Subject(s)
Ataxia , Vertigo , Humans , Child, Preschool , Vertigo/diagnosis , Vertigo/etiology , GaitSubject(s)
Cerebrospinal Fluid Rhinorrhea/diagnosis , Cerebrospinal Fluid Rhinorrhea/history , Glucose Oxidase/metabolism , Glucose/cerebrospinal fluid , Cerebrospinal Fluid Rhinorrhea/enzymology , Diagnostic Tests, Routine/methods , Female , History, 20th Century , Humans , Male , Pediatrics/history , Periodicals as Topic/history , Sensitivity and SpecificityABSTRACT
In a population-based retrospective cohort of 5,353,022 California births from 1991 to 2000, 3,152 newborns were diagnosed with congenital hydrocephalus during the birth hospitalization. We compared demographic and clinical characteristics of infants with and without congenital hydrocephalus, and examined in-hospital fatality rates. The prevalence of congenital hydrocephalus was 5.9 per 10,000. During the study period, there was a decline in congenital hydrocephalus due to spina bifida (1.4 to 0.9 per 10,000), and an increase in congenital hydrocephalus due to obstructive hydrocephalus (0.5 to 1.0 per 10,000). Independent risk factors for congenital hydrocephalus were birth weight <1,500 g (odds ratio [OR] 51.6, 95% confidence interval [CI] 47.7-55.8) and birth weight 1,500-2,000 g (OR 14.1, 95% CI 12.4-16) compared to birth weight greater than 2,000 g, low socioeconomic status (OR 1.5, 95% CI 1.4-1.6), and male sex (OR 1.2, 95% CI 1.1-1.3). Asians had a decreased risk for congenital hydrocephalus (OR 0.7, 95% CI 0.6-0.8) when compared to whites. Thirteen percent of affected neonates died before hospital discharge.
Subject(s)
Hydrocephalus/epidemiology , California/epidemiology , Female , Hospital Mortality , Humans , Hydrocephalus/congenital , Hydrocephalus/mortality , Infant, Newborn , Male , Prevalence , Retrospective Studies , Socioeconomic FactorsABSTRACT
BACKGROUND: Actual prednisone exposure in low-dose prednisone regimens, in part determined by cytochrome P450 metabolism, has been shown to be important for allograft survival. METHODS: Prednisolone (the principal active metabolite of prednisone) metabolism was determined in eight nontransplant patients and in transplant recipients receiving oral prednisone maintenance therapy (20 kidney and 6 liver recipients receiving cyclosporine [CsA] and eight lung recipients receiving ketoconazole and CsA or tacrolimus [FK506]). RESULTS: Prednisolone area under the curve (AUC)-dose-normalized (PNAUCn) to 1 mg/kg was 8,288+/-1,513 ng.hr/mL in kidney recipients, versus 4,826+/-999 ng/mL per hr in healthy subjects (P<0.001); it was also increased in liver recipients versus healthy subjects (11,456+/-1,214 ng.hr/mL, P<0.001). Liver recipients also metabolized prednisolone more slowly than kidney recipients (P<0.001). PNAUCn in lung recipients was similar in kidney recipients despite the effect of ketoconazole to slow CsA metabolism. In kidney transplant recipients, the rate of CsA metabolism was correlated with the rate of prednisolone metabolism (r=0.54, P=.026). Basal cortisol levels in all transplant recipients were lower than in healthy subjects, suggesting more prednisolone exposure in transplant patients. CONCLUSIONS: Prednisolone metabolism is slower in solid-organ transplant recipients than in healthy subjects. The slower metabolism of prednisolone, particularly in liver recipients, may help explain the immunologic effectiveness of low-dose prednisone regimens in these patients.