bs_bs_banner
doi:10.1111/jpc.12781
ORIGINAL ARTICLE
Randomised controlled trial of daily versus stoss vitamin D therapy in Aboriginal children Jason KG Tan,1,2 Paula Kearns,3 Andrew C Martin1 and Aris Siafarikas1,2,4 1
Neonatal Intensive Care Unit, Princess Margaret Hospital, 2School of Paediatrics and Child Health, University of Western Australia, 3Rural Clinical School of Western Australia, Perth and 4Institute for Health Research, University of Notre Dame, Fremantle, Western Australia, Australia
Aim: The prevalence of vitamin D deficiency has risen in countries with a high ultraviolet index and sunny environment such as Australia. There is lack of information on vitamin D status and best possible therapy in Australian Aboriginal children. We aim to (i) describe the vitamin D status in an opportunistic sample of Aboriginal children in Western Australia and (ii) compare the efficacy of oral daily vitamin D with oral stoss vitamin D therapy in this sample. Method: Participants were recruited from a metropolitan area (31' S) and a rural area (17' S). Those with a 25(OH)D level less than 78 nmol/L were randomised to receive daily or stoss vitamin D therapy with follow-up at 4–6 months and 9–12 months. Biochemical and clinical parameters such as 25(OH)D, alkaline phosphatase, calcium and sun exposure were collected. Results: Seventy-three participants were enrolled (61 from a metropolitan and 12 from a rural area). 25(OH)D levels were greater than 78 nmol/L in 9/12 (75%) participants in the rural group and 21/61 (34%) in the metropolitan group. 25(OH)D levels were less than 78 nmol/L in 43/73 (59%) participants. Of these, 34/43 (79%) were insufficient (50–78 nmol/L), 8/43 (19%) mildly deficient (27.5–50 nmol/L) and 1/43 (2%) deficient (78 nmol/L), insufficient (50–78 nmol/L), mildly deficient (27.5–50 nmol/L) and deficient ( 78 nmol/L, compared with 34% (21/61) in the metropolitan group (P ≤ 0.05). Significant differences were observed in 25(OH)D, corrected serum calcium, phosphate and skin phototype between the two groups (Table 1).
Factors that influence 25(OH)D levels Location predicted low 25(OH)D levels (Fisher’s exact test, P = 0.009). 25(OH)D levels were correlated to sun exposure (r2 = 0.18, P < 0.05) and sun exposure score (r2 = 0.16, P < 0.05). The 25(OH)D levels were distributed evenly across skin phototypes (Kruskal–Wallis test, P = 0.85) and seasons (Kruskal–Wallis test, P = 0.443).
Journal of Paediatrics and Child Health 51 (2015) 626–631 © 2014 The Authors Journal of Paediatrics and Child Health © 2014 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
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Vitamin D therapy in Aboriginal children
JKG Tan et al.
Fig. 1 Treatment algorithm based on initial 25(OH)D level.
Daily versus stoss vitamin D therapy We randomised 37 of the 43 participants. Only 14/37 (36%) and 6/14 (43%) had data available for analysis at the first and second time point, respectively (Table 2). Participants in either group reported no adverse events or side effects. The daily group had a greater increase in 25(OH)D levels after treatment than the stoss group (Fig. 3). At 4–6 months, the daily group had a greater mean increase in 25(OH)D levels from baseline than the stoss group with a difference of 18.25 nmol/L (95% CI −17.5 to 54.0, P = 0.32). Similarly, at 8–12 months, the daily group had a greater mean increase in 25(OH)D levels from baseline than the stoss group with a difference of 17.67 nmol/L (95% CI 2.4–32.9, P = 0.03). At both time points, the two groups were similar in age, growth parameters, gender, sun exposure score and initial 25(OH)D levels.
Discussion This study highlights that a considerable proportion of Aboriginal children in Western Australia have low vitamin D levels. We observed a difference between groups living in rural versus metropolitan areas. Oral stoss supplements may be considered a therapeutic alternative to daily supplements. Vitamin D deficiency was found in 12% and insufficiency in 59% of our participants, which are comparable with those reported in Australia. In Perth, vitamin D deficiency ranged from 4.4% in healthy adolescents (low risk), 30% in pregnant women to 39% of refugee children (high-risk group).9,21–23 Two studies reported mean serum 25(OH)D levels of 40 and 628
56.8 nmol/L in Australian Aboriginal adults.13,14 A study from the Northern Territory described the vitamin D status of nonAboriginal and Aboriginal children.24 They used similar definitions for deficiency and insufficiency and found 3.1% and 19.4% had vitamin D deficiency and insufficiency, respectively. We found almost threefold more of children with insufficient 25(OH)D levels, which may be explained by difference in location and weather. Environmental factors may explain the difference in 25(OH)D levels between the rural and metropolitan areas.10,25,26 The rural group on average had a higher annual UV index with more sunny days than the metropolitan group.27 Also, we hypothesise that metropolitan compared with rural children may live a more ‘modern’ life-style (e.g. use of electronic entertainment) that leads to reduced exposure to UVB radiation. We feel that the combination of life-style and UVB exposure explains the differences seen between rural and metropolitan groups. Skin phototype did not have a significant impact on 25(OH)D levels in this study. This may be explained by small sample size and bias. We found that children with a higher skin phototype were more likely to be from the rural group, which had higher average 25(OH)D levels. However, skin phototype likely contributed to the low 25(OH)D levels, which would be in keeping with other studies.28,29 We found the response in the daily therapy group was almost twice as much as the stoss therapy group after 4–8 months, and five times at 8–12 months. The dose of stoss therapy was more conservative than other studies, which may explain the difference seen. The dose used for stoss therapy did result in a rise from baseline of 25(OH)D in our study. Guidelines have
Journal of Paediatrics and Child Health 51 (2015) 626–631 © 2014 The Authors Journal of Paediatrics and Child Health © 2014 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
JKG Tan et al.
Vitamin D therapy in Aboriginal children
Fig. 2 Consort algorithm of enrolment, randomisation and follow-up. *Lost to follow-up: unable to contact (for medication drop-off or blood draw), no withdrawal from study.
suggested that stoss therapy is a safe and effective method of treatment for vitamin D.5,7,30 We propose that oral stoss therapy could be used to treat vitamin D deficiency; however, research to evaluate the optimal dose and schedule is required before widespread use. Our study was limited by the small sample size and selection bias. Our cohort was a sample of convenience comprised of acute illness and day surgery patients. It could be argued that our cohort had low 25(OH)D levels from reduced sun exposure or infection. However, low baseline 25(OH)D levels reflect reduced UVB exposure and dietary vitamin D over a prolonged period of weeks.12 A recent study found that acute bacterial
infection has little effect on baseline 25(OH)D levels in children.31 These studies suggest that acute illness and infection may not influence 25(OH)D levels. We were disappointed by our low rates of follow-up, despite planning for out-of-hospital management. Other studies and programmes have had varied success ranging from early stoppage to 89% follow-up rates.32–35 Learning from these studies will help improve preventative health-care delivery to Aboriginal children. As with all vitamin D research, discussion regarding awareness of sun exposure is important but is beyond the scope of this paper. We concur with the recent guidelines published in the
Journal of Paediatrics and Child Health 51 (2015) 626–631 © 2014 The Authors Journal of Paediatrics and Child Health © 2014 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
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Vitamin D therapy in Aboriginal children
Table 1
JKG Tan et al.
Comparison of metropolitan and rural groups
Female, n (%) Age, years Height (cm) Height Z-score Weight (kg) Weight Z-score BMI (kg/m2) BMI Z-score Sun exposure score Skin phototype 25(OH)D, nmol/L Corrected Ca, mmol/L ALP, mmol/L Phosphate, mmol/L
Metropolitan
Rural
P-value
30/61 (49%) 6.72 (5.59, 7.85) 119.0 (107.6, 130.5) −0.13 (−0.72, 0.46) 25.6 (20.7, 30.6) −0.17 (−0.59, 0.26) 17.3 (15.6, 18.9) −0.09 (−6.90, 0.51) 1.35 (1.27, 1.43) 4.19 (median 4.0) 71.1 (65.1, 77.1) 2.33 (2.31, 2.36) 214.7 (199.7, 229.7) 1.75 (1.67, 1.83)
4/12 (33%) 6.77 (4.04, 9.49) 113.4 (82.5, 144.4) 0.63 (−1.36, 2.63) 34.6 (8.8, 60.4) 0.34 (−1.45, 2.13) 18.0 (14.5, 21.5) 0.79 (−0.12, 1.71) 1.32 (1.08, 1.56) 4.91 (median 5.0) 92.0 (76.1, 107.9) 2.23 (2.04, 2.41) 238.5 (165.4, 311.6) 1.99 (1.59, 2.40)
0.360 0.973 0.656 0.279 0.232 0.403 0.675 0.169 0.811 0.019*† 0.007* 0.026* 0.291 0.05*
*P-value < 0.05. †Mann–Whitney U-test. ALP, alkaline phosphatase; BMI, body mass index; Ca, calcium.
Table 2 Treatment response of daily and stoss therapy Visit
n
Daily therapy
n
Stoss therapy
P-value
Visit 1 (0 weeks) Visit 2 (mean of 28 weeks) Visit 3 (mean of 44 weeks)
8 8 3
56.4 (46.8, 66.0) 93.1 (64.7, 121.6) 81.7 (67.5, 95.8)
6 6 3
58.2 (45.7, 70.7) 76.7 (61.0, 92.3) 65.0 (41.3, 88.7)
0.781 0.293 0.060
initial treatment. If there is poor response, stoss therapy may be an option with two to three monthly follow-ups. Future research is required to validate these findings, determine the optimal therapy schedule for stoss therapy and better understand the extra-skeletal role of vitamin D.
Acknowledgements This research was funded by a seeding grant from the PMH Foundation. We acknowledge and greatly thank all the participants and their families for their participation. We would also like to acknowledge staff from DAHS, the paediatric unit in Derby, Derbal Yerrigan and PMH.
References
Fig. 3
Comparison of daily versus stoss therapy group over time.
Medical Journal of Australia that advises sensible sun exposure. It recommends children with higher skin phototypes should have intermittent sun exposure without UV protection in summer.5 We recommend opportunistic screening of Aboriginal children who attend hospital and use daily supplementation for 630
1 Prentice A. Nutritional rickets around the world. J. Steroid Biochem. Mol. Biol. 2012; 136: 201–6. 2 Huh SY, Gordon CM. Vitamin D deficiency in children and adolescents: epidemiology, impact and treatment. Rev. Endocr. Metab. Disord. 2008; 9: 161–70. 3 Misra M, Pacaud D, Petryk A, Collett-Solberg PF, Kappy M. Vitamin D deficiency in children and its management: review of current knowledge and recommendations. Pediatrics 2008; 122: 398– 417. 4 Holick MF. Vitamin D extraskeletal health. Rheum. Dis. Clin. North Am. 2012; 38: 141–60.
Journal of Paediatrics and Child Health 51 (2015) 626–631 © 2014 The Authors Journal of Paediatrics and Child Health © 2014 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
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5 Paxton GA, Teale GR, Nowson CA et al. Vitamin D and health in pregnancy, infants, children and adolescents in Australia and New Zealand: a position statement. Med. J. Aust. 2013; 198: 142–3. 6 Munns C, Zacharin MR, Rodda CP et al. Prevention and treatment of infant and childhood vitamin D deficiency in Australia and New Zealand: a consensus statement. Med. J. Aust. 2006; 185: 268–72. 7 Shepherd D, Belessis Y, Katz T, Morton J, Field P, Jaffe A. Single high-dose oral vitamin D(3) (stoss) therapy – a solution to vitamin D deficiency in children with cystic fibrosis? J. Cyst. Fibros. 2012; 12: 177–82. 8 Munns CF, Simm PJ, Rodda CP et al. Incidence of vitamin D deficiency rickets among Australian children: an Australian Paediatric Surveillance Unit study. Med. J. Aust. 2012; 196: 466–8. 9 Siafarikas A, Youngs L, Colvin J et al. Skin type and lack of UVB exposure as risk factors for vitamin D deficiency in Western Australia despite sunny ambient conditions [Abstract]. Horm. Res. 2005; 64 (Suppl. 1): 91. 10 Gilchrest BA. Sun exposure and vitamin D sufficiency. Am. J. Clin. Nutr. 2008; 88: 570S–577S. 11 Springbett P, Buglass S, Young AR. Photoprotection and vitamin D status. J. Photochem. Photobiol. B. 2010; 101: 160–8. 12 Armas LA, Dowell S, Akhter M et al. Ultraviolet-B radiation increases serum 25-hydroxyvitamin D levels: the effect of UVB dose and skin color. J. Am. Acad. Dermatol. 2007; 57: 588–93. 13 Benson J, Wilson A, Stocks N, Moulding N. Muscle pain as an indicator of vitamin D deficiency in an urban Australian Aboriginal population. Med. J. Aust. 2006; 185: 76–7. 14 Vanlint SJ, Morris HA, Newbury JW, Crockett AJ. Vitamin D insufficiency in Aboriginal Australians. Med. J. Aust. 2011; 194: 131–4. 15 Fitzpatrick TB. The validity and practicality of sun-reactive skin types I through VI. Arch. Dermatol. 1988; 124: 869–71. 16 Specker BL, Valanis B, Hertzberg V, Edwards N, Tsang RC. Sunshine exposure and serum 25-hydroxyvitamin D concentrations in exclusively breast-fed infants. J. Pediatr. 1985; 107: 372–6. 17 Wagner CL, Greer FR. Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. Pediatrics 2008; 122: 1142–52. 18 Lerch C, Meissner T. Interventions for the prevention of nutritional rickets in term born children. Cochrane Database Syst. Rev. 2007; (4): CD006164. 19 Shah BR, Finberg L. Single-day therapy for nutritional vitamin D-deficiency rickets: a preferred method. J. Pediatr. 1994; 125: 487–90. 20 Ilahi M, Armas LA, Heaney RP. Pharmacokinetics of a single, large dose of cholecalciferol. Am. J. Clin. Nutr. 2008; 87: 688–91. 21 Mutch RC, Cherian S, Nemba K et al. Tertiary paediatric refugee health clinic in Western Australia: analysis of the first 1026 children. J. Paediatr. Child Health 2012; 48: 582–7.
Vitamin D therapy in Aboriginal children
22 Hollams EM, Hart PH, Holt BJ et al. Vitamin D and atopy and asthma phenotypes in children: a longitudinal cohort study. Eur. Respir. J. 2011; 38: 1320–7. 23 Whitehouse AJ, Holt BJ, Serralha M, Holt PG, Kusel MM, Hart PH. Maternal serum vitamin D levels during pregnancy and offspring neurocognitive development. Pediatrics 2012; 129: 485–93. 24 Dyson A, Pizzutto SJ, MacLennan C, Stone M, Chang AB. The prevalence of vitamin D deficiency in children in the Northern Territory. J. Paediatr. Child Health 2014; 50: 47–50. 25 Freedman DM, Cahoon EK, Rajaraman P et al. Sunlight and other determinants of circulating 25-hydroxyvitamin D levels in black and white participants in a nationwide US study. Am. J. Epidemiol. 2013; 177: 180–92. 26 Norman AW. Sunlight, season, skin pigmentation, vitamin D, and 25-hydroxyvitamin D: integral components of the vitamin D endocrine system. Am. J. Clin. Nutr. 1998; 67: 1108–10. 27 Commonwealth of Australia. Average Solar Ultraviolet (UV) Index. 2013. Available from: http://www.bom.gov.au/jsp/ncc/climate _averages/uv-index/index.jsp [accessed February 2013]. 28 Nessvi S, Johansson L, Jopson J et al. Association of 25-hydroxyvitamin D3)levels in adult New Zealanders with ethnicity, skin color and self-reported skin sensitivity to sun exposure. Photochem. Photobiol. 2011; 87: 1173–8. 29 Poopedi MA, Norris SA, Pettifor JM. Factors influencing the vitamin D status of 10-year-old urban South African children. Public Health Nutr. 2011; 14: 334–9. 30 Diamond TH, Ho KW, Rohl PG, Meerkin M. Annual intramuscular injection of a megadose of cholecalciferol for treatment of vitamin D deficiency: efficacy and safety data. Med. J. Aust. 2005; 183: 10–12. 31 Binfield A, Aird C, Murdoch DR, Elder P, Walls T. Are vitamin D levels affected by acute bacterial infections in children? J. Paediatr. Child Health 2014; 50: 643–6. 32 Hull BP, McIntyre PB, Couzos S. Evaluation of immunisation coverage for aboriginal and Torres Strait Islander children using the Australian Childhood Immunisation Register. Aust. N. Z. J. Public Health 2004; 28: 47–52. 33 National Centre for Immunisation Research and Surveillance (NCIRS). Vaccine Preventable Diseases and Vaccination Coverage in Aboriginal and Torres Strait Islander People, Australia 2006–2010. 2013. Available from: http://www.health.gov.au/internet/publications/ publishing.nsf/Content/cda-cdi37suppl.htm/$File/cdi37suppl.pdf [accessed November 2014]. 34 Sibthorpe BM, Bailie RS, Brady MA, Ball SA, Sumner-Dodd P, Hall WD. The demise of a planned randomised controlled trial in an urban Aboriginal medical service. Med. J. Aust. 2002; 176: 273–6. 35 Morris PS. Randomised controlled trials addressing Australian aboriginal health needs: a systematic review of the literature. J. Paediatr. Child Health 1999; 35: 130–5.
Journal of Paediatrics and Child Health 51 (2015) 626–631 © 2014 The Authors Journal of Paediatrics and Child Health © 2014 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
631
doi:10.1111/jpc.12781
ORIGINAL ARTICLE
Randomised controlled trial of daily versus stoss vitamin D therapy in Aboriginal children Jason KG Tan,1,2 Paula Kearns,3 Andrew C Martin1 and Aris Siafarikas1,2,4 1
Neonatal Intensive Care Unit, Princess Margaret Hospital, 2School of Paediatrics and Child Health, University of Western Australia, 3Rural Clinical School of Western Australia, Perth and 4Institute for Health Research, University of Notre Dame, Fremantle, Western Australia, Australia
Aim: The prevalence of vitamin D deficiency has risen in countries with a high ultraviolet index and sunny environment such as Australia. There is lack of information on vitamin D status and best possible therapy in Australian Aboriginal children. We aim to (i) describe the vitamin D status in an opportunistic sample of Aboriginal children in Western Australia and (ii) compare the efficacy of oral daily vitamin D with oral stoss vitamin D therapy in this sample. Method: Participants were recruited from a metropolitan area (31' S) and a rural area (17' S). Those with a 25(OH)D level less than 78 nmol/L were randomised to receive daily or stoss vitamin D therapy with follow-up at 4–6 months and 9–12 months. Biochemical and clinical parameters such as 25(OH)D, alkaline phosphatase, calcium and sun exposure were collected. Results: Seventy-three participants were enrolled (61 from a metropolitan and 12 from a rural area). 25(OH)D levels were greater than 78 nmol/L in 9/12 (75%) participants in the rural group and 21/61 (34%) in the metropolitan group. 25(OH)D levels were less than 78 nmol/L in 43/73 (59%) participants. Of these, 34/43 (79%) were insufficient (50–78 nmol/L), 8/43 (19%) mildly deficient (27.5–50 nmol/L) and 1/43 (2%) deficient (78 nmol/L), insufficient (50–78 nmol/L), mildly deficient (27.5–50 nmol/L) and deficient ( 78 nmol/L, compared with 34% (21/61) in the metropolitan group (P ≤ 0.05). Significant differences were observed in 25(OH)D, corrected serum calcium, phosphate and skin phototype between the two groups (Table 1).
Factors that influence 25(OH)D levels Location predicted low 25(OH)D levels (Fisher’s exact test, P = 0.009). 25(OH)D levels were correlated to sun exposure (r2 = 0.18, P < 0.05) and sun exposure score (r2 = 0.16, P < 0.05). The 25(OH)D levels were distributed evenly across skin phototypes (Kruskal–Wallis test, P = 0.85) and seasons (Kruskal–Wallis test, P = 0.443).
Journal of Paediatrics and Child Health 51 (2015) 626–631 © 2014 The Authors Journal of Paediatrics and Child Health © 2014 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
627
Vitamin D therapy in Aboriginal children
JKG Tan et al.
Fig. 1 Treatment algorithm based on initial 25(OH)D level.
Daily versus stoss vitamin D therapy We randomised 37 of the 43 participants. Only 14/37 (36%) and 6/14 (43%) had data available for analysis at the first and second time point, respectively (Table 2). Participants in either group reported no adverse events or side effects. The daily group had a greater increase in 25(OH)D levels after treatment than the stoss group (Fig. 3). At 4–6 months, the daily group had a greater mean increase in 25(OH)D levels from baseline than the stoss group with a difference of 18.25 nmol/L (95% CI −17.5 to 54.0, P = 0.32). Similarly, at 8–12 months, the daily group had a greater mean increase in 25(OH)D levels from baseline than the stoss group with a difference of 17.67 nmol/L (95% CI 2.4–32.9, P = 0.03). At both time points, the two groups were similar in age, growth parameters, gender, sun exposure score and initial 25(OH)D levels.
Discussion This study highlights that a considerable proportion of Aboriginal children in Western Australia have low vitamin D levels. We observed a difference between groups living in rural versus metropolitan areas. Oral stoss supplements may be considered a therapeutic alternative to daily supplements. Vitamin D deficiency was found in 12% and insufficiency in 59% of our participants, which are comparable with those reported in Australia. In Perth, vitamin D deficiency ranged from 4.4% in healthy adolescents (low risk), 30% in pregnant women to 39% of refugee children (high-risk group).9,21–23 Two studies reported mean serum 25(OH)D levels of 40 and 628
56.8 nmol/L in Australian Aboriginal adults.13,14 A study from the Northern Territory described the vitamin D status of nonAboriginal and Aboriginal children.24 They used similar definitions for deficiency and insufficiency and found 3.1% and 19.4% had vitamin D deficiency and insufficiency, respectively. We found almost threefold more of children with insufficient 25(OH)D levels, which may be explained by difference in location and weather. Environmental factors may explain the difference in 25(OH)D levels between the rural and metropolitan areas.10,25,26 The rural group on average had a higher annual UV index with more sunny days than the metropolitan group.27 Also, we hypothesise that metropolitan compared with rural children may live a more ‘modern’ life-style (e.g. use of electronic entertainment) that leads to reduced exposure to UVB radiation. We feel that the combination of life-style and UVB exposure explains the differences seen between rural and metropolitan groups. Skin phototype did not have a significant impact on 25(OH)D levels in this study. This may be explained by small sample size and bias. We found that children with a higher skin phototype were more likely to be from the rural group, which had higher average 25(OH)D levels. However, skin phototype likely contributed to the low 25(OH)D levels, which would be in keeping with other studies.28,29 We found the response in the daily therapy group was almost twice as much as the stoss therapy group after 4–8 months, and five times at 8–12 months. The dose of stoss therapy was more conservative than other studies, which may explain the difference seen. The dose used for stoss therapy did result in a rise from baseline of 25(OH)D in our study. Guidelines have
Journal of Paediatrics and Child Health 51 (2015) 626–631 © 2014 The Authors Journal of Paediatrics and Child Health © 2014 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
JKG Tan et al.
Vitamin D therapy in Aboriginal children
Fig. 2 Consort algorithm of enrolment, randomisation and follow-up. *Lost to follow-up: unable to contact (for medication drop-off or blood draw), no withdrawal from study.
suggested that stoss therapy is a safe and effective method of treatment for vitamin D.5,7,30 We propose that oral stoss therapy could be used to treat vitamin D deficiency; however, research to evaluate the optimal dose and schedule is required before widespread use. Our study was limited by the small sample size and selection bias. Our cohort was a sample of convenience comprised of acute illness and day surgery patients. It could be argued that our cohort had low 25(OH)D levels from reduced sun exposure or infection. However, low baseline 25(OH)D levels reflect reduced UVB exposure and dietary vitamin D over a prolonged period of weeks.12 A recent study found that acute bacterial
infection has little effect on baseline 25(OH)D levels in children.31 These studies suggest that acute illness and infection may not influence 25(OH)D levels. We were disappointed by our low rates of follow-up, despite planning for out-of-hospital management. Other studies and programmes have had varied success ranging from early stoppage to 89% follow-up rates.32–35 Learning from these studies will help improve preventative health-care delivery to Aboriginal children. As with all vitamin D research, discussion regarding awareness of sun exposure is important but is beyond the scope of this paper. We concur with the recent guidelines published in the
Journal of Paediatrics and Child Health 51 (2015) 626–631 © 2014 The Authors Journal of Paediatrics and Child Health © 2014 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
629
Vitamin D therapy in Aboriginal children
Table 1
JKG Tan et al.
Comparison of metropolitan and rural groups
Female, n (%) Age, years Height (cm) Height Z-score Weight (kg) Weight Z-score BMI (kg/m2) BMI Z-score Sun exposure score Skin phototype 25(OH)D, nmol/L Corrected Ca, mmol/L ALP, mmol/L Phosphate, mmol/L
Metropolitan
Rural
P-value
30/61 (49%) 6.72 (5.59, 7.85) 119.0 (107.6, 130.5) −0.13 (−0.72, 0.46) 25.6 (20.7, 30.6) −0.17 (−0.59, 0.26) 17.3 (15.6, 18.9) −0.09 (−6.90, 0.51) 1.35 (1.27, 1.43) 4.19 (median 4.0) 71.1 (65.1, 77.1) 2.33 (2.31, 2.36) 214.7 (199.7, 229.7) 1.75 (1.67, 1.83)
4/12 (33%) 6.77 (4.04, 9.49) 113.4 (82.5, 144.4) 0.63 (−1.36, 2.63) 34.6 (8.8, 60.4) 0.34 (−1.45, 2.13) 18.0 (14.5, 21.5) 0.79 (−0.12, 1.71) 1.32 (1.08, 1.56) 4.91 (median 5.0) 92.0 (76.1, 107.9) 2.23 (2.04, 2.41) 238.5 (165.4, 311.6) 1.99 (1.59, 2.40)
0.360 0.973 0.656 0.279 0.232 0.403 0.675 0.169 0.811 0.019*† 0.007* 0.026* 0.291 0.05*
*P-value < 0.05. †Mann–Whitney U-test. ALP, alkaline phosphatase; BMI, body mass index; Ca, calcium.
Table 2 Treatment response of daily and stoss therapy Visit
n
Daily therapy
n
Stoss therapy
P-value
Visit 1 (0 weeks) Visit 2 (mean of 28 weeks) Visit 3 (mean of 44 weeks)
8 8 3
56.4 (46.8, 66.0) 93.1 (64.7, 121.6) 81.7 (67.5, 95.8)
6 6 3
58.2 (45.7, 70.7) 76.7 (61.0, 92.3) 65.0 (41.3, 88.7)
0.781 0.293 0.060
initial treatment. If there is poor response, stoss therapy may be an option with two to three monthly follow-ups. Future research is required to validate these findings, determine the optimal therapy schedule for stoss therapy and better understand the extra-skeletal role of vitamin D.
Acknowledgements This research was funded by a seeding grant from the PMH Foundation. We acknowledge and greatly thank all the participants and their families for their participation. We would also like to acknowledge staff from DAHS, the paediatric unit in Derby, Derbal Yerrigan and PMH.
References
Fig. 3
Comparison of daily versus stoss therapy group over time.
Medical Journal of Australia that advises sensible sun exposure. It recommends children with higher skin phototypes should have intermittent sun exposure without UV protection in summer.5 We recommend opportunistic screening of Aboriginal children who attend hospital and use daily supplementation for 630
1 Prentice A. Nutritional rickets around the world. J. Steroid Biochem. Mol. Biol. 2012; 136: 201–6. 2 Huh SY, Gordon CM. Vitamin D deficiency in children and adolescents: epidemiology, impact and treatment. Rev. Endocr. Metab. Disord. 2008; 9: 161–70. 3 Misra M, Pacaud D, Petryk A, Collett-Solberg PF, Kappy M. Vitamin D deficiency in children and its management: review of current knowledge and recommendations. Pediatrics 2008; 122: 398– 417. 4 Holick MF. Vitamin D extraskeletal health. Rheum. Dis. Clin. North Am. 2012; 38: 141–60.
Journal of Paediatrics and Child Health 51 (2015) 626–631 © 2014 The Authors Journal of Paediatrics and Child Health © 2014 Paediatrics and Child Health Division (Royal Australasian College of Physicians)
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