Study data presented at the AAOS 2018 Annual Meeting suggest that although serum vitamin D levels are low in children, the deficiency is not associated with acute low-energy fractures.
“Results of this multisite study, conducted within a large diverse population living in a seasonal climate, underscore the high prevalence of vitamin D (25-OHD) insufficiency and deficiency among pediatric patients as described in the literature,” said coauthor Alexa J. Karkenny, MD, who presented the study.
“Although rickets and osteomalacia are well-understood outcomes of disrupted calcium homeostasis, further research is needed on other clinical musculoskeletal effects. The role of bone health markers and their association with acute low-energy fractures in healthy children has not yet been well-elucidated, and earlier results on vitamin D levels in pediatric fracture patients have been contradictory,” she added.
The researchers’ primary purpose for conducting the study was to evaluate the association between acute low-energy fractures and 25-OHD, parathyroid hormone (PTH), and calcium in children. Secondarily, they sought to assess the behavioral and environmental influences of bone health markers as potential confounders of fracture risk. They hypothesized that children with acute fractures would have lower vitamin D levels than those without an acute fracture.
“A fracture is one of the most common diagnoses treated not only by pediatric orthopaedists, but also community orthopaedists across the country,” Dr. Karkenny said. “A greater understanding of the role of hypovitaminosis D in low-energy fractures can, in turn, help us develop evidence-based guidelines on vitamin D requirements for pediatric fracture prevention, screening for hypovitaminosis D among fracture patients, and postfracture vitamin D supplementation.”
Prospective cross-sectional study
The study involved 222 pediatric patients between the ages of 1 and 17 years who presented to the emergency departments (EDs) at two urban Level 1 hospitals between January 2014 and May 2017. After informed consents from parents/legal guardians were obtained, the patients were recruited into either a fracture cohort (n = 109) or nonfracture (control) cohort (n = 113). The study excluded patients who did not require intravenous access as part of their routine standard medical care and those previously enrolled in the study who made repeat visits to the ED during the study period. Patients diagnosed with the following chronic diseases, known to affect the metabolism of vitamin D, also were excluded:
- primary hyperparathyroidism
- malabsorption syndromes
- skeletal dysplasia
- genetic disorders
- glucocorticoid treatment (including the use of oral or inhaled steroids for more than 30 days within the last 12 months)
The researchers measured serum levels of 25-OHD, intact PTH, and calcium for all patients. A 25-OHD level of less than 20–29.9 ng/mL was defined as insufficient; less than 12–19.9 ng/mL as deficient; and less than 12 ng/mL as severely deficient.
The researchers also collected demographic, diagnosis, season, and mechanism of injury data for all patients. A nutrition and activity survey was administered to document family-reported sun exposure, sunscreen use, diet, time spent participating in physical and sedentary activities, time spent participating in indoor and outdoor activities, multivitamin intake, and history of prior fracture(s).
Statistical analysis revealed a mean 25-OHD level of 22.8 ng/mL in the fracture group versus 24.5 ng/mL in the control group, a difference that the authors noted was not statistically significant. Among the two groups combined, 21.6 percent of patients were 25-OHD sufficient, 41.4 percent were 25-OHD insufficient, 29.7 percent were 25-OHD deficient, and 7.2 percent were severely 25-OHD deficient (Fig. 1). Categorical sufficiency levels were not significantly different between fractures and controls.
Fracture location was not associated with differences in 25-OHD levels. Patients with previous fractures did not have different 25-OHD levels than controls, nor was frequency of prior fracture different between the groups. In addition, higher dairy intake was not associated with higher serum 25-OHD or serum calcium levels. However, younger age, sunscreen use, and greater than three hours per day spent outdoors were significantly associated with higher 25-OHD levels (P = 0.006, P = 0.015, and P < 0.001, respectively). Differences in 25-OHD levels between the ethnic groups were also significant. The mean 25-OHD level among patients enrolled in winter months was 20.1 ng/mL versus 25.8 ng/mL in summer months (P < 0.001).
The mean PTH level in the fracture group (38 pg/mL) was significantly higher than in the control group (26.6 pg/mL), (P < 0.001). All the hyperparathyroid patients had insufficient, deficient, or severely deficient levels of 25-OHD.
“The results of our study revealed a higher rate of combined 25-OHD deficiency and insufficiency (78 percent) among children and adolescents than the previously reported rates of 42 percent to 52 percent. However, the observed racial disparities were consistent with prior studies, with the lowest levels of 25-OHD among African-American, Asian, and Hispanic children,” Dr. Karkenny said. “Also, to the authors’ knowledge, this study is the first of its kind to report a statistically significant difference in PTH between pediatric fracture and control cohorts. PTH was elevated to the level defined as hyperparathyroidism (> 65 pg/mL) in 5.7 percent of fracture patients and 1 percent of control patients.
“This study not only contributes to the growing body of research on vitamin D and bone health among pediatric orthopaedic patients, but also sheds new light on our understanding of PTH after a fracture,” Dr. Karkenny said. “While a rise in PTH has been documented in the year following a hip fracture, observations on PTH and acute fractures have not been previously discussed in pediatric orthopaedic literature. Whether subclinical increased PTH is a reflection of the patient’s baseline vitamin D status itself, a biological response to fracture, or both is a worthwhile question.”
Dr. Karkenny’s coauthors of “Pediatric Fractures: Does Vitamin D Play a Role?” are Jahn Avarello, MD; Ashley Elizabeth Burlage, MD; Rocio Amanda Llanio Crabb; Kelly Meghan McNally, BS; Jacob Foster Schulz, MD; Sara Merwin, MPH; and Selina Poon, MD.
Maureen Leahy is assistant managing editor of AAOS Now. She can be reached at firstname.lastname@example.org.
- Holick, M.F., Vitamin D deficiency. N Engl J Med, 2007. 357(3): p. 266-81.
- Sullivan, S.S., et al., Adolescent girls in Maine are at risk for vitamin D insufficiency. J Am Diet Assoc, 2005. 105(6): p. 971-4.
- Gordon, C.M., et al., Prevalence of vitamin D deficiency among healthy adolescents. Arch Pediatr Adolesc Med, 2004. 158(6): p. 531-7.
- Nesby-O’Dell, S., et al., Hypovitaminosis D prevalence and determinants among African American and white women of reproductive age: third National Health and Nutrition Examination Survey, 1988-1994. Am J Clin Nutr, 2002. 76(1): p. 187-92.