RESUMO
A recent survey found that approximately 4% of very low birth weight infants in Japan were treated with glucocorticoids postnatally for circulatory collapse thought to be caused by late-onset adrenal insufficiency. We identified 11 preterm infants with clinical signs compatible with this diagnosis (hypotension, oliguria, hyponatremia, lung edema, and increased demand for oxygen treatment) and matched them for gestational age with 11 infants without such signs. Blood samples were obtained for cortisol and its precursors from the patient group before the administration of hydrocortisone, and from the control group during the same postnatal week. All samples were analyzed using a gas chromatography-mass spectrometry system. Cortisol concentrations did not differ between the two groups (6.6 +/- 4.5 vs 3.4 +/- 2.7 microg/dL); however, the total concentration of precursors in the pathway to cortisol production was significantly higher in the patient group (72.2 +/- 50.3 vs 25.0 +/- 28.5 microg/dL; p < 0.05). We conclude that the clinical picture of late-onset adrenal insufficiency in preterm infants is not a result of an absolute deficiency of cortisol production, but may be a result of a limited ability to synthesize sufficient cortisol for the degree of clinical stress.
Assuntos
Insuficiência Adrenal/sangue , Hidrocortisona/sangue , Doenças do Prematuro/sangue , Recém-Nascido Prematuro , Choque/sangue , Insuficiência Adrenal/complicações , Insuficiência Adrenal/tratamento farmacológico , Estudos de Casos e Controles , Feminino , Cromatografia Gasosa-Espectrometria de Massas , Idade Gestacional , Glucocorticoides/uso terapêutico , Humanos , Recém-Nascido de Peso Extremamente Baixo ao Nascer , Recém-Nascido , Doenças do Prematuro/tratamento farmacológico , Recém-Nascido de muito Baixo Peso , Masculino , Choque/tratamento farmacológico , Choque/etiologiaRESUMO
To investigate the efficacy of the long-term treatment with pranlukast, a specific cysteinyl leukotriene receptor antagonist, in pediatric patients with mild to moderate asthma, 77 pediatric asthmatic patients who received pranlukast for up to 36 months (mean duration, 13 months) were evaluated retrospectively. Treatment with pranlukast resulted in improvements from the pretreatment baseline in asthma attacks per month, episodes of hospitalization, and episodes of intravenous amynophiline treatment on emergent clinic visits. The percentage of responders who had marked or moderate improvements in the above-mentioned parameters of asthma control was 79%. In conclusion, pranlukast caused significant improvements in long-term asthma control in pediatric patients with mild to moderate asthma.