RESUMO
OBJECTIVE: To evaluate the effectiveness of initial treatment of children with acute immune thrombocytopenic purpura (ITP) with anti-D immune globulin (anti-D) or pooled IgG immune globulin (IVIg). STUDY DESIGN: The medical charts of 33 children diagnosed with acute ITP from May 1995 to October 1997 were reviewed. Patient data were eligible for analysis if, for the new diagnosis of acute ITP, the patient had received either anti-D at 45 to 50 microg/kg (WinRho SD, NABI) or IVIg at 0.8 to 1 g/kg (Gammagard SD, Baxter-Highland). The platelet response time for each treatment group was compared by the Mann-Whitney U test. RESULTS: Time to achieve a platelet count >/=20 x 10(9 )/L (20,000/mm3 ) was 1.54 +/- 0.51 days in the IVIg group (n = 13) and 1.26 +/- 0.82 days in the anti-D group (n = 14) (P =.34). Time to achieve a platelet count >/=40 x 10(9 )/L (40,000/mm3 ) was 1.77 +/- 0.74 and 1.49 +/- 1.01 days for the IVIg and anti-D groups, respectively (P =.32). Children given IVIg were hospitalized for 2.1 +/- 0.87 days, whereas those given anti-D were hospitalized for 1.94 +/- 1.08 days. A net decrease in hemoglobin concentration was observed after receipt of IVIg (9.1 +/- 7.3 g/L [0.91 +/- 0.73 g/dL]) and after anti-D therapy (4.5 +/- 10.3 g/L [0.45 +/- 1.03 g/dL], P =.23). No patient required intervention for hemolysis. CONCLUSIONS: In this retrospective analysis anti-D was as effective as IVIg for the treatment of acute ITP in children. However, randomized, controlled trials are needed to establish the role of anti-D in the treatment of acute ITP in children.
Assuntos
Imunoglobulinas Intravenosas/uso terapêutico , Isoanticorpos/uso terapêutico , Púrpura Trombocitopênica Idiopática/tratamento farmacológico , Adolescente , Criança , Pré-Escolar , Feminino , Hemoglobinas/efeitos dos fármacos , Humanos , Lactente , Masculino , Contagem de Plaquetas/efeitos dos fármacos , Púrpura Trombocitopênica Idiopática/sangue , Estudos Retrospectivos , Imunoglobulina rho(D)RESUMO
We administered lovastatin to two sisters, aged 4 and 17 years, who had cholesterol ester storage disease, an autosomal recessive disorder manifested by hypercholesterolemia and hypertriglyceridemia. The drug, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, was taken orally for 6 months. Serum lipid concentrations were determined monthly. Computed tomography of the liver was performed before and during therapy to evaluate liver fat content. The younger sister had liver biopsies before and after 6 months of lovastatin therapy to assess hepatic cholesterol stores. Both patients had marked decreases in serum levels of cholesterol, triglycerides, and low-density lipoprotein-cholesterol; high-density lipoprotein-cholesterol levels increased. Computed tomography during treatment demonstrated a significant increase in linear attenuation, suggesting a decreased liver fat content. Liver tissue obtained 6 months after lovastatin therapy was initiated had 13% less esterified cholesterol than the liver sample obtained before treatment. We conclude that lovastatin may be effective in treating children with cholesterol ester storage disease.