Search

BACKGROUND A prospective study was conducted to evaluate low-density lipoprotein-cholesterol (LDL-C) lowering efficacy and tolerability of ezetimibe as monotherapy in children and adolescents with polygenic hypercholesterolemia (PH) or familial hypercholesterolemia (FH). METHODS AND RESULTS Children with PH (n=6) or FH (n=11) aged 5-15 years were consecutively enrolled to receive ezetimibe as monotherapy at 10 mg/day for 11.3 +/- 7.3 and 15.9 +/- 10.1 months, respectively. Plasma biochemical and lipid profiles were assessed before and after treatment. Ezetimibe significantly lowered total cholesterol (TC) and LDL-C in patients with PH and FH: TC from 260.5 +/- 12.4 to 180.0 +/- 21.6 mg/dl (p = 0.02) and from 315.3 +/- 41.8 to 233.3 +/- 36.8 mg/dl (p = 0.003), respectively, and LDL-C from 177.1 +/- 17.7 to 102.6 +/- 16.7 mg/dl (p = 0.02) and from 243.0 +/- 41.8 to 170.0 +/- 29.8 mg/dl (p = 0.003), respectively. However, high-density lipoprotein-cholesterol (HDL-C) only decreased significantly (from 58.1 +/- 10.0 to 49.3 +/- 9.1 mg/dl) (p < 0.01) in patients with FH and remained unaltered in patients with PH. Triglyceride levels remained unchanged in both groups. Biochemical profile (hemogram, transaminases, creatinine, calcium, phosphorus and liposoluble vitamins A and E) remained unchanged; no adverse effects were observed. CONCLUSIONS Our data show that ezetimibe as monotherapy significantly lowered TC and LDL-C in children with PH and FH.

Background Age at pubertal growth spurt (PGS) onset varies and is sex-dependent. We present anthropometric pubertal growth data for five 1-year interval age maturity groups: very early, early, intermediate, late and very late. Methods Longitudinal growth study of 458 healthy children (223 boys, 235 girls). Ages at PGS onset and at adult height attainment, total pubertal growth (TPG), and peak height velocity (PHV) were evaluated. PGS begins between the ages of 10 and 15 in boys and 8 and 13 in girls; children were allocated to the corresponding 1-year interval age maturity group. Results For each sex, the earlier the start of PGS onset, the higher were PHV and TPG gain. However, adult heights were similar among the five pubertal maturity groups. Height SDS values for mean values of the very early, early, late and very late maturity groups calculated according to data from the five pubertal maturity groups taken together as a single group differed from zero in both sexes, mainly during the pubertal years for the very early (> +1) and very late (> -1) maturers. These differences disappeared at adult height. Conclusions Our data might contribute to better clinical evaluation of pubertal growth according to individual pubertal maturity tempo.

Aim To assess thyroid function in 76 sick preterm infants 30-36 weeks gestational age. Patients and methods Measurement of serum TSH, T4, T3, free T4 and rT3 in the mother and cord at delivery, and in the infant at 1 and 24 hours, 1 and 3 weeks, 2, 4, 6 and 12 months of postnatal age. These values were compared with those of 75 healthy age-matched controls. Gestational age was 30 weeks in 24, 31 weeks in 23, 32 weeks in 13, 33 weeks in 13, 34 weeks in one, 35 weeks in one and 36 weeks in one. Hypothyroxinemia at each postnatal age was defined as serum free T4 values under -2 SD of the mean of controls. Results Forty-four patients were normothy-roxinemic at all times, and 32 presented hypothyroxinemia at 24 hours (29 patients), 1 week (seven patients) and 3 weeks (two patients). Follow-up of 31 patients who were normothyroxinemic at 24 hours of life showed that at one week three (9.7%) were hypothyroxinemic and at 3 weeks all were normothyroxinemic. At 24 hours of life, all patients with patent ductus arteriosus and all patients treated with dopamine were in the hypothyroxinemic range. Conclusion Hypothyroxinemia may be present in sick preterm infants 30-36 weeks of gestational age, particularly in those treated with dopamine and/or presenting patent ductus arteriosus.

Background: Maximum bone mass accretion in the fetal skeleton is acquired during the third trimester of gestation, and may he compromised in premature newborns. Objective: To ascertain the incidence and evolution of osteopenia, a longitudinal study was performed to evaluate areal bone mineral density (aBMD) in the lumbar spine in premature newborns followed during the first 2 years of life. Methods: aBMD values were assessed in lumbar spine (L2-L4) by DEXA and expressed as grams hydroxyapatite/cm 2 in 80 premature newborns, 41 boys and 39 girls, of gestational ages 24.5-35.7 weeks. aBMD values were evaluated at (mean ′ SD) 0.2 ′ 0.1 years (at discharge from the neonatal unit), 0.9 ′ 0.2 years and 2.0 ′ 0.5 years of postnatal age, and compared with those of age- and sex-matched full-term newborns with normal intrauterine and postnatal growth. Results: aBMD values recovered progressively from the first to the third evaluations, and were 0.139 ′ 0.06 g/cm 2 (-2.4 ′ 1.4 SDS) at 0.2 ′ 0.1, 0.270 ′ 0.06 g/cm 2 (-1.0 ′ 1.0 SDS) at 0.9 ′ 0.2 and 0.410 g/cm 2 (-0.08 ′ 1.0 SDS) at 2.0 ′ 0.5 years. Conclusions: Our data show a significant catch-up of aBMD, reaching values similar to those of full-term newborns at the age of 0.2 ′ 0.5 years, regardless of the gestational age at birth.