Re: British Paediatric and Adolescent Bone Group’s position statement on vitamin D deficiency
6 February 2013
We read with interest the responses to our position statement from Professor Nussey and Drs Scheimberg and Cohen (1). We are not a committee but a current comprehensive group of clinicians managing children with bone disease in the UK. Our opinions are based on our combined clinical experience of vitamin D deficiency in infants, children and adolescents across the UK. Our statement was a concise expression of our position rather than an exposition of the evidence. However, careful consideration of the extant literature does underpin our statement (whilst we acknowledge the paucity of studies which examine clinical outcomes in relation to serum 25-hydroxy vitamin D (25OHD) concentrations).
Our cut-off value for 25OHD, 25nmol/l, is that used by NICE for deficiency - based on the systematic reviews undertaken by Cochrane, the Scientific Advisory Committee on Nutrition and the Institute of Medicine, and by the Department of Health for “low vitamin D status” (recently endorsed in the recent letter from the UK Chief Medical Officers) (2). Nonetheless, rather than the value for serum 25OHD alone (dependent in part upon the laboratory method) determining the development of rickets, other crucial factors need to be taken into consideration including low serum phosphate and/or a low dietary intake of calcium resulting in elevation of serum parathyroid hormone. In contrast to the adult autopsy data cited, Edouard et al found no evidence of defects of bone mineralisation in bone biopsies from 37 children with serum 25OHD concentrations between 13 and 50nmol/l (3). It is true that we have not addressed the important question of whether current recommended doses of vitamin D raise serum 25OHD levels adequately but there is not yet an agreed definition of “adequate”.
No reference is presented by Nussey to support the statement that a few children with rickets have “several” fractures. The evidence suggests that, in a mobile child with rickets, if they fracture a single fracture is the norm. The National Diet and Nutrition Survey showed that up to 30% of South Asian toddlers in the UK have a 25OHD concentration <25nmol/l (4). Vitamin D status in infants in this group is likely to be the same or even lower. If serum 25OHD <25nmol/l was associated with fragility fractures then we might expect to see hundreds of cases of fractures of ribs or proximal humeri captured on the thousands of chest radiographs performed for indications such as bronchiolitis each year. This is not our experience. We also know that the prevalence of clinical signs of rickets is far lower than the incidence of deficiency, <1 in 1000 (5).
The sensitivity of conventional radiology in detecting rickets may be unclear (quoted reports from 1909 and 1923 regarding the timing of radiological changes, are of limited value given the improvements in radiography over the last century). However, we suppose that the authors are not proposing bone biopsy as a clinical tool to diagnose rickets. Whilst we accept radiological changes of rickets can be subtle, we stress that biochemical changes should be present in all cases of vitamin D deficiency.
The use of the term “subclinical rickets” is problematic in the absence of a clear definition. Supposing a definition could be found there would remain the question as to whether it matters. This would have to be established through assessment of bone strength and resistance to fracture which ought not to be assumed to be reduced.
Finally the histopathological changes of dead infants with 25OHD levels >50nmol/l described by Scheimberg and Cohen are interesting but lack crucial details, including any dietary information (e.g. calcium intake) and biochemical data, including the actual 25OHD concentration.
We stand by our original statement and trust that the guidance provided will be useful for clinicians managing children with vitamin D-related problems.
1. Arundel P, Ahmed SF, Allgrove J, Bishop NJ, Burren CP, Jacobs, B, Mughal MZ, Offiah AC, Shaw NJ. British Paediatric and Adolescent Bone Group’s position statement on vitamin D deficiency. BMJ. 2012 Dec 3;345:e8182
2. Letter from Chief Medical Officers of the United Kingdom. Vitamin D – Advice on supplements for at risk groups. Department of Health. 02 February 2012
3. Edouard T, Glorieux FH, Rauch F. Relationship between vitamin D status and bone mineralization, mass, and metabolism in children with osteogenesis imperfecta: histomorphometric study. J Bone Miner Res. 2011 Sep;26(9):2245-51
4. Lawson M, Thomas M. Vitamin d concentrations in Asian children aged 2 years living in England: population survey. BMJ. 1999 Jan 2;318(7175):28
5. Callaghan AL, Moy RJ, Booth IW, Debelle G, Shaw NJ. Incidence of symptomatic vitamin D deficiency. Arch Dis Child. 2006 Jul;91(7):606-7
P Arundel, consultant in paediatric metabolic bone disease and secretary of British Paediatric and Adolescent Bone Group (1)
S F Ahmed, Samson Gemmell Chair of Child Health (2)
J Allgrove, consultant paediatric endocrinologist (3)
N J Bishop, professor of paediatric bone disease (4)
C P Burren, consultant paediatric endocrinologist and diabetologist (5)
B Jacobs, consultant paediatrician (6)
M Z Mughal, consultant in paediatric bone disorders (7)
A C Offiah, HEFCE clinical senior lecturer (4)
N J Shaw, consultant paediatric endocrinologist (8)
1. Sheffield Children’s NHS Foundation Trust, Sheffield, UK
2. School of Medicine, University of Glasgow, Glasgow, UK
3. Great Ormond Street Hospital, London. UK
4. Academic Unit of Child Health, University of Sheffield, Sheffield, UK
5. Bristol Royal Hospital for Children, Bristol, UK
6. Royal National Orthopaedic Hospital, Stanmore, UK
7. Royal Manchester Children’s Hospital, Manchester, UK
8. Birmingham Children’s Hospital, Birmingham, UK
Competing interests: None declared
Sheffield Children’s NHS Foundation Trust, Western Bank, Sheffield, S10 2TH
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