264 vitamin d group 



1. Hypervitaminosis D 



The pathologic effects of overdosage with vitamin D have been studied 

 chiefly in individuals who have received massive doses of calciferol in the 

 treatment of arthritis. In children there have been additional cases re- 

 ported as a side effect of vitamin D treatment for tuberculosis or after 

 receiving imperfectly irradiated ergosterol preparations containing large 

 amounts of toxic intermediates (vigantol). The basic pathologic effect is the 

 precipitation of calcium in various tissues. As a result of metastatic cal- 

 cification in the kidneys, kidney insufficiency may develop. Finally, 

 withdrawal of large amounts of calciimi into these abnormal foci may re- 

 sult in demineralization of bone. 



The gross and histologic findings have been frequently reported and are 

 similar in both children and adults, although fatalities seem to occur more 

 frequently in the young. There is diffuse calcinosis affecting the joints, syn- 

 ovial membranes, kidneys, myocardium, pulmonary alveoli, parathyroid 

 glands, pancreas, skin, lymph glands, large and medium-sized arteries, the 

 conjunctivae and cornea, and the acid-secreting portion of the stomach. The 

 abnormal calcification can be seen grossly as a w^hitish, chalky material. 

 The bones in the early stages may show accelerated calcification of the 

 provisional zone of calcification with thickening of the periosteum. In 

 more advanced cases, however, there is interference with cartilage growth, 

 and several authors^^ have demonstrated diffuse demineralization of the 

 bones. Shelling and Asher^^ pointed out that osteoporosis produced by hy- 

 pervitaminosis differs from that produced by parathormone in that the 

 resorbed areas are not replaced by fibrous tissue. Freeman et al}^ have re- 

 ported an instance in a child in which doses of ertron resulted in a nega- 

 tive calcium balance. The most serious involvement is that of the kidneys, 

 and most of the fatal cases terminated in uremia. The best evidence seems 

 to indicate that the initial kidney damage is due to deposition of calcium in 

 the basement membranes of the cells of the distal tubules.-^ There results 

 an inflammatory reaction, and later complete obstruction. As a result of 

 the obstruction, several nephrons at first dilate and then atrophy. As a 

 result of the inflammatory reaction, the lesion may spread rapidly through 

 the entire kidney. The kidney damage in turn is responsible for such path- 

 ology as hypertension, hypertensive retinopathy, and chemical evidence of 

 renal insufficiency. 



23 D. H. Shelling, The Parathyroids in Health and Disease. C. V. Mosby Co., St, 



Louis, 1935. 

 2* D. H. Shelling, and D. Remsen, Bull. Johns Hopkins Hosp. 57, 158 (1935). 

 " S. Freeman, P. S. Rhoads, and L.B. Yeager, J. Am. Med. Assoc. 130, 197 (1946). 

 26 R. H. Freyberg and J. M. Bauer, Univ. Hosp. Bull. (Michigan) 11, 61 (1945); 



T. S. Danowski, A. W. Winkler, and J. P. Peters, Ann. Internal Med. 23, 22 (1945). 



