ABSTRACT
Background: The pathogenesis of renal scarring following acute pyelonephritis [APN] remains unclear
Objectives: We sought to investigate the implication of the common polymorphisms in the renin-angiotensin system [RAS] genes, and other risk factors, in the development of renal scarring following APN in Egyptian children
Methods: 414 patients with culture-confirmed urinary tract infection were examined by DMSA-scans for diagnosis of APN and voiding cystourethrogram to test for vesicoureteric reflux [VUR]. Genetic polymorphisms at three RAS genes [ACE I/D, ATR-1 A1166C and AGT M235T] were analyzed by PCR and DNA sequencing in APN patients and 140 control children. Follow up DMSA-scans were performed 6-9 months later to detect renal scarring
Results: APN was diagnosed in 63 patients [34 boys and 29 girls] aging 2 months-12 years. Renal scarring was detected in 40 patients. VUR was the only independent risk factor for renal scarring [P=0.01]. The D-allele of ACE gene was significantly more frequent in the scarring group [76.25%] compared to non-scarring group [57.8%] and controls [56.7%]; P=0.035 and 0.003, respectively. However, the frequencies of ATR-1 and AGT genotypes and alleles in scarring and non-scarring groups did not show significant difference. The ACE I/D polymorphism was significantly and tightly associated with renal scarring [OR=2.6, CI=1.04-4.94, P=0.039]. In contrast, AGT and ATR-1 polymorphisms could not be associated with renal scarring after APN [P=0.108 and P=0.821, respectively]
Conclusion: VUR is an independent risk factor for renal scarring following APN. The ACE D allele may be one of the genetic susceptibility factors contributing to adverse renal prognosis in Egyptian children
ABSTRACT
To assess the efficacy of atropine treatment for infantile hypertrophic pyloric stenosis, 20 infants [17 boys and 3 girls] with infantile hypertrophic pyloric stenosis were evaluated initially clinically and sonographically then atropine was give intravenously and then orally and the patients were followed clinically and sonographically for 6 months. It was found that 14 patients [70%] showed complete cure clinically. Six patients [30%] showed no satisfactory improvement clinically and surgical interference was the alternative option. Long-term follow up showed no significant difference clinically or sonographically between patients treated medically with atropine and those who were treated surgically after 6 months
ABSTRACT
The study included 50 full term newborns with a 5 minute Apgar score
Conclusion: the consequences of perinatal asphyxia and HIE are tremendous. Both metabolic and biochemical changes are recorded. Enzymes as well as increases in injurious oxygen free radicals [L.per and NO] with decreases in the cell defence antioxidants [SOD and T.th] occur. Factors that lead to HIE are in the major part preventable [by good antenatal and perinatal care with fetal monitoring]. The present study has highlighted areas of intervention and treatment of HIE. Knowledge of cellular and biochemical events that occur in HIE may lead to recognition of certain steps that may be amenable to pharmacologic intervention to limit or even prevent neuronal cell damage due to HIE. The bleak outcome of HIE may be improved. Apgar score commonly used to judge asphyxia was not found to be a reliable indicator of HIE severity and/or outcome
ABSTRACT
To evaluate the prognosis of breath-holding spells [BHS] after iron treatment, 30 children [20 boys and 10 girls] aged between 10 months and 7 years [mean age 20.2 months] were followed prospectively for 3 months on iron therapy. It was found that spells were cyanotic in 60%, pallid in 26.7% and mixed in 13.3%. All patients were evaluated initially for hematological indices and EEG. All patients received iron therapy for 3 months [6mg/kg/day]. There was marked reduction in the frequency, duration and severity of BHS after iron therapy