EFFECTS ON THE LIVER 329 



capillaries. The liver-cells are decreased in size, with finely granular cytoplasm 

 (no steatosis), and pycnotic nuclei. The iron-reaction is constant, though 

 variable in intensity, but is not characteristic of athrepsia. 



Schelble ('10) made a careful histological study of the liver in 35 cases of 

 pedatrophy (with early fixation in 16), but could find no constant, marked or 

 characteristic lesions. 



Lesage ('n, '14) noted a weight of only 109 g. in the liver of an atrophic 

 infant, the normal being 300 g. The hepatic cells may become atrophic, 

 and fail to secrete the bile necessary for digestion. Lesage and Cleret ('14) 

 found in congenital spasmodic atrophy a marked sclerosis of the liver and other 

 organs. Maillet ('13) noted lesions in the liver of athreptic infants. 



Hayashi ('14) made a special study (with review of the literature) of the 

 liver fat in atrophic infants, using optical and microchemical methods. In 8 

 cases, 5 showed neither fats nor lipoids; 1 showed partial and 2 marked fatty 

 degeneration. Hayashi concluded that the hepatic fat in athrepsia differs 

 from that found in experimental inanition. 



Mattei ('14) usually found in athreptic infants but little change in the liver 

 structure, which appeared normal in 5 out of 15 cases. In some zones the 

 columns of liver-cells appeared slightly compressed between the dilated blood 

 capillaries. The hepatic cells are sometimes swollen by vacuoles (fat droplets) 

 of variable size, which may occur around either the central vein or portal vessels. 

 Some cells contain pigment (probably siderosis of hematic origin). Atrophic 

 cells with karyolytic nuclei may occur throughout the gland. Sometimes the 

 cells appear more deeply stained in the periphery of the lobule, and clearer 

 toward the center (not due to difference in glycogen content). There may be 

 periportal sclerosis. 



Nobecourt ('16) reviewed the literature and concluded that in atrophic 

 infants the liver may be either normal or diminished in size. Congestion is 

 characteristic and a variable degree of fibrosis, steatosis or siderosis may be 

 found. 



Marfan ('21) held that the hepatic siderosis in athreptic infants is related to 

 the hemolysis and anemia found in these cases. Huebschmann ('21) claimed 

 that in acute nutritional disorders (intoxications, "Mehlnahrschaden") there 

 is a toxic disturbance of the general cell metabolism resulting in a characteristic 

 steatosis of the liver and a related disappearance of suprarenal lipoids. Ste- 

 phani ('23) likewise noted severe fatty degeneration in acute cases, but not in 

 chronic malnutrition, in which hepatic hemosiderosis occurred. 



In famine-stricken children of various ages, Nicolaeff ('23) found the liver 

 weight always over 20 (sometimes 45-55) per cent subnormal for age, being 

 smallest in edematous subjects. The histologic structure appears variable. 

 In non-edematous cases, there is frequent venous and capillary hyperemia; 

 atrophy of the hepatic cell-cords, especially near the center of the lobule; and 

 complete absence of fat and glycogen. In edematous subjects, there is venous 

 hyperemia, and adipose infiltration in the periphery of the lobule. Stefko ('23) 

 observed the reestablishment of normoblasts in the liver of children who died 

 from starvation. 



