Surveillance

Canadian Paediatric Surveillance Program
Vitamin D Deficiency Rickets

Principal investigator

Dr. Leanne Ward, University of Ottawa, Division of Endocrinology and Metabolism, Department of Paediatrics, Children’s Hospital of Eastern Ontario, 401 Smyth Rd., Ottawa ON  K1H 8L1; tel.: (613) 737-2253; fax: (613) 738-4236; e-mail: ward_l@cheo.on.ca

Co-investigators

Dr. Stanley Zlotkin, University of Toronto, Division of Gastroenterology and Nutrition, Departments of Paediatrics and Nutritional Sciences, The Hospital for Sick Children

Dr. Moyez Ladhani, McMaster University, Department of Paediatrics, McMaster Children’s Hospital

Study Results

Results can be found in the CPSP 2004 Results (pdf format).

Study publications/presentations

CPSP highlights

• What does the CPSP have to do with public health?
• The multiple facets of bone diseases.
• CPSP 2002 Results: What have we learned?
• A risk of northern climate!

Presentations

• The changing face of bone diseases.
• The many faces of Osteogenesis imperfecta.
• Vitamin D deficiency in rickets (VDDR) among children living in Canada: A new look at an old disease.
• Vitamin D Deficiency Rickets among Children Living in Canada: A New Look at an Old Disease.
• Public health impact of the Canadian Paediatric Surveillance Program (CPSP).
• Risk factors for vitamin D deficiency rickets among children living in Canada: Results of an incidence study through the Canadian Pediatric Surveillance Program. Ward LM, Gaboury I, Ladhani M, Zlotkin S. Presented at the Canadian Society of Endocrinology and Metabolism’s Annual Meeting, Ottawa, October 2003.

News Release

• Canadian Paediatric Society confirms that rickets still a major health issue (June 17, 2004)

Background

Vitamin D is critical for calcium homeostasis and for mineralization of the skeleton, especially during the growing years. A deficiency in vitamin D is costly for the paediatric patient as it leads to rickets (a mineralization defect at the epiphyseal growth plates) and osteomalacia (a mineralization defect of bone tissue). These effects are associated with pain, fractures, skeletal deformity, growth retardation, dental enamel defects, delayed developmental milestones and, in severe cases, hypocalcemic tetany and seizures. If not recognized and properly treated, vitamin D deficiency may have long-term sequelae. On the other hand, the disease is entirely preventable with simple dietary measures or vitamin supplementation.

The two main sources of vitamin D are skin exposure to sunshine and dietary intake. In Canada, infants and children cannot depend on adequate skin exposure to sunlight for vitamin D synthesis due to our northern latitude. Therefore, as a regulated public health measure, all fluid dairy products (excluding yogurt drinks) are fortified with vitamin D. Human milk, advocated by paediatricians and nutritionists as the ideal fluid source for infants in the first year of life, is not rich in vitamin D. Furthermore, the Canadian Paediatric Society has recommended that all exclusively breast-fed infants receive a daily supplement of oral vitamin D. The Canada’s Food Guide also recommends that older children maintain a diet that is adequate in calcium and vitamin D.

Despite these public health measures, evidence indicates that vitamin D deficiency is persistent in Canada (1) and in developed countries worldwide (2-4). In fact, concern has been raised that the disease is on the rise (5). The literature and our own experience suggest that the etiology of vitamin D deficiency rickets over the past decade has been multi-factorial. Firstly, not all health-care providers/parents of breast-fed infants are aware that breast milk is not a rich source of vitamin D and that supplementation is necessary. Furthermore, adequate nutrition and vitamin supplementation are not readily available to some children, such as those living in the immigrant, First Nations (6,7) and Inuit (8) populations. Thirdly, health food alternatives given to infants and children with severe allergies and eczema may result in dietary deficiency of calcium and vitamin D (9). The prevention of excessive ultraviolet radiation in childhood through sunscreen programs has also contributed to the rise in rickets worldwide (10). Finally, infants who are breast-fed by mothers with poor vitamin D intake or inadequate sun exposure (due to veiling/northern latitudes/dark skin) are also at risk (11).

The precise incidence of vitamin D deficiency rickets in Canada is unknown. To date, prospective studies to determine the true incidence of the disease have not been performed. Incidence estimates are complicated by the fact that many cases do not reach tertiary care institutions but rather are treated in community practices. Therefore, even regional estimates based on data from tertiary care paediatric hospitals are imprecise. The lack of available incidence and prevalence data and the concern that this preventable disease is on the rise underline the importance of a prospective surveillance study.

The ultimate aim of this study, then, is to provide the public health community with unique and current data on the incidence and etiology of vitamin D deficiency rickets in Canada. Countries worldwide, including the United Kingdom and Australia, have in fact recognized the importance of vitamin D deficiency rickets as a public health issue in the year 2002 and are launching similar surveillance programs. By determining which geo-ethnic populations in Canada are at risk, it will be possible to develop specific health policies for the prevention and early identification of vitamin D deficiency rickets.

Objectives

1. To ascertain the incidence of simple vitamin D deficiency (also known as nutritional rickets) among children living in Canada by identifying all newly diagnosed cases over a two-year period.
2. To obtain demographic and medical information which will assist in the:
   • identification of risk factors for development of the disease in Canada (i.e., poor dietary intake of Vitamin D, lack of Vitamin D supplementation when indicated, inadequate sun exposure);
   • evaluation of current preventive strategies.
3. To supply data that will help develop novel public health policies to prevent vitamin D deficiency rickets among children living in Canada.

Methods

Paediatricians who participate in the CPSP monthly survey will be asked to report all biochemically and radiographically confirmed cases of vitamin D deficiency rickets (as outlined in the case definition). Participants will also be asked to complete a detailed case report form for each new case identified.

Case definition

Children up to and including 18 years of age with calcipenic rickets secondary to simple Vitamin D deficiency (also known as nutritional rickets).

Inclusion criteria

1. Low serum 25-hydroxyvitamin D (25OHD)
2. Elevated serum alkaline phosphatase

Supplemental data ideally to be obtained prior to treatment (and expected results*):

1. Serum ionized calcium (normal or low)†
2. Serum phosphate (normal or low)
3. Serum PTH (elevated)
4. Serum 1,25-dihydroxyvitamin D (1,25(OH)2D); low, normal or high)
5. X-ray confirmation of rickets at the distal ulnar or femoral epiphysis‡

* These results are not essential for reporting.
† If ionized calcium is not available, obtain total calcium and serum albumin.
‡ In rare instances, the x-ray features of rickets may not be present at the time of diagnosis, for example, if linear growth is arrested (and growth plate activity is blunted) or in the very early phase of the disease when x-ray changes at the growth plate are not yet visible. For this reason, x-ray confirmation of rickets is not a strict inclusion criterion but should be obtained during the initial patient evaluation.

Exclusion criteria

1. Vitamin D deficiency rickets associated with underlying disease, such as fat malabsorption, liver disease and renal insufficiency. Patients receiving total parenteral nutrition are also excluded.
2. Vitamin D deficiency secondary to heritable disorders of vitamin D metabolism, including:
   • 1a-hydroxylase deficiency (pseudo-vitamin D deficiency rickets)
   • Vitamin D receptor defects (hypocalcemic vitamin D resistant rickets
3. Phosphopenic rickets of any etiology (where hypophosphatemia is the primary cause of the rickets, and not due to calcipenic rickets with secondary hyperparathyroidism)

Duration

July 2002 to June 2004

Ethical approval

• Research Ethics Board, Children’s Hospital of Eastern Ontario, University of Ottawa
• Research Ethics Board, The Hospital for Sick Children, University of Toronto
• Research Ethics Board, McMaster University Health Centre, McMaster University

Date for analysis and publication

Data analysis and preparation of abstracts will be undertaken by December 2004. Manuscript preparation will be completed by July 2005.

References

1. Binet A, Kooh SW. Persistence of vitamin D-deficiency rickets in Toronto in the 1990s. Can J Public Health 1996;87(4):227-30.
2. Blok BH, Grant CC, McNeil AR, Reid IR. Characteristics of children with florid vitamin D deficient rickets in the Auckland region in 1998. N Z Med J 2000; 113(1117):374-6.
3. Pal BR, Shaw NJ. Rickets resurgence in the United Kingdom: Improving antenatal management in Asians. J Pediatr 2001;139(2):337-8.
4. Rowe PM. Why is rickets resurgent in the USA? Lancet 2001;357(9262):1100.
5. McCaffree J. Rickets on the rise. J Am Diet Assoc 2001;101(1):16-7.
6. Moffatt ME. Current status of nutritional deficiencies in Canadian aboriginal people. Can J Physiol Pharmacol 1995;73(6):754-8.
7. Lebrun JB, Moffatt ME, Mundy RJ, Sangster RK, Postl BD, Dooley JP, Dilling LA, Godel JC, Haworth JC. Vitamin D deficiency in a Manitoba community. Can J Public Health 1993;84(6):394-6.
8. Godel JC, Hart AG. Northern infant syndrome: A deficiency state? Can Med Assoc J 1984;131(3):199-204.
9. Carvalho NF, Kenney RD, Carrington PH, Hall DE. Severe nutritional deficiencies in toddlers resulting from health food milk alternatives. Pediatrics 2001;107(4):E46.
10. Zlotkin S. Vitamin D concentrations in Asian children living in England. Limited vitamin D intake and use of sunscreens may lead to rickets. BMJ 1999; 318(7195):1417.
11. Nozza JM, Rodda CP. Vitamin D deficiency in mothers of infants with rickets. Med J Aust 2001;175(5):253-5.