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Concentrations of serum alkaline phosphatase and total urinary hydroxyproline were measured in 36 children to study the effect of phenobarbital administration with respect to the development of rickets in patients receiving anticonvulsive medications over prolonged periods of time. Administration of phenobarbital led to the appearance of increased AP and HOP values very early in the course of treatment and without any obvious bone changes suggestive of rickets; a single large oral dose of vitamin D had no appreciable effects in restoring the biochemical derangement. On the other hand, the administration of vitamin D in a daily dose of 4,000 IU for a period of two months hampered the appearance, or restored already existing changes of latent rickets, in children receiving anticonvulsive medication. The results in the present study favor the concept that phenobarbital administration is implicated in the development of rickets. The need for simultaneous daily administration of supplements of vitamin D in subjects receiving anticonvulsive drugs is stressed.

The necessary daily amount of vitamin D3 in premature infants was calculated by Hövels and his group as being 25 mcg (1000 I.U.). This was in agreement with our own investigations. Without vitamin D3, however, the incidence of rikkets in premature and small-for-dates newborns occurred usually at the beginning of the second month of life. Clinical signs of rickets are still absent at this time, while an increased activity of the serum alkaline phosphatase signals the beginning of the illness. Three groups of prematurely born infants received up to 50 days daily oral doses of 12.5 mcg vitamin D3 (=500 I.U.), 25 mcg vitamin D3 (=1000 I.U.) or 9 mcg 25-hydroxycholecalciferol (25-HCC), respectively, while one untreated group served as control. No differences were noted between the four groups in the serum values of calcium and phosphorus. The activity of the alkaline phosphatase tended to be higher in the untreated and the 500 I.U. groups. The differences were prouved by the chi2-test to be significant (see table 2 and 3). It appeared that 9 mcg of 25-HCC prevented the rise in alkaline phosphatase slightly better than 25 mcg of vitamin D3 (1000 I.U.). On a mcg base 25-HCC seems three times as effective as cholecalciferol. One could speculate about a delayed hydroxylation of cholecalciferol (vitamin D3) to 25-HCC.

Ten years of experience with daily prophylaxis of rickets brought about isolated knowledge which corrected old mistakes and demands a revision of older attitudes towards the usual prophylaxis. Prophylaxis of vitamin D according to the most modern and reliable knowledge in the best way promotes the growth and mineralisation of the skeleton with dosages of 400 to 800 I.U. smaller or higher dosages are disadvantageous. By observing the above given dosage, rickets and hypercalcaemia are rare and only conceivable under special pathological conditions. The diagnosis of beginning rickets must be well known, otherwise unspecific symptoms of rickets may induce the administration of unnecessarily high amounts of vitamin D. The symptoms of rickets show a gradual increase: the increase of serum alkaline phosphatase precedes the clinical and radiological symptoms. The reliable radiographic deformities of the hand can first be seen at the Ulna, then at the Radius and later at the secondary centers of Metacarpals. Among the relatively reliable clinical symptoms there its first the rosary later the Marfan-sign and eventually the deformation of the long bones. For infants protected by vitamin D, craniotabes as a sign of rickets is completely unreliable as well as the Harrison grooves and rachitic kyphosis. If one observes all these rules and rachitic kyphosis. If one observes all these rules and criterions vitamin D is as reliable in the prophylaxis as in the therapy of vitamin D deficiency rickets.

The prevalence of vitamin D deficiency was reassessed in April and May 1971, 10 years after the discovery of widespread late rickets and osteomalacia in the Glasgow Pakistani community. Evidence of vitamin D deficiency was found in 28 out of 115 adults and children examined (24%). Children at the age of puberty were most severely affected by rickets, whereas most infants and younger children in the survey were protected by vitamin D supplements. Mild biochemical osteomalacia was common in Pakistani women.A total of 21 Pakistani and Indian children with rickets were admitted to Glasgow hospitals during 1968-70. These comprised 10 children with infantile rickets and 11 with late rickets. Four of the latter group required osteotomy for severe rachitic deformity.Late rickets and osteomalacia in Pakistani and Indian immigrants are not primarily due to nutritional deficiency of vitamin D, though the high phytate content of their diet may be of aetiological importance. A combination of environmental, social, and endogenous factors, the relative importance of which is not at present clear, may also be involved. Advice on the prophylaxis of vitamin D deficiency should be given to all Pakistani and Indian communities in the United Kingdom.