• rickets
• Asian

We welcome the timely review by Shaw and Pal¹ on the continuing problem of vitamin D deficiency among South East Asians living in the UK. Since our report in 1999,² we have continued to see 8–10 non-white toddlers with florid vitamin D deficiency rickets per year, at our inner city general paediatric unit. A recent national survey showed that 20–34% of South East Asian children had biochemical evidence of vitamin D deficiency.³ However, there is no information on the prevalence of clinical rickets among non-Caucasian children in the UK.

We opportunistically studied 6–36 month old children from ethnic minority backgrounds who were brought to a child health clinic in Central Manchester between 30 May 2001 and 12 July 200 for immunisations, weight checks, hearing tests, and developmental assessments. A structured questionnaire was used to determine if the children were receiving vitamin D supplements and whether they had been prescribed by health professionals or bought “over the counter” by the parents. Arms and legs of children were examined for deformities and swelling of the metaphyses due to rickets. Children with clinical stigmata of rickets had an x ray of their left wrist and estimation of serum calcium, phosphorus, alkaline phosphatase (ALP), parathyroid hormone (PTH), 25-hydroxyvitamin D (25OHD), and 1,25-dihydroxyvitamin D (1,25(OH)₂D). Ethnicity was self determined by parents as South East Asian (Pakistani, Bangladeshi, or Indian), African, Afro-Caribbean, and Middle Eastern origin. The study was approved by the Central Manchester Research Ethics Committee.

A total of 124 children (mean age 15.4 (8.2) months) were studied. Seventy seven per cent of children were of South East Asian origin and almost 50% were of Pakistani origin. Thirty (24%) children were receiving vitamin supplements; in 13 (43%) multivitamin preparations had been bought “over the counter” by the parents. Three children had clinical stigmata of rickets. Table 1 shows biochemical results. Two (1.6%) of these had radiological features of moderately severe rickets (fig 1) and the third had metaphyseal sclerosis, indicating healed rickets. One child was noted to be pale; his haemoglobin was 62 g/l (normal >110 g/l).

The Department of Health’s Committee on Medical Aspects of Food Policy (COMA) recommends vitamin D supplements for all children up to 3 years, and up to 5 years in those at high risk of developing vitamin D deficiency.⁴ It was therefore disappointing that less that a quarter of the subjects studied were receiving vitamin D supplements. Two children (cases 1 and 2) were found to have clinical and radiological evidence of active rickets. As shown in table 1, they also had biochemical features of rickets with elevated serum ALP activity for age, low serum 25OHD (a measure of an individual’s vitamin D status), and secondary hyperparathyroidism. All three had been breast fed for periods ranging between four and nine months after birth and none had been prescribed vitamin D supplements.

According to the 1991 census data there were appproximately 4000, 6–12 month old children of ethnic minority background resident in the city of Manchester. We found that 1.6% of the children examined had rickets. If this figure were extrapolated to all 6–36 month old non-Caucasian children living in the Manchester area, we estimate that there would be approximately 60 children with rickets at the time of this study. Rickets is not a historical disease, as it seems to be perceived by many health professionals. However, it is an entirely preventable by use of vitamin D supplements as recommended by the COMA.⁴ We wholeheartedly agree with Shaw and Pal¹ that a nationwide campaign, similar to the “Stop Rickets” campaign in the 1980s is needed to tackle this problem.

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Figure 1

Radiograph of the wrist (case 1, table 1), showing wideing, cupping, and fraying of the distal radius and ulna.