Lipid profile and thyroid hormone concentrations in children with epilepsy treated with oxcarbazepine monotherapy: a prospective long-term study.

BACKGROUND AND PURPOSE: To evaluate prospectively the changes and possible associations in lipid and thyroid profiles in children treated with oxcarbazepine (OXC) monotherapy. METHODS: Serum total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TGs), lipoprotein (a) [Lp(a)], free thyroxine (FT4), free triiodothyronine (FT3), thyrotropin (TSH) and gamma-glutamyltransferase (GGT) concentrations were measured in 23 children with epilepsy, before and at 8 and 18 months of OXC monotherapy. RESULTS: Total cholesterol was significantly increased at 8 months (P = 0.033), whereas LDL-C was significantly increased at 8 and 18 months (P < 0.001 and P = 0.004, respectively) of treatment. Lp(a) was significantly increased at 8 months (P = 0.042) and borderline significantly increased at 18 months (P = 0.050) of treatment. FT4 was significantly decreased at 8 and 18 months (P < 0.001 and P = 0.002, respectively), and TSH levels were significantly increased at 8 and 18 months (P = 0.002 and P = 0.001, respectively) of OXC monotherapy. GGT levels were significantly increased at 8 and 18 months (P < 0.001) of treatment. There were no significant alterations in HDL-C, TGs and FT3 levels during the study. Significant positive correlations were found between GGT and LDL-C levels at 8 (r = 0.468, P = 0.024) and 18 months (r = 0.498, P = 0.016), and between TSH and TC at 18 months (r = 0.508, P = 0.013) of treatment. CONCLUSIONS: OXC monotherapy may cause significant and persistent alterations in lipid and thyroid profiles in children with epilepsy. The increase in LDL-C and TC levels may be associated with liver enzymes induction and thyroid dysfunction. Further long-term prospective studies are required to confirm these findings and to determine their clinical significance.

Cardiovascular impairment in children, adolescents, and young adults with type 1 diabetes mellitus (T1DM).

Left ventricular (LV) function was assessed in 42 patients (mean age +/- SD, 18.45 +/- 3.76 years; 17 males) with type I diabetes mellitus (T1DM; mean duration 9.89 years) and in 43 healthy controls (mean age +/- SD, 18.27 +/- 3.36 years; 18 males). Systolic, diastolic cardiac function and LV dimensions were assessed using M-mode and Doppler echocardiography. Neural autonomic function was assessed by measuring RR variation during deep breathing, Valsava maneuver, 30/15 ratio, and blood pressure response to standing. Fractional shortening, peak velocity of early ventricular filling (E wave), peak velocity of LV filling (A wave), E/A ratio, deceleration time, isovolumic relaxation time, LV dimensions (interventricular septum, posterior wall thickness, end diastolic diameter [EDD] and systolic diameter [ESD]) were all comparable between patients with T1DM and controls. However, in 11 T1DM patients with microalbuminuria and/or retinopathy, EDD, ESD, E/A ratio, and E wave were all lower (p = 0.0011, p = 0.019, p = 0.0011, and p = 0.030, respectively) while, A wave, heart rate, and diastolic blood pressure were all higher (p = 0.008, p = 0.0024 and p = 0.004, respectively) compared to matched for age and sex controls. Furthermore, in six of the 11 T1DM patients with microangiopathy who had E/A <1.12 (<2 SD of the control mean), significant and marginally significant correlations were found between E/A ratio and the duration of the disease as well as the mean HbA1c of the last year (r = -0.38, p = 0.011 and r = -0.287, p = 0.064, respectively). In conclusion, it has been found that impairment of diastolic, but not systolic, LV function can be detected early in young patients with T1DM and microangiopathy.

Relation of serum leptin levels to lipid profile in healthy children.

The association of leptin with body fat concentration is well established. There is also experimental evidence of a direct effect of leptin on lipid metabolism. The aim of this study was to evaluate whether leptin levels are related to the corresponding serum lipid levels independently of body fat mass. The study population consisted of 294 phenotypically healthy school children aged 6 to 12 years. Age, sex, body weight, height, Tanner stage, and triceps skinfold thickness were recorded for all participating subjects. A blood sample was drawn in the morning after a 12-hour fast, and serum total, high-density lipoprotein (HDL), and low-density lipoprotein cholesterol; triglyceride; and leptin levels were determined. Multiple regression analysis showed that triglyceride values were positively correlated with the ln(log(e))-transformed leptin levels (beta =.01, P <.001), whereas HDL levels were inversely associated with lnleptin values (beta = -.06, P =.05) after controlling for age, sex, Tanner stage, and body mass index when each of the lipid parameters was tested separately in the regression model. However, the introduction of both triglycerides and HDL values in the same model eliminated the significance of association of HDL with lnleptin, and the positive relationship of triglycerides with lnleptin remained significant. Our results indicate that triglycerides are independently associated with leptin levels after controlling for any known confounder.