XI. PATHOLOGY 505 



may gain oiilrance to the body. Such agents may be of intestinal bacterial 

 origin. The therapeutic efTect of B12 on the neurologi(- lesions of pernicious 

 anemia, which is not e.xerted by PGA, suggests that B12 is concerned whh 

 metabolic processes affecting the integrity of neurones. 



The elfectiveness in pernicious anemia of refined and concentrated liver 

 extracts appears to depend entirely on their content of B12 (cyanocobala- 

 min) and its analogs, such as Biob (hydroxocobalamin). The claims of some 

 investigators that Bi.> constitutes incomplete treatment of pernicious anemia 

 and that superior results are obtained from the use of crude liver extracts 

 have not been substantiated and are counter to the accaimulated experience 

 of a great manj' clinical observers. 



The megaloblastic anemia associated with some cases of Diphyl- 

 lobothrium latum infestation is apparently due to diversion of B12 in the ali- 

 menatry tract from the host to the nutritional requirements of the tape- 

 worm. Anemia following gastrectomy is presumably in part the result of 

 elimination of the source of intrinsic factor, but other disturbances of di- 

 gestion or absorption are undoubtedly factors in its production. Intestinal 

 anastomoses, strictures, and blind loops cause complex nutritional distur- 

 bances which depend upon diminished absorptive surface, altered motility, 

 stasis and changes in bacterial flora. Megaloblastic anemia is of common 

 occurrence in such situations and may result from deficiencies of both B12 

 and PGA in varying degrees. 



Observations on the effect of B12 administration to children with retarded 

 physical development have indicated that the vitamin may have growth- 

 promoting properties even though the diets of such children have not been 

 obviously inadequate. It has been proposed that in such cases B12 supple- 

 mentation may correct a variety of metabolic derangements which are 

 collective!}'' responsible for the slow-down in the rate of growth. Addi- 

 tional careful nutritional studies will have to be carried out before the role 

 of B12 as a growth-promoting agent in children can be adequately evaluated. 



Therapeutic success has been claimed for B12 in relieving sensory dis- 

 turbances in a number of neurologic disorders other than pernicious anemia. 

 Although deficiency of B12 may be a factor in some nutritional disorders 

 associated with neuropath}^, it would appear that in most of the conditions 

 treated there is no evidence for the existence of such deficiency. Whatever 

 benefit follows the use of massive doses of the vitamin must be attributed 

 to a pharmacologic action rather than to correction of a metabolic defect. 



