Abstract

Background: Patients with anorexia nervosa (AN) experience bone as well as kidney complications including low bone mineral density (BMD), increased fracture rate, kidney stones, hypercalciuria and chronic renal failure. However, the mechanisms of those complications are not fully understood (1). The aim of this study is to investigate the interrelationship of central measures of calcium vitamin D metabolism and bone and kidney health in adolescents with newly diagnosed AN. Methods: This is a cross-sectional study that included newly diagnosed adolescents with AN referred to the Eating Disorder Program (EDP) at the Hospital for Sick Children over a two-year period. In addition to demographic and auxiological data, information on vitamin D and calcium intake was obtained. BMD and blood and urine samples for central measures of calcium vitamin D metabolism were investigated. In addition to descriptive statistics, multiple linear regression was performed to examine the association between PTH and various predictors. Results: A total of 61 patients (55 female, 6 male, mean age 15.2 ± 1.56 years) were included. Overall levels of serum calcium, phosphate, magnesium and 25-hydroxyvitamin D (25OHD) were normal and urinary calcium to creatinine ratio was increased (0.87 ± 0.47mmol/mmol, normal<0.7). However, a novel observation was made regarding low PTH levels in 35% of this cohort (<22ng/L, normal 22-88ng/l (2)). Low PTH levels did not appear to be a result of partial or complete hypoparathyroidism (normal calcium and phosphate levels), oral calcium intake (no significant correlation, p= 0.59) or magnesium deficiency (normal magnesium levels). As previously described, a significant negative correlation between PTH and 25OHD levels below 100 nmol/L was noted (p=0.007). However, 25OHD levels in the range of 100-200 nmol/L, did not contribute to the lower PTH levels (p= 0.39). Mean lumbar spine (L2-4) BMD Z-score was -0.69 ± 1.14. Conclusion: This study indicates reduced PTH levels in 1/3 of adolescents with AN at presentation to a tertiary care EDP. As in previous studies (1), this data suggests that the reduction in PTH may be due to a subtle increase in ionized serum calcium resulting from reduced bone formation and reduced mineralization with ongoing bone resorption. Reduced PTH levels in these patients may contribute to both the renal and bone complications in AN.

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