Atrial natriuretic peptide in bronchial asthma in children

The hormone atrial natriuretic peptide [ANP] causes bronchodilatation and partially protects against direct and indirect bronchial challenges in patients with asthma. The present study was carried out to determine the role of ANP in bronchial asthma in children. Twenty asthmatic children with age ranged from 1.5 to 11 years old were subjected to clinical, laboratory and radiological studies. Plasma ANP has been measured for the asthmatic group during acute sever asthma and at least 4 weeks later while clinically stable, as well as, for a control group who included 15 clinically free children with appropriate age and sex. The mean plasma value of ANP during acute sever asthma [9.25 +/- 2.95 pg/me was significantly higher [P<0.001] than the corresponding values of clinically stable asthmatic children [6.13 +/- 2.72 pg/ml] and the-control group [1.45 +/- 1.12 pg/ml]. Also, the difference between the mean plasma ANP values of clinically stable asthmatic children and the control group was statistically highly significant [P<0.001]. We concluded that ANP could be considered one of the mediators of asthma modulation that increased in asthmatic children to protect against bronchocontriction

Imbalance between free radical propagation and antioxidant status in children with nephrotic syndrome

Oxygen radicals have been implicated in a variety of disease processes including nephrotic syndrome. In this study we investigated the free radical activation products and antioxidant status in children with nephrotic syndrome compared with a control group. Serum lipid peroxides [LP] and selenium levels and red blood cell glutathione peroxidase [GSH-Px] and superoxide dismutase [SOD] activities were measured in 35 children [28 males and 7 females] with nephrotic syndrome. Similar number of apparently healthy children with appropriate age and sex were used as a control group. Children with nephrotic syndrome had significantly higher levels of LP [3.37 +/- 0.5 nmol/ml] and lower levels of serum selenium [150 +/- 35 ug/L] and red blood cell GSH- Px and SOD [32.6 +/- 7.8 U/g Hb and 1116 +/- 151 U/g Hb respectively] when compared with the corresponding levels of the control group [2.53 +/- 0.6 nmol/ml, 230 +/- 43 ug/L, 51.8 +/- 13.8 U/g Hb and 1422 +/- 277 U/g Hb respectively]. We concluded that imbalance between generation of oxygen radicals and antioxidant status may have etiological implications for nephrotic syndrome