260 VITAMIN D GROUP 



phosphorus concentration and heaUng of the ricketic lesion in the bones. 

 Increased dosage of vitamin D or its administration in highly dispersed 

 form in a watery dispersion or parenteral administration of the vitamin 

 may solve the difficulty in some of these cases. In other cases functional 

 disease of the kidney or diseases of the parathyroids may explain the persis- 

 tence of the ricketic state and its progress in spite of therapy. In some in- 

 stances much larger doses of vitamin D will suffice, whereas in others sup- 

 plementation of vitamin D with other substances is required. In one such 

 case, Albright, Butler, and Bloomberg found it necessary to increase the 

 daily dose of vitamin D to 1,500,000 units in order to initiate healing and to 

 give 150,000 units daily in order to maintain the normal state. However, 

 before one concludes that a patient has refractory rickets, one must be 

 certain that he is not dealing with some endocrine imbalance (hyperpara- 

 thyroidism) or some other abnormality such as a disturbance of acid-base 

 equilibrium, renal insufficiency, hypercalcemic rickets, liver damage, the 

 De Toni-Fanconi syndrome, the hyperplastic form of chondrodystrophy, 

 or rickets due to a disturbance of cysteine metabolism or due to biliary ob- 

 struction. 



Refractoriness due to chronic acidosis should be treated with alkalies in 

 addition to large doses of vitamin D. Some cases of chronic acidosis are 

 due to a defect in the ammonia-producing mechanism in the renal tubules. 

 This is corrected by the administration of large amounts of base such as 

 sodium, potassium, calcium, or magnesium, an alkaline ash-yielding diet, 

 along with adequate doses of vitamin D, or simple sodium bicarbonate or 

 citrate. A form of rickets associated with chronic renal disease and hyper- 

 chloremia has been described. This responds to a mixture of sodium citrate 

 and citric acid, in addition to massive doses of vitamin D. In the De Toni- 

 Fanconi syndrome there is evidence of renal tubular dysfunction. There is 

 normal excretion of ammonia, but the blood shows a low bicarbonate, evi- 

 dence of compensated acidosis, marked and persistent hypophosphatemia, 

 occasional hypocalcemia, and, in the later stages, a decrease in the blood 

 sodium, potassium, and chlorides. Treatment is ineffective. 



Although the practice is widespread of discontinuing prophylactic use of 

 the vitamin after the age of 2, when a mixed diet is ingested. Park's studies 

 have demonstrated histological evidence of rickets in children even up to 

 14 years.^^ This would indicate the need for the continuance of sup- 

 plementary vitamin D up to that age, in doses about half that for infants. 

 Normal adults may rely on sunshine and incidental ingestion of the vitamin, 

 but women during pregnancy and lactation require about 1000 units daily 

 to avoid the deleterious effects of vitamin D deficiency. 



Single massive doses of vitamin D sometimes may be used. This method 



" R. H. Follis, Jr., D. Jackson, M. M. Eliot, and E. A. Park, Am. J. Diseases 

 Children 66, 1 (1943). 



