236 INANITION AND MALNUTRITION 



of the muscle cells undergo vacuolation and the elastic layers are more wrinkled 

 (due to the shrinkage of the vessel). The stellate connective tissue cells of the 

 adventitia undergo fatty degeneration, and extensive hemorrhages into the 

 surrounding tissue are frequent. In animals amply refed after inanition, these 

 changes in the vascular wall have largely disappeared, excepting slight necrosis 

 and fatty degeneration which still persisted in the cells near the ligature. 



In dystrophic infants, according to Lesage ('11), the blood vessels usually 

 appear normal in structure, although arteriosclerosis sometimes appears. 



Stefko ('23) calls attention to the frequent hemorrhagic diathesis (purpura) 

 in cases of human starvation. The condition appears to be due to degeneration 

 in the walls of the blood vessels, which results from the impoverishment of the 

 blood. Possibly this hemorrhagic condition should be ascribed to the exhaustion 

 of vitamin C, as occurs in scurvy. 



Protein Deficiency. — Many investigators of malnutritional edema ascribe 

 the condition primarily to an injury of the capillary walls (Lange '17; Schitten- 

 helm and Schlecht ('19); Maver '20; Burger '20; Maase and Zondek '20; etal.). 

 Oberndorfer ('18) considered the universal capillary congestion of significance, 

 and Maver, Maase and Zondek mention the possibility of direct toxic injury to 

 the capillary walls. The question is closely related to that of the role of the 

 capillaries in the production of edema in general, the literature upon this topic 

 being reviewed by Lange ('17). 



Although, as previously stated, protein deficiency has usually been accepted 

 as the primary cause of famine edema, the question has been raised as to whether 

 this (as also other edemas) may not involve also a calcium deficiency. The 

 work of Herbst upon invertebrates (see Chapter III) showing the effects of 

 calcium deficiency in dissolving the intercellular cement substance has been cited 

 in this connection; as well as in disorders such as scurvy, with characteristic 

 capillary hemorrhages. Chiari ('10) has reviewed the evidence indicating 

 that calcium deficiency in general tends to increase the permeability of the capil- 

 lary walls. 



In pellagra (presumably due chiefly to protein deficiency), vascular changes 

 have been described. Fraenkel ('6o-'7o) mentioned pigmentation of the 

 capillaries and fatty degeneration of the adventitia in the brain vessels. 

 Primary degeneration and sclerosis of the blood vessels was emphasized by Marie 

 ('08, 'jo), Nicholls ('12), Kozowsky ('12), Raubitschek ('15) and Harris ('19) 

 as of importance in the pathogenesis of pellagra. 



In rickets, Kassowitz ('12), as previously mentioned, has long advocated the 

 theory that the characteristic changes in the zone of enchondral ossification are 

 primarily due to hyperemia and increased vascular proliferation in the region. 

 This theory, however, has not met with general acceptance. 



In relation to vitamin deficiency, vascular changes have been noted especially 

 in connection with scurvy (deficiency of vitamin C), in which the hemorrhages 

 form a constant and conspicuous lesion, and petechial extravasations have 

 been described as occurring in nearly every organ. The exact cause of the 

 hemorrhagic tendency is uncertain. Direct toxic injury to the capillary wall 

 has been suggested by Sato and Nambu ('08). The possibility of a calcium- 



