Dexamethasone Versus Prednisone or Prednisolone for Acute Pediatric Asthma Exacerbations in the Emergency Department: A Meta-Analysis.

OBJECTIVE: This study evaluates the efficacy and tolerability of dexamethasone (DEX) as an alternative to prednisone/prednisolone (PRED) for the treatment of pediatric asthma exacerbations in emergency department (ED). METHODS: Fixed-effects meta-analyses of selected endpoints were performed by using data taken from relevant studies identified by following a priori eligibility criteria after a comprehensive literature search in several electronic databases. RESULTS: Data from 10 studies (3208 pediatric asthma patients [1616 DEX treated and 1592 PRED treated], 4.77 years [95% confidence interval, 3.80-5.56 years], 63% [57.76%-62.68%] males) were used. Risk of vomiting drug was significantly lower in DEX group than in PRED group (risk ratio, 0.29 [0.18-0.48]; P ˂ 0.00001). Emergency department stay between DEX and PRED treated patients was statistically different (0.16 [0.03-0.40] hours; P = 0.02) but may not be clinically meaningful. The number of ß-agonist therapies received by DEX- and PRED-treated patients was similar. Treatments with both DEX and PRED were associated with improvement in asthma status assessment scores, and there was no significant difference between the groups. There were also no differences between the groups in hospitalization rate, ED revisit rate, and hospital admission rate after relapse. CONCLUSIONS: Dexamethasone is a suitable alternative to PRED for the treatment of pediatric asthma exacerbation in ED.

Effect of chronic intermittent hypoxia on the expression of Nip3, cell apoptosis, beta-amyloid protein deposit in mice brain cortex.

BACKGROUND: Chronic intermittent hypoxia (CIH) is the most important pathophysiologic feature of sleep apnea syndrome (SAS). To explore the relationship between SAS and dementia, the effects of CIH on the expression of Nip3, neuron apoptosis and beta-amyloid protein deposit in the brain cortex of the frontal lobe of mice were evaluated in this study. METHODS: Thirty male ICR mice were divided into four groups: control group (A, n = 10, sham hypoxia/reoxygenation), 2 weeks CIH group (B, n = 5), 4 weeks CIH group (C, n = 5), and 8 weeks CIH group (D, n = 10). The ICR mice were placed in a chamber and exposed to intermittent hypoxia (oxygen concentration changed periodically from (21.72 +/- 0.55)% to (6.84 +/- 0.47)% every two minutes, eight hours per day). Neuron apoptosis of the cortex of the frontal lobe was detected by means of terminal deoxy-nucleotidyl transferase-mediated in situ end labeling (TUNEL). Immunohistochemical staining was performed for measuring expression of Nip3 and beta-amyloid protein. The ultrastructure of neurons was observed under a transmission electron microscope. RESULTS: TUNEL positive neurons in each square millimeter in the cortex of the frontal lobe were categorized by median or Ri into group A (1, 5.5), group B (133, 13), group C (252, 21), and group D (318, 24). There were significant differences among the above four groups (P = 0.000). The significance test was performed between the control group and each CIH group respectively: group A and B (P > 0.05); group A and C (P < 0.01); and group A and D (P < 0.005). The number of apoptotic neurons kept increasing in the ICR mice under CIH condition, and reached the peak in the group D, but there was no significant difference between groups B and C, between groups B and D, and between groups C and D. Nip3 positive neurons in each square millimeter in the cortex of the frontal lobe in each group were calculated by median or Ri as follows: group A (2, 5.5), group B (117, 13), group C (227, 26.2), and group D (479, 21.4). There were significant differences among the four groups (P = 0.000). The statistical test was performed between the control group and each CIH group respectively: groups A and B (P > 0.05); groups A and C (P < 0.005); and groups A and D (P < 0.005). There was no significant difference between groups B and C, groups B and D, and groups C and D. The expression of Nip3 was closely correlated with neuron apoptosis in the brain (P < 0.05). The expression of beta-amyloid protein in the brain of mice was negative in all CIH groups and the control group. Ultrastructure observation showed karyopyknosis of nucleus, swelling of chondriosomes, deposit of lipofuscins and degeneration of neural sheath in all CIH groups but not in the control group. CONCLUSION: The results of this study indicate that CIH could up-regulate the expression of Nip3, and result in neuron apoptosis and ultrastructural changes in neurons of the frontal cortex.