Rheumatic fever in children: a 15-year experience in a developing country.

Clinical data from 91 patients with rheumatic fever (RF), who were hospitalized at a tertiary hospital in Lebanon between 1980 and 1995, were reviewed retrospectively. Age on hospitalization was 11.1+/-2.9 years (mean +/- SD, range 3-17 years). Nineteen patients were <6 years of age. Manifestations included carditis (93%), arthritis (39%), Sydenham's chorea (2%), erythema marginatum (4%), subcutaneous nodules (1%), fever (62%), arthralgia (55%), and acute congestive heart failure (CHF) on initial presentation (44%). Pericardial effusion occurred in 11%. There was positive family history of RF in 14%. Mitral insufficiency and aortic insufficiency occurred in 67 and 35%, respectively. Both mitral and aortic valves were involved in 30% of cases. Tricuspid insufficiency developed in 3% and pulmonary insufficiency in 1%. Mitral stenosis developed in 19%. Twenty-eight patients underwent surgical intervention: mitral valve repair and commissurotomy in 9/91 (10%), mitral valve replacement in 18/91 (20%), and aortic valve replacement in 9/91 (10%). Overall mortality was 12%: 5 following surgical intervention (3 after mitral valve surgery and 2 after mitral and aortic valve surgery). All patients that died had CHF on initial presentation (p = 0.006). This study includes hospitalized patients with predominant rheumatic heart disease. Initial presentation with CHF is a risk factor for surgical intervention and mortality. A significant high surgical intervention rate is noted that is probably related to the nature of the selected group studied. This study emphasizes the significant morbidity and death in patients with RF and carditis.

Transient hypertrophic cardiomyopathy in the newborn following multiple doses of antenatal corticosteroids.

Postnatal exposure to steroids has been associated with hypertrophic cardiomyopathy (HCM) in the newborn. Such an effect has not been described in infants born to mothers who received antenatal steroids. We report three newborns whose mothers were treated with betamethasone prenatally in different doses, duration of time, and who developed various degrees of HCM diagnosed by echocardiography. There was no maternal evidence of diabetes except for one infant whose mother had a normal fasting and post-prandial blood glucose prior to steroid therapy, but an abnormal one hour postprandial glucose after 8 weeks of betamethasone therapy, with a normal HbA1 C level. There was no family history of HCM, no history of maternal intake of other relevant medications, and no hypertension in all three newborns. Follow-up echocardiography revealed complete resolution of the HCM changes in all infants. We suggest that repeated antenatal maternal steroid intake may cause changes of HCM in the newborn. These changes appear to be dose- and duration-related and are mostly reversible. Further prospective controlled studies to evaluate these observations and to investigate potential mechanisms are warranted.