An update on the prevalence of glucose-6-phosphate dehydrogenase deficiency and neonatal jaundice in Tehran neonates

Abolghasemi, Hassan; Mehrani, Hossein; Amid, Ali

doi:10.1016/j.clinbiochem.2003.11.010

Cited by 29 publications

(25 citation statements)

References 25 publications

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“…The genetic basis for the condition has been identified as a polymorphism in the promoter for the gene which leads to reduced enzyme activity and subsequently caused decreased bilirubin conjugation 4,10,17. Some investigators suggested that rate limiting enzyme in the production of bilirubin was increased in G6PD enzyme deficiency which subsequently aggravate the bilirubin level 6,10 .In this study, higher serum bilirubin and higher ALT levels in G6PD deficient group and their negative correlation with erythrocyte G6PD levels support liver cells enzyme defect in this group of neonates.…”

Section: Figuresupporting

confidence: 54%

“…In the last two decades, numerous studies have shown that G6PD deficiency is a potential cause of neonatal jaundice. Investigators from different countries reported that significantly higher serum bilirubin level is a usual finding in neonates with G6PD deficiency 3,4,5,6 . They also reported about different values of serum bilirubin level in erythrocyte G6PD deficient neonates, some of them found >20 mg/dl 7,11 in this group of neonates.…”

mentioning

confidence: 99%

“…They also reported about different values of serum bilirubin level in erythrocyte G6PD deficient neonates, some of them found >20 mg/dl 7,11 in this group of neonates. Decreased conjugation and excretion of bilirubin by the liver had major contribution to the development of neonatal jaundice in G6PD deficient neonates 6,7 . Some investigators reported that most of this enzyme deficient neonates developed exaggerated jaundice due to deficiency of the enzyme in the liver cells.…”

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confidence: 99%

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Some Aspects of Liver Function Status in G6PD Deficient Neonates and Its Relationship with G6PD

Akhter

Begum

Ferdousi

2012

J Bangladesh Soc Physiol

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Background: Neonatal jaundice is a common cause of newborn hospital admission. G6PD enzyme defects is one of the factor to develop neonatal hyperbilirubinemia, which may be related to abnormal liver function in this group of neonates. Objective: To observe some aspects of liver function status by measuring serum bilirubin and alanine amino transferase levels in G6PD deficient neonates and also their relationship with erythrocyte G6PD levels. Methods: The study was conducted on 30 male, term neonates with G6PD deficiency in the Department of Physiology, Bangabandhu Sheikh Mujib Medical University (BSMMU) between 1st July 2007 to 30th June 2008. For comparison age and sex matched 30 apparently healthy neonates without deficiency (control group) were also included in the study. Erythrocyte G6PD level was measured by Spectrophotometric method by using kit of Randox. Alanine amino transferase level was done by Schumann and Klauke method. For statistical analysis independent sample "t" test and Pearson's correlation coefficient test were performed as applicable by using SPSS for windows version-13 Results: In this study, significantly (p<0.001)higher level of serum bilirubin & ALT were found in G6PD deficient group in comparison to those of non-deficient group. Further more, serum bilirubin & ALT levels were negatively (r=-.671, (r= -.534) correlated with erythrocyte G6PD level and it was statistically significant (p<0.01) in G6PD deficient group. Again, significant (p<0.05) positive (r=+.429) correlation of serum bilirubin level was observed in non deficient group. Whereas, non significant positive (r=+.041) correlations of ALT was found in non deficient group. Conclusion: From the study results it can be concluded that higher level of alanine amino transferaseand hyperbilirubinemia were present in G6PD deficient neonates & increase serum bilirubin and serum alanine amino transferase levels were associated with degree of G6PD enzyme deficiency.

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confidence: 54%

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confidence: 99%

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confidence: 99%

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Some Aspects of Liver Function Status in G6PD Deficient Neonates and Its Relationship with G6PD

Akhter

Begum

Ferdousi

2012

J Bangladesh Soc Physiol

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“…In our study, the male to female ratio in G6PD deficient neonates was 5.5:1. In other studies in the city of Dhahran (Saudia Arabia), 19 Yanbu(Saudi Arabia), 20 Pinjab (India), 21 Tehran (Iran) 14 male to female ratio in G6PD deficient neonates was reported as 2:1, 3:1, 1.8:1 and 6:1, respectively. It seems that the incidence of G6PD deficiency in the Iranian female population is lower than in other female populations.…”

Section: Discussionmentioning

confidence: 99%

Newborn screening for glucose-6-phosphate dehydrogenase deficiency in Isfahan, Iran: a quantitative assay

et al. 2008

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Objectives To determine the prevalence of glucose-6-phosphate dehydrogenase (G6PD) deficiency in Isfahan, the central state of Iran. Methods From February to March 2006, a total of 2501 samples were screened for the quantitative measurement of G6PD activity by enzymatic colorimetric assay by a commercial kit (GAMMA, Belgium). The neonates were referred from 17 delivery units to the Isfahan neonatal screening center at 3–7 days after birth. Any neonate with a value < 6.4 U/gHb was considered G6PD deficient. Results Of the 2501 newborns (1307 males, 1194 females) screened, 79 neonates were found to have G6PD deficiency (67 males, 12 females). The overall incidence of G6PD deficiency was 3.2%. Frequency in male population was 5.1 % (67 out of 1307 male neonates) and in female population was 1% (12 out of 1194 female neonates).The female:male ratio was 1:5.5 ( P = 0.0001). The mean enzyme activity in deficient patients was 3.22 ± 1.8 U/gHb (male deficient group; 3.17 ± 1.74 U/gHb, female deficient group; 3.49 ± 2.17 U/gHb, P = 0.58). Conclusion Routine neonatal screening in Isfahan, Iran with a relatively high prevalence of G6PD deficiency is justified and meets the World Health Organization recommendation.

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“…The prevalence rates reported in the studies reviewed were not comparable with the prevalence rate observed in Sistan and Balouchestan province. For example, screening of newborns in a Tehran hospital for G6PD deficiency showed that 2.1% (3.6% of males and 0.6% of females) were G6PD-deficient [40]. Similarly, the proportion of the neonates born in the city of Arak hospitals with enzyme deficiency was 2.2% [41].…”

Section: Discussionmentioning

confidence: 99%

Prevalence of glucose-6-phosphate dehydrogenase (G6PD) deficiency in southeast Iran: implications for malaria elimination

Tabatabaei

Khorashad

Sakeni

et al. 2015

J Infect Dev Ctries

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Introduction: Glucose-6-phosphate dehydrogenase deficiency (G6PD) is an X-linked genetic disorder with a relatively high frequency in malaria-endemic regions. It is an obstacle to malaria elimination, as primaquine administered in the treatment of malaria can cause hemolysis in G6PD-deficient individuals. This study presents information on the prevalence of G6PD deficiency in Sistan and Balouchetsan province, which hosts more than 90% of Plasmodium vivax malaria cases in Iran. This type of information is needed for a successful malaria elimination program. Methodology: A total of 526 students were randomly recruited through schools located in southeast Iran. Information was collected by interviewing the students using a structured questionnaire. Blood samples taken on filter papers were examined for G6PD deficiency using the fluorescent spot test. Results: Overall, 72.8% (383/526) of the subjects showed normal G6PD enzyme function. Mild and severe G6PD deficiency was observed in 14.8% (78) and 12.2% (64) of subjects, respectively. A total 193/261 males (73.9%) and 190/265 (72%) females had normal enzyme activity. Mild G6PD deficiency was observed in 10.8% (28) and 18.9% (50) of male and female subjects, respectively. However, in comparison with females, a greater proportion of males showed severe enzyme deficiency (15.3% versus 9.1%). All these differences were statistically significant (p < 0.006). Conclusions: G6PD deficiency is highly prevalent in southeast Iran. G6PD-deficient individuals are susceptible to potentially severe and lifethreatening hemolytic reactions after primaquine treatment. In order to achieve malaria elimination goals in the province, G6PD testing needs to be made routinely available within the health system.

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An update on the prevalence of glucose-6-phosphate dehydrogenase deficiency and neonatal jaundice in Tehran neonates

Cited by 29 publications

References 25 publications

Some Aspects of Liver Function Status in G6PD Deficient Neonates and Its Relationship with G6PD

Some Aspects of Liver Function Status in G6PD Deficient Neonates and Its Relationship with G6PD

Newborn screening for glucose-6-phosphate dehydrogenase deficiency in Isfahan, Iran: a quantitative assay

Prevalence of glucose-6-phosphate dehydrogenase (G6PD) deficiency in southeast Iran: implications for malaria elimination

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