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 Table of Contents  
ORIGINAL ARTICLE
Year : 2021  |  Volume : 11  |  Issue : 4  |  Page : 81-84

Prevalence of glucose-6-phosphate dehydrogenase deficiency among neonates with hyperbillirubinemia in the West of Iran


1 Department of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
2 Autism Spectrum Disorders Research Center, Hamadan University of Medical Sciences, Hamadan, Iran

Date of Submission07-Feb-2021
Date of Decision10-Apr-2021
Date of Acceptance01-Jun-2021
Date of Web Publication16-Oct-2021

Correspondence Address:
Ensiyeh Jenabi
Autism Spectrum Disorders Research Center, Hamadan University of Medical Sciences, Hamadan
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/aihb.aihb_12_21

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  Abstract 


Introduction: Hyperbilirubinemia is a common complication among neonates. The objective of this cross-sectional study was the prevalence of glucose 6-phosphate dehydrogenase (G6PD) deficiency among neonates with hyperbilirubinemia in the west of Iran. Materials and Methods: In this retrospective cross-sectional study, the records of neonates with hyperbilirubinemia who were hospitalised in Hamadan located in the west of Iran, from 2011 to 2016 were reviewed. After reviewing and studying each of the mentioned files, the necessary information was entered in the relevant checklists. Then, the neonates were divided into two groups, including the group with G6PD enzyme deficiency in the case study group and the G6PD enzyme-free group in the control study group. All statistical analyses were conducted in SPSS version 21 software and P < 0.05 was statistically considered significant. Results: A total of 1545 neonates with hyperbilirubinemia was reviewed. Among them, 40 neonates were in the case group and 1505 were in the control group. The prevalence of G6PD deficiency in the present study was 2.58% among neonates with hyperbilirubinemia which has a similar gender distribution. There were statistically significant differences between case and control groups based on total bilirubin, direct bilirubin, reticulocyte count, time of appearance of jaundice, duration of receiving phototherapy and hospitalisation (P < 0.05). Conclusion: We proposed that cord blood G6PD screening be conducted among neonates. This can be affected in identifying G6PD-deficient neonates who might require a longer hospital stay after birth, with monitoring of their serum bilirubin before and after discharge.

Keywords: Glucose 6-phosphate dehydrogenase deficiency, glucose phosphate dehydrogenase deficiency, neonatal hyperbilirubinemia, prevalence


How to cite this article:
Eghbalian F, Aqaie R, Jiriaee N, Jenabi E. Prevalence of glucose-6-phosphate dehydrogenase deficiency among neonates with hyperbillirubinemia in the West of Iran. Adv Hum Biol 2021;11:81-4

How to cite this URL:
Eghbalian F, Aqaie R, Jiriaee N, Jenabi E. Prevalence of glucose-6-phosphate dehydrogenase deficiency among neonates with hyperbillirubinemia in the West of Iran. Adv Hum Biol [serial online] 2021 [cited 2021 Dec 4];11:81-4. Available from: https://www.aihbonline.com/text.asp?2021/11/4/81/328387




  Introduction Top


Hyperbilirubinemia is a common complication among neonates. It happens among 60% of full-term and 80% of preterm neonates in the first 3 days of birth.[1] The severe hyperbilirubinemia secondary to reduced glucose 6-phosphate dehydrogenase (G6PD) activity is complicated by kernicterus and it is a serious neurological disease.[2] The G6PD deficiency is an X-linked recessive disease affecting males more than females.[3]

The G6PD deficiency is seen most frequently in approximately all of Africa, Asia, and the countries near the Mediterranean Sea.[4] G6PD deficiency is an important disorder of hexose monophosphate shunt in erythrocyte metabolism. The activity of the enzyme G6PD is essential for the survival of red blood cells because it only catalyses the metabolic pathway that is capable of producing reducing power to these mitochondrial cells.[5]

Oduola et al., in Nigeria, reported that total bilirubin was significantly higher in G6PD-deficient neonates than in G6PD-normal neonates.[6] Isa in 2017 showed that G6PD deficiency is an important risk factor for severe neonatal indirect hyperbillirubinemia. They showed that 42% of neonatal indirect hyperbilirubinemia had G6PD-deficient which was double compared with the normal population.[7]

Other study in Turkey reported that the prevalence of G6PD deficiency is only in 1%–5% of the population and 3.8% of neonatal indirect hyperbilirubinemia had G6PD deficiency.[8] M Abo El Fotoh and Rizk in Egypt reported that G6PD deficiency was found to be one important cause of neonatal jaundice after 2 days of birth.[9]

The aim of this cross-sectional study was the prevalence of G6PD deficiency among neonates with hyperbilirubinemia in the west of Iran.


  Materials and Methods Top


In this retrospective cross-sectional study, the records of neonates with hyperbilirubinemia who were hospitalised in Hamadan located in the west of Iran, from 2011 to 2016 (6 years) were reviewed. Ethical approval for the study was obtained from Hamadan University of Medical Sciences with the code of IR.UMSHA.REC.1399.290.

Inclusion criteria were all neonates with hyperbilirubinemia who were admitted to the NICU ward of Hospital in Hamadan City during the years 2011–2016. Exclusion criteria were direct hyperbilirubinemia (more than 20% of total bilirubin is direct bilirubin), sepsis, congenital anomalies and neonates with incomplete records.

According to the results of the study, the prevalence of hyperbilirubinemia in neonates with G6PD deficiency was reported 3.2%.[10] Therefore, we assumed P to be 0.032, we arrived at a sample size of 1239 at 95% significance level. Finally, after reviewing all 6-year records, the number of 1545 neonates (782 males and 763 females) was included in the present study.

After reviewing and studying each of the mentioned files, the necessary information was entered in the relevant checklists. Then, the neonates were divided into two groups based on the presence or absence of G6PD enzyme, including the group with G6PD enzyme deficiency in the case study group and the G6PD enzyme-free group in the control study group.

The checklist included data on birth weight, gender, RH, blood group, total bilirubin, indirect bilirubin and direct bilirubin, reticulocyte count, time of appearance of jaundice, duration of receiving phototherapy and hospitalisation. The validity and reliability of the checklist were assessed.

Qualitative data were summarised with frequency and percentage and quantitative variables with mean (standard deviation). Statistical analysis was performed using the independent t-test for comparison continuous variables. All the Statistical Package for the Social Science (SPSS) software for Windows (IBM Corp. Armonk, NY, USA) version 21.0 software and P < 0.05 was statistically considered significant.


  Results Top


A total of 1545 neonates with hyperbilirubinemia, 782 (50.61.3%) males and 763 (49.39%) females, was reviewed. Among them, 40 neonates were in the case group (G6PD deficient) and 1505 were in the control group (G6PD normal).

In the present study, from 1545 newborns, 1299 neonates (84.07%) were diagnosed as having physiological jaundice, ABO incompatibility was diagnosed in 123 neonates (7.96%), Rh incompatibility in 50 neonates (3.23%), ABO and Rh incompatibility in 22 neonates (1.42%), G6PD deficiency in 40 neonates (2.58%) and urinary tract infection in 11 neonates (0.71%) [Table 1]. Therefore, the prevalence of G6PD deficiency among neonates with hyperbilirubinemia in the present study was 2.58% which has a similar gender distribution (P = 0.378)
Table 1: The etiology of hyperbilirubinemia among neonates

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There were statistically significant differences between case and control groups based on total bilirubin, direct bilirubin, reticulocyte count, time of appearance of jaundice, duration of receiving phototherapy and hospitalisation (P < 0.05). There was no significant difference based on birth weight and indirect bilirubin between case and control groups [Table 2].
Table 2: Clinical and laboratory findings in the case and control groups

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  Discussion Top


According to our findings, G6PD deficiency had a prevalence of 2.58% among neonates with hyperbilirubinemia with a similar gender distribution. We also found that there was no significant relationship between birth weight and the prevalence of G6PD deficiency. In neonates with G6PD deficiency, serum total bilirubin, direct bilirubin and peripheral blood reticulocyte levels were higher than controls. We also found that G6PD can prolong the duration of hospitalisation and receiving phototherapy compared with the control group.

The prevalence of G6PD deficiency in Middle Eastern countries was between 1% and 2%.[11] Isa et al. in 2017 showed that 42% of neonatal with indirect hyperbilirubinemia had G6PD-deficient.[7] Eghbalian and Monsef in Iran reported that the frequency of G6PD deficiency without haemolysis in the hospitalised icteric newborns was 2.6%.[12] Furthermore, other study in Turkey reported that the prevalence of G6PD deficiency is only in 1%– 5% of the population and 3.8% of neonatal indirect hyperbilirubinemia had G6PD deficiency.[8] In our study, G6PD deficiency had a prevalence of 2.58% among neonates with hyperbillirubinemia. Various results in the field of G6PD deficiency indicate racial or ethnic dependence in the incidence of this disease.

In the present study, the mean of total and direct bilirubin in G6PD deficient individuals was significantly higher than in the control group. This finding is consistent with the studies of Pahlavanzadeh et al.[13] and Isa et al.[7]

According to the results of the present study, the time of appearance of jaundice occurred in neonates with G6PD deficiency at older ages. This finding was consistent with the study of Isa et al.[7] Therefore, this finding can be effective in clinical suspicion of this genetic defect in neonates who have late jaundice symptoms.

In the present study, there was no relationship between birth weight and G6PD deficiency, which was consistent with the study of Pahlavanzadeh et al.[13] as well as the study of Khodashenas et al.[14]

The duration of hospitalisation and phototherapy in neonates with G6PD deficiency was significantly longer than in the control group. This finding was consistent with a study conducted in Bahrain.[7] Therefore, early diagnosis of this disease can prevent prolonged hospital stay and reduce the costs associated with it.

We may have included G6PD-deficient neonates in the normal group because testing for G6PD may be falsely negative during acute haemolysis.[15] Therefore, this was the limitation of the present study.

We proposed that cord blood G6PD screening be conducted among neonates. This can be affected in identifying G6PD-deficient neonates who might require a longer hospital stay after birth, with monitoring of their serum bilirubin before and after discharge. In addition, neonates with normal G6PD may be discharged earlier and have routine follow-up.


  Conclusion Top


Our findings reported that G6PD deficiency had a prevalence of 2.58% among neonates with hyperbilirubinemia neonates with a similar gender distribution. We also found that there was no significant relationship between birth weight and the prevalence of G6PD deficiency. In neonates with G6PD deficiency, serum total bilirubin, direct bilirubin and peripheral blood reticulocyte levels were higher than controls. We also found that G6PD can prolong the duration of hospitalisation and receiving phototherapy compared with the control group.

Acknowledgement

We thank from Hamadan University for its financial support.

Financial support and sponsorship

The protocol of this study was financially supported by Hamadan University of Medical Sciences, Iran, with Code 9907014455.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Koosha A, Rafizadeh B. Evaluation of neonatal indirect hyperbilirubinaemia at Zanjan Province of Iran in 2001-2003: Prevalence of glucose-6-phosphate dehydrogenase deficiency. Singapore Med J 2007;48:424-8.  Back to cited text no. 1
    
2.
Cunningham AD, Hwang S, Mochly-Rosen D. Glucose-6-Phosphate Dehydrogenase Deficiency and the Need for a Novel Treatment to Prevent Kernicterus. Clin Perinatol 2016;43:341-54.  Back to cited text no. 2
    
3.
Luzzatto L. G6PD deficiency: A polymorphism balanced by heterozygote advantage against malaria. Lancet Haematol 2015;2:e400-1.  Back to cited text no. 3
    
4.
Frank JE. Diagnosis and management of G6PD deficiency. Am Fam Physician 2005;72:1277-82.  Back to cited text no. 4
    
5.
Jatau E, Toma O, Egesie O, Damulak D, Ayuba Z, Ewuga J, et al. Glucose-6-phosphate dehydrogenase activity in newborn in Jos: A necessary evaluation for icteric neonates. J BioMed Res Clin Pract 2019;2:191-6.  Back to cited text no. 5
    
6.
Oduola T, Bunza F, Yusuf MT, Dallatu MK, Ndakotsu MA, Panti A, et al. Prevalence of glucose-6-phosphate dehydrogenase deficiency among neonates in usmanu danfodiyo university teaching hospital (UDUTH), Sokoto, Nigeria: Oxidative stress markers in g6pd deficient neonates. Int Blood Res Rev 2018;8:1-6.  Back to cited text no. 6
    
7.
Isa HM, Mohamed MS, Mohamed AM, Abdulla A, Abdulla F. Neonatal indirect hyperbilirubinemia and glucose-6-phosphate dehydrogenase deficiency. Korean J Pediatr 2017;60:106-11.  Back to cited text no. 7
    
8.
Atay E, Bozaykut A, Ipek IO. Glucose-6-phosphate dehydrogenase deficiency in neonatal indirect hyperbilirubinemia. J Trop Pediatr 2006;52:56-8.  Back to cited text no. 8
    
9.
M Abo El Fotoh WM, Rizk MS. Prevalence of glucose-6-phosphate dehydrogenase deficiency in jaundiced Egyptian neonates. J Matern Fetal Neonatal Med 2016;29:3834-7.  Back to cited text no. 9
    
10.
Mafinezhad S, Bayani G, Bozorgnia Y, Araghi Z. Prevalence of G6PD deficiency among newborns with hyperbilirubinemia in North Khorasan and its correlation with jaundice complication. J North Khorasan Univ Med Sci 2015;7:167-73.  Back to cited text no. 10
    
11.
Ali N, Anwar M, Ayyub M, Bhatti FA, Nadeem M, Nadeem A. Frequency of glucose-6-phosphate dehydrogenase deficiency in some ethnic groups of Pakistan. J Coll Physicians Surg Pak 2005;15:137-41.  Back to cited text no. 11
    
12.
Eghbalian F, Monsef EA. Evaluation of Glucose-6-Phosphate Dehydrogenase Deficiency Without Hemolysis in Icteric Newborns; 2007;17:35-40.  Back to cited text no. 12
    
13.
Pahlavanzadeh M, Hekmatimoghaddam S, Teremahi Ardestani M, Ghafoorzadeh M, Aminorraaya M. G6PD enzyme deficiency in neonatal pathologic hyperbilirubinemia in Yazd. Iran J Ped Hematol Oncol 2013;3:69-72.  Back to cited text no. 13
    
14.
Khodashenas E, Kalani MF, Araghi Z, Khodaparast M, Yazdani Z. Glucose-6-phosphate dehydrogenase deficiency and neonatal hyperbilirubinemia; 2015:6: 28-31.  Back to cited text no. 14
    
15.
Samanta S, Kumar P, Kishore SS, Garewal G, Narang A. Donor blood glucose 6-phosphate dehydrogenase deficiency reduces the efficacy of exchange transfusion in neonatal hyperbilirubinemia. Pediatrics 2009;123:e96-100.  Back to cited text no. 15
    



 
 
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