VIII. REQUIREMENTS 259 



calcium and phosphorus are ingested simultaneously and in a fixed ratio 

 to each other and to vitamin D. When concentrated forms of vitamin D are 

 used they should preferably be given in water-dispersed form in doses of 

 3000 units per day because of possible defective absorption of some fats 

 and fat-soluble vitamins. Occasionally, larger doses are required. The actual 

 amounts may have to be determined by the method of trial and error, 

 controlled ^vith serial x-rays of the extremities and repeated determinations 

 of plasma, calcium, inorganic phosphorus, and phosphatase. Prematurely 

 born infants may require a somewhat larger dose. 



This therapy should be continued throughout the year, rather than de- 

 pend on chance solar irradiation during the summer months. When mothers 

 cannot be depended upon to continue this medication or where conditions 

 exist that make adequate medical supervision impossible or in the presence 

 of prolonged infection, the large single dose of 600,000 units every 6 months 

 apparently may be used with favorable results. Clinical and pathological 

 studies show that there is little risk of hypervitaminosis with such therapy. 



For the treatment of rickets in the otherwise normal child a similar dose 

 will suffice. Vitamin D highly dispersed in milk or in water seems to be 

 more effective than when administered as a concentrated fish oil. As little 

 as 400 units of vitamin D in milk will in due time cure the majority of rick- 

 etic children. When administered as vitamin D in oil, 1000 units daily is 

 usually required. It is important that the diet contain adequate amounts 

 of calcium and phosphorus, preferably in a 2 : 1 ration, as well as a mixture 

 of good proteins. 



Where rickets persists in spite of adequate vitamin D dosage, an expla- 

 nation must be sought in a careful study of the organism itself. A number 

 of such refractory cases have been described, and many of these have been 

 subjected to exhaustive metabolic study. Defects of absorption (coeliac 

 disease, cystic fibrosis of the pancreas, sprue, idiopathic steatorrhea, in- 

 testinal shunts, intestinal anomalies, ulcerative colitis) may explain the 

 refractory state. 



Where bile fails to enter the intestinal tract, as in acquired common duct 

 obstruction, congenital absence of bile ducts, or atresia of these structures 

 or biliary fistulae, absorption of fat-soluble vitamins, including vitamin D 

 is impaired and rickets may fail to respond to the usual doses of vitamin D, 

 Similarly, in cases of liver damage, as in cirrhosis, additional vitamin D 

 may be needed both to prevent as well as to cure rickets. For the child with 

 defective intestinal absorption the vitamin is preferably given in the form 

 of a water dispersion. 



In some unknown manner infections may reduce the Ca X P product in 

 the blood plasma, giving rise to ricketic changes in the bones that are de- 

 monstrable histologically but not clinically or radiologically. Subsidence 

 of the infection results in a correction of the plasma calcium and inorganic 



