RACHITIC INVOLVEMENT of the skeleton in infants and children occurs occasionally in association with other disease processes. Examples of this are the combination of rickets and congenital syphilis, rickets and infantile scurvy, rickets and lead poisoning, and rickets and erythroblastic anemia. A case of osteogenesis imperfecta seen in the Children's Hospital has been previously reported (Bromer, 1), in which rickets developed at the age of three months and signs of infantile scurvy at the age of twenty-one months. The roentgen diagnosis of rickets and associated conditions is often difficult. Lack of autopsy material prevents, to a great extent, confirmatory study of the underlying histologic picture of the associated processes. Rickets and Infantile Scurvy Infantile scurvy and rickets are now much less prevalent than in the decade of 1920–30 and earlier years. Their etiology is definitely established and, when they do occur, it is because of ignorance or lack of adequate preventive or curative treatment. Borderline cases, however, are still seen, and occasionally a fully developed case is encountered. McIntosh (7) has stated that it was common in the past to make a diagnosis of coincidental clinical rickets in a large proportion of patients showing unmistakable scurvy. With the development of roentgenographic and chemical criteria for the detection of rickets, the tendency to make that diagnosis in addition to scurvy; largely because of the rosary, has declined. MeIntosh further states that histologic evidence shows that the two conditions do at times occur in the same patient. In his series of 186 cases of scurvy from the Babies Hospital there were 15 patients (8 per cent) who had craniotabes, one of them also showing signs of tetany. Evans (4) made the diagnosis of associated rickets in 36 of the 93 (38.7 per cent) cases of scurvy constituting his series. Follis, Jackson, and Park (5), in a series of 57 autopsies on children between three and nine months of age, in whom scurvy was proved by histo histologic examination of the bones, found rickets, demonstrated in similar fashion, in 26 (46 per cent). They believed that in all probability rickets was present in a greater percentage, because, when the scurvy was extreme, they could not always be sure that it did not mask the rickets. They found that such criteria as a history of vitamin deficiency, the season of the year when the patient came under observation, results of clinical and roentgen examination, and measurements of calcium, inorganic phosphorus and phosphatase of the blood serum, were not satisfactory. The roentgen examination did not reveal rickets unless the disease was well developed. Wimberger (10), in his study of rickets and scurvy in Vienna following the first World War, stated that when scurvy develops in the healing period of severe or moderately severe rickets the roentgen recognition of both is possible.
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