Search

Children treated for acute lymphoblastic leukemia may develop reduced bone mineral density during treatment, but there is little information on the mechanisms involved. In a prospective, longitudinal study on 15 children with ALL, we undertook serial measurements of markers of bone and collagen turnover, insulin-like growth factor (IGF)-I and its binding proteins (IGFBPs)-3 and -2 during the second year of continuing chemotherapy. In eight patients we also measured lower leg length by knemometry. Height SD scores, lower leg length velocity, IGF-I, and markers of bone collagen turnover did not differ significantly from healthy children. However, bone alkaline phosphatase, a marker of the differentiated osteoblast, was lower (mean SD score, -0.64; p < 0.0001), whereas procollagen type III N-terminal propeptide (P3NP, a marker of soft tissue collagen turnover; mean SD score, +0.93, p < 0.05), IGFBP-3 (mean SD score, +0.76; p < 0.01), and IGFBP-2 (mean SD score, +1.24, p = 0.01) were all higher than in healthy children. IGFBP-3 decreased during episodes of afebrile neutropenia (p < 0.05). Within 3 mo after completion of treatment, bone ALP increased in all eight patients, but collagen markers showed little change. IGFBP-2 returned to normal posttreatment, but P3NP and IGFBP-3 remained significantly elevated compared with healthy children (mean SD scores, +1.51 and +1.36, respectively; p < 0.01). We conclude that continuing chemotherapy was associated with normal growth and bone collagen turnover but enhanced soft tissue collagen turnover. Bone bone alkaline phosphatase was low throughout treatment, which suggests impaired osteoblast differentiation resulting from a direct effect of chemotherapy on bone. Although the effect was reversible, the long-term implications for bone health in survivors remain uncertain.

Correlations between knemometric (lower leg length) growth rates and urine free cortisol excretion, respectively, and serum concentrations of IGF-I, IGF binding protein-3, osteocalcin, carboxy terminal propeptide of type I collagen (PICP), carboxy terminal pryridinoline cross-linked telopeptide of type I procollagen (ICTP), and amino terminal propeptide of type III procollagen (PIIINP) were investigated in 17 asthmatic children aged 7-14 y during treatment with fluticasone propionate, 200 micrograms, and beclomethasone dipropionate, 400 and 800 micrograms/d, taken from dry powder inhalers. The study was a double blind, crossover trial with three active treatment periods and two wash-out periods. All periods were 15 d long. Overnight urine free cortisol/ creatinine x 10(6) did not correlate with knemometric growth rates or any of the serum markers. Significant correlations (Pearson's correlation coefficient, P) between knemometric growth rates and IGF-I (0.41; 0.006), IGFBP-3 (0.35; 0.02), PICP (0.44; 0.003), ICTP (0.35; 0.001), and PIIINP (0.46; 0.002) were found. Compared with fluticasone propionate, 200 micrograms, beclomethasone dipropionate, 400 and 800 micrograms, caused significant suppression of lower leg growth rate (F = 12.41; p = 0.002, and F = 23.30; p = 0.0001, respectively) and of urine free cortisol/creatinine x 10(6) (F = 10.52; p = 0.003, and F = 13.74; p = 0.001). Beclomethasone, 800 micrograms, caused suppression of PICP compared with fluticasone propionate, 200 micrograms (F = 8.31; p = 0.008), and beclomethasone, 400 micrograms (F = 7.53; p = 0.01). Both low (F = 6.82; p = 0.02) and high (F = 23.35; p = 0.0001) doses of beclomethasone were associated with reduced concentrations of ICTP, the high dose being the most suppressive (F = 4.42; p = 0.05). Beclomethasone 400 (F = 9.75; p = 0.004) and 800 micrograms (F = 23.61; p = 0.0001) resulted in reduced levels of PIIINP. Reduced short-term knemometric growth rates in children treated with inhaled glucocorticosteroids reflect suppressive effects on type I and type III collagen turnover.

A hand-held electronic knemometer, resembling a pair of callipers, for measuring knee-heel length in preterm infants was developed to improve the accuracy of measuring linear growth velocity in infants. The measuring system is based on a magnetic encoder and has a resolution of 0.01 mm. The knee-heel length is recorded automatically when the pressure applied on the heel reaches a preset value. The result of a measurement sequence is expressed as the average of five sequential readings. The error of one measurement sequence was 0.82 mm, corresponding to a coefficient of variation of 0.8% or 2 d of growth in knee-heel length. It includes the technical error and an error component due to the correlation of the readings within a series. The estimated error on the measurement of the knee-heel growth velocity (expressed as mm/d), measured over a 3-wk period, was 0.04 mm, corresponding to a coefficient of variation of 8%. Longitudinal growth data from 11 healthy preterm infants (birth weight 918–1482 g) are presented. Knee-heel length velocity from birth until day of regained birth weight was similar to the velocity during the following weeks, showing that there was no deceleration of growth immediately after birth. In conclusion, the method is accurate and gentle in measuring linear growth velocity over short periods and can be useful in monitoring the progress of ill infants and in growth studies of preterm and mature infants, in which linear growth is a more relevant short-term outcome than weight gain.

Background: Adequate nutrition of infants with a birth weight II (group2: n=3) showed a lower growth velocity (n.s.). Conclusions: Regular measurements of growth help to monitor and improve nutrition of infants with a birth weight < 1500g. In this context knemometry is a useful tool. All data are given as median (25./ 75. quartiles).

Introduction:: Knemometry is a useful tool in assessing short term growth in premature infants. By daily measurements of lower leg length, day by day growth can be detected. In the following study, short term growth in formula fed premature infants was compared to that of breast milk fed infants.

Impairment of growth in BPD is well described but the amount by which growth is disturbed and the stage at which impairment occurs is unclear. We have compared lower leg growth, measured by knemometry, and weight gain, in 16 babies who needed home oxygen, 22 babies who needed oxygen for more than 28 days but were discharged in air and 24 babies who needed supplementary oxygen for less than 28 days All groups exhibited an initial weight loss followed by steady weight gain, with no apparent difference in weight gain for the two oxygen dependent groups. Changes in leg length are shown in the figure. Comparison of leg length velocities demonstrated differences in the three groups between 0-13 days (p=0,12); 14-27 days (p=0.0001) and 28-41 davs (p=0.006). A significant impairment of growth in the early postnatal period is seen in those babies who will develop moderate and severe BPD. This may occur despite apparently similar weight gains

To assess the growth promoting potential of GRF, we studied so far 4 boys (age 5 - 13 yrs) with short stature (height SDS -2.2 to -3.8) due to partial HGH deficiency, diagnosed by arginin and insulin stimulation tests and nocturnal HGH secretion profile. None of them received any prior hormonal therapy. Before, after 2 weeks and at the end of 12 weeks of GRF therapy, each child had an i.v. GRF 1-29 bolus test (2 μg/kg, AM, fasted) with determination of plasma HGH, basal serum somatomedin C (SMC) and urinary hydroxyproline excretion (OHP). Lower leg length, measured by knemometry was determined under standard conditions once a week for 3 - 15 months before and twice a week during GRF treatment. Synthetic GRF 1-29 was given s.c. in a dose of 3 - 4 μg/kg b.i.d., at 0700 and 1900 h. After 2 weeks of GRF treatment, the peak HGH response after GRF i.v. stimulation increased from (means) 31 to 74 ng/ml. SMC increased from 1.07 to 2.25 IU/ml and OHP from 119 to 210 μg/mg creatinine. Knemometric growth rate increased by 1.6 to 2.8-fold from (means) 0.44 to 0.93 mm/week. Such increased growth rates were never observed in any of these patients during the pretreatment period. The knemometric growth patterns during CRF therapy appear to be similar to those observed during the initiation of HGH substitution therapy. Our preliminary data suggest that GRF 1-29, given s.c. twice daily, induces longitudinal growth via increased endogenous HGH and SMC secretion and thus may be of therapeutic value in GRF deficient short children.

SHORT TERM RESPONSE TO SOMATREM IN TURNER SYNDROME ASSESSED BY KNEMOMETRY AND CONVENTIONAL AUXOLOGY

It is now possible to study short-term growth by knemometry, a non-invasive technique measuring the exact distance between heel and knee in sitting children. During the measurement the lower leg length (LLL) is determined by repeatedly moving the child's knee under the measuring board. Each single measurement consists of six independent estimations, the SD of which is