ICCBH2017 Poster Presentations (1) (209 abstracts)
1Royal Manchester Childrens Hospital, Manchester, UK; 2Great Ormond Street Hospital for Children NHS Trust, London, UK; 3Northwick Park Hospital, London, UK; 4Royal Free London NHS Foundation, London, UK; 5Royal College of Paediatrics & Child Health, British Paediatric Surveillance Unit, London, UK; 6Childrens University Hospital, Temple Street, Dublin, Ireland; 7Royal Hospital for Sick Children, Glasgow, UK; 8Birmingham Childrens Hospital, Birmingham, UK.
Background: Rickets is a disorder of the growing child arising from impaired mineralisation of the growth plate and osteoid. The most common cause of NR in the UK is thought to be secondary to vitamin D deficiency [VDD; serum 25-hydroxyvitamin D (25OHD) <25 nmol/l], although in some African & South Asian countries dietary calcium deficiency (DCaD) by itself, or together with VDD is an important cause of NR (Ann Trop Paediatr. 2006;26:116). Currently, the data on new cases of NR is being collected monthly (March 2015March 2017) from 3500 Paediatricians, using the BPSU reporting methodology.
Objective: Eight cases of NR who did not meet the criteria for VDD (serum 25OHD <25 nmol/l) but had clinical and radiological features of rickets/osteomalacia have been reported to BPSU, during 22 months of surveillance (Table). In these patients, DCaD is likely to have contributed to the causation of NR.
Results: The table summarises the patient characteristics and biochemical features of NR.
Discussion: Since one of the criteria for reporting cases of NR to the BPSU is a serum 25OHD<25 nmol/l, some cases in which DCaD may have contributed to the causation of NR may have been missed. Provision of vitamin D along with recommended dietary intake of calcium for the age of the child is important for prevention of NR.
Conclusion: We conclude that DCaD, along with inadequate vitamin D status (serum 25OHD >25 but <50 nmol/l), contributes to the causation of NR in the UK.
Age in months and gender | Ethnicity | Ca mmol/l | P mmol/l | ALP IU/l | PTH | 25OHD Nmol/l |
9; M | A&C | 2.2 | 1.06 (1.31.9) | 1794 (<300) | 19.8 pmol/ (1.31.9) | 27.3 |
17; M | U | 2.53 | 1.22 (0.91.8) | 1634 (110440) | 16.5 pmol/l (1.66.9 | 27 |
22; F | SA | 2.21 | 1.2 (0.91.8) | 914 (60425) | 24.6 pmol/l (1.66.9) | 29 |
10; F | A/C | 2.29 | 0.84 (0.812,26) | 911 (126524) | 247 ng/ml (1070) | 31 |
25; M | A/C | 2.23 | 1.15 (0.81.4) | 1096 (0281) | 389 ng/ml (550) | 33 |
20; M | A-C | 1.88 | 0.5 (0.81.4) | 6000 (0281) | 1051 ng/ml (550) | 44 |
27; F | A-C | 2.09 | 0.97 (0.91.8) | >1500 (60435) | 89.4 pmol/l (06.4) | 48 |
176; F | SA | 1.39 | 1.0 (0.81.5) | 539 (50390) | 87.1 pmol/l (1.57.6) | 28 |
Legend: M- male; F- female; A&C African & Caucasian; A/C African or Afro-Caribbean; U-Unknown. SA- South Asian; Ca serum calcium; P- serum inorganic phosphate; ALP serum alkaline phosphatase; PTH- plasma parathormone; 25OHD serum 25-hydroxyvitamin D. Age related reference range from local laboratories given in parentheses. |
Disclosure: The authors declared no competing interests.