:: Volume 1, Issue 4 (10-1999) ::
J Babol Univ Med Sci. 1999; Volume 1 Back to browse issues page
The prevalence of G6PD deficiency in the newborns of Babol, 1995
Y ZahedPasha *
Abstract:   (10700 Views)
Objective: The G6PD deficiency is the most common enzyme disorder in the human beings. It causes severe jaundice, kern icterus and death in the neonates and sever hemolysis or even death while having beans and some chemical materials in the other ages, so we decided to survey its prevalence in our region by studying on the umbilical cord blood. Methods: This is a descriptive-analytic study. The samples were gathered by a simple randomized procedure. Enzyme activity was measured with the method of (FST) divided into 3 categories of sufficient (S), deficient (D) and severely deficient (SD). D and SD were considered as the G6PD deficiency. Chi square and Fisher exact tests were used to analyze the data and P<0.05 was considered as significant. Findings: From total 2046 neonates, 50.5% were male and 49.5% were female. 12.5% of the boys, 8.4% of the girls and over all, 8.7% of the neonates were G6PD deficient. P value was 0.005 regarding to the correlation of positive familial history with the disease and 0.001 for the positive first line family history. Conclusion: According to the results, the G6PD deficiency is more common in boys than girls and there were some significant differences between the positive familial history with the disease in the boys and at all but not in the girls. Due to the high risk of jaundice in neonates and acute hemolysis in other age groups which are mentioned as a threatening factor for public health, we suggest using the screening umbilical cord blood tests on the neonates, to diagnose the G6PD deficiency, and to increase the primary health care (PHC) quality and public information by teaching.
Keywords: Neonate, Umbilical cord blood, G6PD deficiency, Screening, Jaundice
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Type of Study: Research | Subject: Biochemical
Accepted: 2014/05/25 | Published: 2014/05/25


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Volume 1, Issue 4 (10-1999) Back to browse issues page