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Clinical Review Lesson of the week

Florid rickets associated with prolonged breast feeding without vitamin D supplementation

BMJ 1999; 318 doi: (Published 02 January 1999) Cite this as: BMJ 1999;318:39
  1. M Z Mughal, consultant paediatrician (mmughal{at},
  2. H Salama, specialist registrar in paediatricsa,
  3. T Greenaway, general practitionerb,
  4. I Laing, consultant biochemisa,
  5. E B Mawer, professor of bone and mineral metabolism.c
  1. aSt Mary's Hospital, Central Manchester Healthcare Trust, Manchester M13 0JH
  2. bAlexandra Practice, Manchester M16 8NG
  3. cUniversity Department of Medicine, Manchester Royal Infirmary, Manchester M13 9WL
  1. Correspondence to: Dr Mughal

    The incidence of rickets caused by vitamin D deficiency, once a common health problem among British Asian children, seems to have declined during the past decade.1 We describe six cases of florid rickets in infants aged 10to 28months who were referred to our paediatric unit by local general practitioners between 1995and 1997.They were all born in the United Kingdom to parents who were either postgraduate students or recent immigrants. All the children had been breast fed for a prolonged period without vitamin D supplementation. The mothers of these infants had not received vitamin D supplements during pregnancy or lactation.

    Case reports

    All six patients had several of the clinical signs and symptoms of rickets: bow legs, rickety rosary, swelling of the ends of long bones, frontal bossing of the skull, delayed dentition, poor growth, and slow motor development. They all had classic radiological features of rickets, including generalised osteopenia, widening of the growth plates, and cupping of metaphyseal regions of long bones (figure). As shown in table 1,biochemical features of the disease included increased serum alkaline phosphatase activity for their age, low serum concentrations of 25-hydroxycholecalciferol (a measure of vitamin D status;concentrations <5ng/ml are associated with rickets or osteomalacia), and secondary hyperparathyroidism leading to hypophosphataemia and normal or above normal serum concentrations of 1,25-dihydroxycholecalciferol. Two subjects had asymptomatic hypocalcaemia. All the subjects had been breast fed, either exclusively or for prolonged periods of time (table 1).No infant had received vitamin D supplements. Treatment with oral cholecalciferol (vitamin D3) successfully healed the rickets in all subjects.


    Radiograph of knee in case 1 showing generalised osteopenia, widening, cupping, and fraying of the metaphyses

    Table 1

    Characteristics of cases of rickets

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    All infants were born in the United Kingdom at full term. Their mothers had not received vitamin D supplements during pregnancy or while nursing their infants. None of the patients received supplementary vitamin D after birth. Four out of five mothers of the toddlers who agreed to undergo biochemical testing were deficient in vitamin D, with low serum 25-hydroxycholecalciferol concentrations (table 1). These four mothers were all practising Muslims who wore concealing clothing when attending the hospital. Further inquiries revealed that three of them had non-specific aches and pains in their legs.


    Rickets resulting from vitamin D deficiency is a disorder of growing children in which the newly formed bone matrix does not become mineralised. In humans the main source of vitamin D is formed by conversion of 7-dehydrocholesterol in the skin to cholecalciferol (vitamin D3) with exposure to the sun's ultraviolet B radiation. This cutaneous synthesis is compromised in people with increased skin pigmentation2 and those who wear concealing clothing or live predominantly an indoor life for religious and cultural reasons.

    Environmental factors that reduce the penetration of antirachitic ultraviolet B radiation (290-310nm) through the atmosphere include cloudy skies, pollution, and residence in northern latitudes, where the sun is too low in the sky during winter months. Under these conditions of insufficient exposure of the skin to sunlight, dietary and supplemental sources of vitamin D are important in preventing rickets in children and osteomalacia in adults.

    Table 2

    Reference nutrient intake for vitamin D in children under 3 years old5

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    Infants born to mothers with subclinical vitamin D deficiency have reduced umbilical cord blood concentrations of 25-hydroxycholecalciferol.3 The prolonged consumption of breast milk is another risk factor for developing vitamin D deficiency as human milk contains only about 1µg of vitamin D per litre, with concentrations varying according to maternal vitamin D status.4 Thus, exclusively breast fed infants with insufficient exposure to ultraviolet B radiation consuming 750-1000ml of breast milk per day would fail to receive the 7-8.5µg of vitamin D per day needed to prevent rickets.5 In Saudi Arabia, despite the abundance of sunshine throughout the year, vitamin D deficiency rickets has been reported among infants owing to prolonged breast feeding and voluntary avoidance of sunshine.6

    Thus, vitamin D deficiency rickets in our patients probably resulted from a combination of factors, including maternal vitamin D deficiency leading to reduced maternofetal transfer of vitamin D during pregnancy, prolonged breast feeding by mothers deficient in vitamin D, residence in the United Kingdom (Manchester's latitude is 53° north of the equator), and probably reduced exposure to the sun during summer months. More importantly, the infants with rickets and their mothers did not receive vitamin D supplements. The Committee on Medical Aspects of Food Policy's recommendations for vitamin D intakes for children up to 3years of age are given in table 2.5 The committee also recommends that children at high risk of vitamin D deficiency should be encouraged to take supplements throughout the first five years and that all pregnant and lactating mothers should receive 10µg of vitamin D daily.5

    Historically, rickets has been associated with poverty, but clinical vitamin D deficiency occurred in the infants and spouses of three comparatively affluent and well educated overseas postgraduate students. Complacency in implementing the vitamin D supplementation policy, in our view, contributed to local resurgence of a completely preventable condition. Our cases serve to re-emphasise the importance of providing vitamin D supplements to growing children and pregnant and lactating women when their exposure to sunshine is limited, regardless of their socioeconomic status.


    We thank Drs S Rimmer and S Russell for radiological assessments and Drs A Kapoor, P L Harris, and A Maw for referring three of the patients.

    Funding: None.

    Conflict of interest: None.


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