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A 10-day course of amoxicillin at a dosage of 40 mg per kilogram per day was compared with conventional (lower dosage) penicillin V therapy in the treatment of culture-proven Group A streptococcal pharyngitis in children 3 to 18 years of age in a prospective, randomized, and singleblinded study. Children had to have signs and symptoms compatible with the diagnosis of streptococcal pharyngitis and to have a throat swab positive for Group A streptococci. A second throat culture was obtained 10 to 14 days after the completion of therapy. Serotyping was performed to help differentiate carrier states from reinfections. Of 161 children enrolled, 113 were evaluable; 55 received penicillin and 58 received amoxicillin. At the completion of therapy 70.9% (39/55) of patients in the penicillin group vs 87.9% (51/58) of patients in the amoxicillin group were asymptomatic (clinical cure, P=0.025). At the completion of therapy, 54.5% (30/55) of patients in the penicillin group vs 79.3% (46/58) of patients in the amoxicillin group had negative throat cultures (bacteriologic cure, P=0.005). The carrier rate (children who were well but who were still carrying the same serotype of Group A streptococcus) also differed betweent the groups: 13 (23.6%) in the penicillin group compared with six (10.3%) in the amoxicillin group. Amoxicillin at 40 mg/kg/day was significantly more effective than lower dosages of penicillin V for clinical and bacteriologic cure in the treatment of Group A streptococcal pharyngitis in children. The current perception that penicillin is declining in effectiveness may be due to inadequate dosing.

• Atherosclerosis is a process that begins in early life. Coronary heart disease is the result of complex interactions among a variety of risk factors of which hypercholesterolemia is but one. During routine screening, 500 children were identified with total cholesterol levels above the 95th percentile of 5.2 mmol/L (200 mg/dL). Lipoprotein profiles were then performed to confirm and delineate their lipid abnormalities. A definable lipid disorder was present in 85% of such children. Abnormal lipoprotein patterns included 292 children with type IIa, 99 with type IIb, and 25 with type IV phenotypes. An abnormally low high-density lipoprotein cholesterol level of less than 0.9 mmol/L (35 mg/dL) was observed in 20 children. Only 5% of patients were identified as being hypercholesterolemic because they had high-density lipoprotein cholesterol levels above the 95th percentile of 1.8 mmol/L (70 mg/dL). Thirty-two percent of children with total cholesterol levels above 5.2 mmol/L had a family member (sibling, parent, uncle, aunt, or grandparent) with a myocardial infarction prior to 55 years of age. Data from this study support universal cholesterol testing after 3 years of age and lipoprotein profiles for those with levels above 5.2 mmol/L. ( AJDC . 1991;145:147–150)

Several studies have documented that hypercholesterolemia is common in American children. Other studies have shown that elevated cholesterol levels in childhood remain elevated well into adult life. Autopsy studies of adolescents have also found a strong positive correlation between antemortem cholesterol levels and early atherosclerotic changes in their aortas and coronary arteries. Collectively, these studies provide strong and consistent evidence that atherosclerosis begins in childhood. The evidence is also overwhelming that lowering elevated low density lipoprotein cholesterol levels reduces the risk of heart attacks caused by coronary heart disease, at least among middle-aged men. As a result, routine cholesterol and coronary heart disease risk factor surveillance in childhood is both productive and appropriate. Premature coronary heart disease may be largely preventable and atherosclerosis, if not preventable, can be significantly delayed.

ALTHOUGH cervical lymphadenitis is a frequent finding in the pediatric age group there is little information concerning this abnormality in standard textbooks, particularly regarding its pathogenesis. The relative frequency with which the various causative agents may produce adenitis has not been well established. Tuberculous cervical lymphadenitis1 2 3 and scrofula caused by the atypical mycobacteria4 5 6 7 have been described in detail. Cat-scratch disease has also received widespread attention as a cause of regional adenitis.8 Adamson9 found a relatively high incidence of Group A streptococci in cervical lymph nodes of children in bacteriologic studies of post-mortem specimens, and cervical lymphadenitis is a frequent finding . . .