110 VITAMINS A AND CAROTENES 



specialized functions which are suppressed by the deficiency. Xo satisfac- 

 tory explanation can be offered for the fact that the reparative activities 

 of basal cells of many different epithelia in vitamin A deficiency end in an 

 identical stratified keratinizing epithelial product comparable in all details 

 with epidermis. 



The gross pathologic features in man and animals are largely the result 

 of the accumulation of keratinized epithelial cells in glands and their ducts, 

 in other organs, and in conjunctival sacs. Cysts of considerable size, filled 

 with yellowish cheesy masses of keratinized cells, may be formed in many 

 glands. In the lungs of human infants and in experimental animals this 

 process produces occlusion of bronchi, atelectasis, and formation of bron- 

 chiectatic cavities filled with keratinized cells. Early workers regarded such 

 cysts and bronciectatic cavities as abscesses, and therefore vitamin A was 

 regarded as an anti-infective vitamin. The plugs of desquamated epithelial 

 cells in ducts, trachea, and bronchi which communicate with regions nor- 

 mally harboring bacteria act as a culture medium, yet rarely in man and 

 experimental animals does invasion of tissue result, presumably because of 

 the barrier presented by the stratified epithelium. 



Because most features of the gross and microscopic pathology of vitamin 

 A deficiency are the result of keratinizing metaplasia, detailed accounts of 

 the various tissues and organs of the body will not be presented. Emacia- 

 tion — ^a consequence of most severe deficiencies — may be taken for granted. 

 The effect upon skeletal growth and consequent damage to a growing cen- 

 tral nervous system will l)e presented in some detail because of confusion, 

 now current in the literature, of the mechanisms invoh'ed and of cause 

 and effect. 



a. Eye 



The night blindness of vitamin A deficiency in the adult is a reversible 

 phenomenon and is probably unaccompanied by morphologic changes dem- 

 onstrable by available techniques. Irreversible loss of vision does occur in 

 young animals and is fully explained by pressure effects upon optic nerA-e 

 and blood vessels, resulting from retardation of the growth of the skull. 

 Johnson^ has carefully studied the retina of rats placed upon a vitamin A- 

 deficient diet at 23 days of age. The earliest change was edema of the retina; 

 then followed slight degenerative changes of the outer segments of rods. 

 Recovery after replacement therapy was rapid. A later lesion, complete 

 degeneration of the outer segments of rods "(and possibly the inner sig- 

 ments as well)," retiuired a longcM- period of therapy. Lesions invoh'ing 

 "the greater part of the outer nuclear lay(n-, or more" proved to be irrep- 



' Myr:i I.. .Jolinsoii, Arch. ()/>h/li<ihin>l . (Cliinn/o) 29, T'.to (WlV.i). 



