OBJECTIVE:To investigate which of the currently applied parameters to assess childhood overweight best predict cardiovascular risk factors. DESIGN: Cross-sectional study comparing ®ve different methods to de®ne overweight with respect to their power to predict cardiovascular risk factors. SUBJECTS: A total of 838 healthy children from the Prevention-Education-Program (Nuremberg, Germany; age 4 ± 9 y, 405 boys, 433 girls). MEASUREMENTS: Obesity parameters Ð body mass index (BMI), ponderal index (PI), the sum of triceps and subscapular skinfold thickness (SFT), percentage body fat (%BF) using SFT and two different regression formulas (Slaughter, %BF-SL; Dezenberg, %BF-DZ). Overweight de®ned by the 90th age-and sex-speci®c percentile of each obesity parameter. Comparison of LDL-and HDL-cholesterol, apolipoprotein-B (apo-B), triglycerides (TG), ®brinogen and blood pressure values (SBPaDBP) between normal-weight and overweight children. RESULTS: When overweight is de®ned by BMI or PI, all cardiovascular risk factors are signi®cantly (P`0.01) different between overweight and normal-weight children (BMI: TG 20.5%, HDL-chol. 7 8.6%, LDL-chol. 9.6%, apo-B 6.8%, SBP 7.4%, DBP 8.6%, ®brinogen 13.2%; PI: TG 24.3%, HDL-chol. 7 6.1%, LDL-chol. 9.0%, apo-B 7.4%, SBP 5.9%, DBP 6.7%, ®brinogen 13.9%), while SFT, %BF-SL and %BF-DZ did not predict all cardiovascular risk factors. A sex-speci®c analysis showed that in girls BMI and PI both predict cardiovascular risk factors, while in boys this is only valid for BMI. CONCLUSION: In prepubescent children, height-to-weight indices such as BMI or PI better predict cardiovascular risk factors than obesity parameters using skinfold measurement. The BMI may be superior to the PI as the association between BMI and cardiovascular risk factors is less affected by gender.
Low density lipoprotein (LDL-) particles can be subfractionated in large-buoyant (lb), intermediate-dense (id) and small-dense (sd) LDL-subtypes. Fibrates improve the LDL-subtype profile by reducing proatherogenic sd-LDL which are prominent in diabetic dyslipoproteinemia. We evaluated the effect of etofibrate on the LDL-subtype distribution in patients with type 2 diabetes mellitus (n = 13, 55 +/- 18 years, BMI 27.9 +/- 5.5 kg/m2, HbA1c 10.1 +/- 3.9 %) and diabetic dyslipoproteinemia (triglycerides 343 +/- 253 mg/dl, HDL-cholesterol 36 +/- 7 mg/dl, LDL-cholesterol 110 +/- 37 mg/dl). Plasma lipids (enzymatic methods) and LDL-subtypes (7 LDL-subfractions, density gradient ultracentrifugation) were measured before and during etofibrate therapy (500 mg/d, 7 - 16 weeks). Etofibrate significantly (p < 0.05, Wilcoxon-test) reduced triglycerides (- 31 +/- 60 %) and increased HDL-cholesterol (+ 24 +/- 22 %), whereas total cholesterol and LDL-cholesterol did not change. Cholesterol concentration decreased in sd-LDL by 12 % (p < 0.05), while it increased in id- and lb-LDL (+ 26 %,+ 39 %, respectively). Thus, the LDL-subtype profile showed a relative increase of the fraction of lb- (+ 13 +/- 32 %, n.s.) and id-LDL (+ 23 +/- 33 %, p < 0.05) and a relative decrease of the fraction of sd-LDL (- 19 +/- 18 %, p < 0.05). We conclude that etofibrate not only decreases triglycerides and increases HDL-cholesterol but also improves the LDL-subtype profile and thus may reduce the cardiovascular risk in patients with an abundance of sd-LDL such as diabetic patients.
We describe the case of a 32-year old male patient who presented with a pathological fracture of his right humerus, splenomegaly and thrombocytopenia, the typical symptoms of Gaucher's disease, a lysosomal storage disease. Diagnosis was confirmed by bone marrow biopsy (detection of lipid engorged macrophages - Gaucher cells), by a markedly diminished activity of acid, beta-Glucosidase and by showing two different mutations (764T/A, 1187G/A) in the gene encoding acid beta-Glucosidase. The first mutation causes an amino-acid substitution (phenylalanine to tyrosine). The second mutation causes a premature termination at amino-acid position 396. Enzyme replacement therapy was started with 60 Units/kg body weight, because of severe bone symptoms. Following the decrease in spleen size and increase in platelet count the dose was gradually tapered to 20 U/kg. After two years of enzyme replacement therapy platelet count and spleen volume have normalized and the bone lesions have almost disappeared.
Although in routine clinical practice an improvement in HbA1c results in better lipid values. This improvement is small and is usually not sufficient to reach lipid target levels.
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