Low bone mineral density and high incidences of fractures and vitamin D deficiency in 52 pediatric cancer survivors.

OBJECTIVE: To evaluate bone mineral density (BMD), fractures, and vitamin D deficiency in pediatric patients in complete remission of solid tumor; and to identify risk factors for these three abnormalities. STUDY DESIGN: Data were collected prospectively after completion of cancer treatment. Hormonal and vitamin D deficiencies were treated. The patients were evaluated again 1 year later. PATIENTS: 52 consecutive patients, 30 boys and 22 girls. Among them, 21 completed the second evaluation. MEASUREMENTS: A clinical examination, nutritional assessment, and laboratory workup were performed. BMD was measured by absorptiometry. RESULTS: Calcium intake was inadequate in 75% of patients and vitamin D reserves were low in 61.5%. BMD was low at the spine in 32.7%, and at the femur in 24% of patients. Spinal and femoral BMD Z-scores correlated significantly with each other. Femoral BMD Z-score showed significant positive correlations with changes in body mass index, urinary calcium/creatinine ratio, and time since treatment completion, and a significant negative correlation with treatment duration. Fractures were noted in 10 patients but were not correlated with BMD. In the 21 re-evaluated patients, no significant improvements were found in calcium intake, vitamin D status, or BMD Z-score. CONCLUSIONS: Survivors of childhood solid cancer have high rates of insufficient calcium intake, vitamin D deficiency, low bone mass and fractures.

Evaluation of lean body mass in obese children.

UNLABELLED: Multiple skinfold anthropometry (MSA) and bioelectrical impedance analysis (BIA) are useful as clinically non-invasive, inexpensive and portable techniques, although it is not clear if they can be used interchangeably in the same patient to routinely assess her/his body composition. In order to compare BIA, MSA and DXA in the estimation of lean body mass (LBM) of a pediatric obese population, 103 obese [body mass index (BMI) > 97th percentile] children (median age: 11 years; range: 5.4-16.7 years) underwent nutritional evaluation. After an overnight fast, the subjects' anthropometric measurements were performed by the same investigator: body weight (BW), height, skinfold thickness (four sites); fat body mass (FBM) using Brook or Durnin equations and dual X-ray absorptiometry (DXA). BIA was performed using a bioelectrical impedance analyzer (Analicor-Eugedia, 50 kHz) and Houtkooper's equation to calculate LBM. Linear regression analysis was performed to evaluate the relationship between the prediction of LBM by MSA, DXA and BIA. The differences between the three techniques were analysed using Student's t-test for paired observations and the Bland and Altmann method. A considerable lack of agreement was observed between DXA- and BIA-LBM (delta = -4.37 kg LBM; delta-2sigma = -11.6 kg LBM; delta+2sigma = +2.8 kg LBM); between DXA- and MSA-LBM (delta = -1.72 kg LBM; delta-2sigma = -8.2 kg LBM; delta+2sigma = +4.8 kg LBM) and between BIA- and MSA-LBM (delta = -2.65 kg LBM; delta-2sigma = -10.5 kg LBM; delta+2sigma = +5.2 kg LBM). CONCLUSION: In obese children, DXA, BIA and MSA should not be used interchangeably in the assessment of LBM because of an unacceptable lack of agreement between them. The discrepancies between methods increase with the degree of obesity.

Impact of total cumulative glucocorticoid dose on bone mineral density in patients with 21-hydroxylase deficiency.

OBJECTIVE: It remains controversial whether long-term glucocorticoids are charged of bone demineralization in patients with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency. The aim of this study was to know whether cumulative glucocorticoid dose from the diagnosis in childhood to adulthood in patients with CAH had a negative impact on bone mineral density (BMD). DESIGN: This was a retrospective study. METHODS: Thirty-eight adult patients with classical and non-classical CAH were included. BMD was measured in the lumbar spine and femoral neck. Total cumulative glucocorticoid (TCG) and total average glucocorticoid (TAG) doses were calculated from pediatric and adult files. RESULTS: We showed a difference between final and target heights (-0.82+/-0.92 s.d. for women and -1.31+/-0.84 s.d. for men; P<0.001). Seventeen patients (44.7%) had bone demineralization (35.7% of women and 70% of men). The 28 women had higher BMD than the 10 men for lumbar (-0.26+/-1.20 vs -1.25+/-1.33 s.d.; P=0.02) and femoral T-scores (0.21+/-1.30 s.d. versus -1.08+/-1.10 s.d.; P=0.007). In the salt-wasting group, women were almost significantly endowed with a better BMD than men (P=0.053). We found negative effects of TCG, TAG on lumbar (P<0.001, P=0.002) and femoral T-scores (P=0.006, P<0.001), predominantly during puberty. BMI was protective on BMD (P=0.006). CONCLUSION: The TCG is an important factor especially during puberty for a bone demineralization in patients with 21-hydroxylase deficiency. The glucocorticoid treatment should be adapted particularly at this life period and preventive measures should be discussed in order to limit this effect.

Low bone mineral density in young children with cystic fibrosis.

RATIONALE: Low bone mineral density (BMD) is a frequent problem for adult patients with cystic fibrosis (CF). Only limited information is available for young patients. OBJECTIVES: The aim of this study was to evaluate BMD of children with CF younger than 6 years. METHODS: BMD was measured at the lumbar spine (LS) after adjustment for height, sex, and pubertal status in 25 children with CF younger than 6 years, 53 prepubertal children aged 6 to 10 years, and 36 adolescents aged 11 to 18 years. Nutritional status, body composition, pulmonary disease severity, corticosteroid usage, dietary calcium, caloric intake, and vitamin D status were evaluated as potential correlates of BMD. MEASUREMENTS AND MAIN RESULTS: The mean LS z score in the youngest group was significantly lower than normal (-0.96; SEM, 0.3). It did not differ significantly from that of children aged 6 to 10 years (-0.91; SEM, 0.2) or adolescents (-1.4; SEM, 0.2). LS z score was positively correlated with fat-free mass in multiple regression analysis. LS z score was less than -1 in 34% of the patients with mild pulmonary disease and normal nutritional status. CONCLUSIONS: These data suggest that the origin of CF bone disease in early childhood may be independent of nutritional status or disease severity.

Treatment of growth failure in juvenile chronic arthritis.

We retrospectively assessed linear growth and final height in a group of 24 patients suffering from juvenile idiopathic arthritis (JIA) during childhood, receiving steroid therapy. In these patients, a significant loss of height (-2.7 +/- 1.5 SDS) occurred in the first years of the disease which was positively correlated with prednisone therapy duration. After remission of the disease and prednisone discontinuation, most of the patients (70%) had catch-up growth but 30% had a persistent loss of height. Their mean final height was strongly correlated with their mean height at the end of steroid therapy and was significantly different between the group of patients with catch-up growth (-1.5 +/- 1.6 SDS) and the group without catch-up growth (-3.6 +/- 1.2 SDS). This pattern of growth observed in JIA patients should help us to define strategies of GH treatment in these patients in order to improve their final height. We have previously reported the beneficial effects on growth and body composition of a 1-year GH treatment in a group of 14 growth-retarded patients suffering from juvenile idiopathic arthritis, receiving glucocorticoid therapy. These patients (n = 13) were treated again with GH at the same dosage (0.46 mg/kg/week) for another 3-year period. GH treatment markedly increased growth velocity in these patients, but had a minor effect on SDS height suggesting that these children will remain short at adult age. Using GH earlier in these patients during the course of their disease may prevent growth deterioration and metabolic complications induced by chronic inflammation and long-term steroid therapy.

Effects on growth and body composition of growth hormone treatment in children with juvenile idiopathic arthritis requiring steroid therapy.

OBJECTIVE: Decreased growth velocity and abnormal body composition including severe osteoporosis are common in glucocorticoid-treated patients with juvenile idiopathic arthritis (JIA). We evaluated the effects of recombinant human growth hormone (GH) given for 3 years on growth velocity, height standard deviation score (SDS), and body composition, together with potential adverse effects on glucose tolerance. METHODS: Thirteen patients received GH (0.46 mg/kg/week) for 3 years. Body composition was assessed by dual-energy x-ray absorptiometry and glucose tolerance by annual oral glucose tolerance tests. RESULTS: Median growth velocity increased from 2.1 to 6.0 cm/year (p = 0.002) in the first year and remained higher than baseline in the second year of treatment. Height SDS did not change significantly (-4.6 SDS at baseline vs -4.3 SDS at study completion), but the growth response varied markedly across patients. Compared with baseline, lean mass increased by 33%, fat mass remained stable, and lumbar bone mineral density increased by 36.6%. Transient glucose intolerance developed in 6 patients, but glycosylated hemoglobin concentrations did not change significantly and diabetes mellitus did not occur. CONCLUSION: Treatment with GH restored linear growth without inducing catch-up growth, significantly improved body composition, and prevented further bone loss. Prolonged followup is needed to assess the benefits of GH and longterm consequences of hyperinsulinism.