AMILIAL HYPERCHOLESTEROLemia is the paradigm of the established relationship between increased low-density lipoprotein cholesterol (LDL-C) and cardiovascular disease. 1,2 This monogenic disorder is characterized by exposure to severely elevated LDL-C levels from birth onward. 3,4 Endothelial function, measured as flow-mediated dilatation of the brachial artery, is already impaired in prepubertal children with familial hypercholesterolemia. 5 In addition to these early functional changes, accumulation of LDL-C in children with familial hypercholesterolemia leads to deterioration of the vascular morphology and gives rise to increased intimamedia thickness (IMT) of the carotid arteries. 6-9 As a sequel to these observations, myocardial ischemia and coronary artery stenoses have been documented in young adults with this disorder. 10,11 The sequence of events in untreated children proceeds from endothelial dysfunction to increased

The potential use of an adjunctive therapy of metronidazole plus amoxycillin for the subgingival elimination of Actinobacillus actinomycetemcomitans in periodontitis patients was investigated. 22 patients participated in this study, 11 with localized juvenile periodontitis (LJP) and 11 with rapidly progressive periodontitis (RPP). 14 patients had received periodontal treatment in the past. All patients were subgingivally infected with A. actinomycetemcomitans. After mechanical subgingival debridement in combination with the antibiotic treatment, elimination of A. actinomycetemcomitans was achieved in all patients but one. With this one exception, clinical improvements were observed in all patients, resulting in reduced pocket probing depths as well as in a significant reduction in bleeding on probing. Re-examination of 16 patients after 9-11 months revealed that A. actinomycetemcomitans was still undetectable and further clinical improvement was observed. It was concluded that the combination of metronidazole plus amoxycillin is a valuable adjunct to mechanical therapy in A. actinomycetemcomitans associated periodontal infections.

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Background-We previously demonstrated in a randomized placebo-controlled trial that 2-year pravastatin treatment induced a significant regression of carotid intima-media thickness (IMT) in 8-to 18-year-old children with familial hypercholesterolemia. Subsequently, we continued to follow up these children to explore the relation between the age of statin initiation and carotid IMT after follow-up on statin treatment. We also examined safety aspects of statin therapy during this long-term follow-up. Methods and Results-All 214 children who initially participated in the previous placebo-controlled study were eligible for the follow-up study. After completion of the placebo-controlled study, all children continued treatment with pravastatin 20 or 40 mg, depending on their age. Blood samples were taken on a regular basis for lipids and safety parameters, and a carotid IMT measurement was performed after an average treatment period of 4.5 years. Follow-up data for 186 children were available for the statistical analyses. Multivariate analyses revealed that age at statin initiation was an independent predictor for carotid IMT after follow-up with adjustment for carotid IMT at initiation of statin treatment, sex, and duration of treatment. Early initiation of statin treatment was associated with a subsequently smaller IMT. Furthermore, no serious laboratory adverse events were reported during follow-up, and statin treatment had no untoward effects on sexual maturation. Conclusions-These data indicate that early initiation of statin treatment delays the progression of carotid IMT in adolescents and young adults. The present study shows for the first time that early initiation of statin therapy in children with familial hypercholesterolemia might be beneficial in the prevention of atherosclerosis in adolescence. (Circulation.

Background-Elevated LDL cholesterol (LDL-C) levels in childhood predict cardiovascular disease (CVD) later in life.Familial hypercholesterolemia (FH) represents the paradigm of this relation. Methods and Results-The objectives of this study were to (1) establish the LDL-C level that provides the most accurate diagnosis of FH in children from families with known FH and (2) assess whether lipoprotein variation in these children is associated with premature CVD in relatives. Foremost, however, it was our objective to identify children with FH who are at high risk and in need of early intervention. A total of 1034 consecutive children from FH kindreds were investigated. First, LDL-C levels Ͼ3.50 mmol/L had a 0.98 post-test probability (95% CI, 0.96 to 0.99) of predicting the presence of an LDL receptor mutation. Second, children with FH in the highest LDL-C tertile (Ͼ6.23 mmol/L) had a 1.7-times higher incidence (95% CI, 1.24 to 2.36) of having a parent with FH suffering from premature CVD (Pϭ0.001). In addition, such a parent was found 1.8 times more often (95% CI, 1.20 to 2.59) among children with FH who had HDL-C Ͻ1.00 mmol/L (Pϭ0.004). Last, children with FH whose lipoprotein(a) was Ͼ300 mg/L had a 1.45-times higher incidence (95% CI, 0.99 to 2.13) of having a parent with FH suffering from premature CVD (Pϭ0.05). Conclusions-In FH families, LDL-C levels allow accurate diagnosis of FH in childhood. Moreover, increased LDL-C and lipoprotein(a) and decreased HDL-C levels in children identify FH kindreds with the highest CVD risk. (Circulation.