosis has been i answered in the 

 affirmative by most observers (E. Meyer (c)). According to the later 

 work of Abderhalden(c) inorganic iron is beneficial in anemia not only 

 because of its indirect stimulation of the blood-forming organs, but also 

 because it is absorbed, assimilated and converted into hemoglobin precisely 

 like food-iron. The elimination of iron in the urine and feces of chlorotic 

 patients has been found variable. The results of different observers have 

 been reviewed by Morawitz(&) and by Kemierknecht. Whereas some in- 

 vestigators give normal figures for urinary iron in chlorosis, others report a 

 decreased or increased elimination. The large excretion of iron in the 

 feces noted by von H6sslin(6) has been interpreted by him to mean that 

 the anemia of chlorosis may be due to the excessive loss of iron through the 

 intestine. Such a conception of the etiology of chlorosis is according to 

 the critical analysis of Morawitz quite unlikely. He is inclined to the 

 view that neither the faulty absorption nor the increased elimination of 

 iron plays an important part in the causation of chlorosis. According 

 to this observer further additions to our knowledge of the etiology of 

 chlorosis will come not from the balance experiments thus far recorded, 

 but rather from a better understanding of the intermediary iron metab- 

 olism in this disease. 



The occurrence of excessive blood destruction in the hemolytic ane- 

 mias gives the observations on iron elimination in these conditions par- 

 ticular significance. In the severe anemia produced experimentally by 

 pyrodin, which gives rise to considerable breaking down of red cells, 

 Samuely(a) noted an increased excretion of iron only in the feces; whereas 

 patients with , pernicious anemia with increased hemolysis may show :i 

 marked increase in the output of iron in the urine. In one patient three 

 weeks before death, W. Hunter found as much as 32.26 milligrams of 

 iron in the twenty-four-hour period of urine, and other observers (Hop- 

 kins, Jolles, Mayer(a)) report similar findings. The patients studied by 

 Kennerknecht showed increased quantities of iron not only in the urine 

 but also in the feces during certain periods of the disease. In their care- 



