Indian Journal of Public Health

: 2012  |  Volume : 56  |  Issue : 2  |  Page : 146--148

Glucose-6-phosphate dehydrogenase screening of babies born in a tertiary care hospital in West Bengal

Sukamal Bisoi1, Sumanta Chakraborty2, Dipankar Chattopadhyay1, Biswajit Biswas3, Sarbajit Ray4,  
1 Assistant Professor, Department of Community Medicine, IPGME and R, Kolkata, India
2 MBBS, Department of Community Medicine, IPGME and R, Kolkata, India
3 Professor, Department of Community Medicine, IPGME and R, Kolkata, India
4 Demonstrator, Department of Community Medicine, IPGME and R, Kolkata, India

Correspondence Address:
Sukamal Bisoi
64/2/1, Danesh Sk. Lane, Howrah-9, West Bengal


About 400 million individuals worldwide have been affected by the inherited disorder of glucose-6-phosphate dehydrogenase (G6PD) deficiency that predisposes individuals to neonatal jaundice or hemolytic crisis due to drugs or infections. A descriptive observational study with longitudinal design was undertaken among 109 live newborns, delivered in labor room of IPGME and R, Kolkata during the period from June to August 2009. An objective of the study was to estimate the occurrence of G6PD deficiency among newborns and its association with different socio-demographic, clinical and gestational characteristics. 14.68% newborns were found G6PD deficient. This occurrence was not significantly related to gender, religion and ethnicity, consanguineous marriage of the parents, gestational age and birth weight of the baby. Development of severe jaundice (total serum bilirubin >15 mg/dl) was found 23.8% among G6PD deficient babies and 12.5% among non-G6PD deficient. This difference was statistically not significant.

How to cite this article:
Bisoi S, Chakraborty S, Chattopadhyay D, Biswas B, Ray S. Glucose-6-phosphate dehydrogenase screening of babies born in a tertiary care hospital in West Bengal.Indian J Public Health 2012;56:146-148

How to cite this URL:
Bisoi S, Chakraborty S, Chattopadhyay D, Biswas B, Ray S. Glucose-6-phosphate dehydrogenase screening of babies born in a tertiary care hospital in West Bengal. Indian J Public Health [serial online] 2012 [cited 2022 Aug 17 ];56:146-148
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Full Text

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an inherited condition in which the body does not have enough of the enzyme G6PD, which helps red blood cells function normally. This deficiency can cause hemolytic anemia, usually after certain medications, foods or even injections. In rare cases, G6PD deficiency leads to chronic anemia. With the right precautions, a child with G6PD deficiency can lead a healthy and active life. [1] About 60% of term babies and 80% of pre-term infants develop some degree of jaundice during their first week of life. [2] But, the jaundice due to G6PD deficiency occurs in the 1 st day of life and usually severe (pathological) in nature. [3] G6PD deficiency was discovered half a century ago and is the most common inherited enzyme defect. Clinically, deficiency of G6PD affects as many as 400 million individuals worldwide. It is most commonly prevalent in African, South East Asian and Middle Eastern populations. It affects about 1 in 10 African-American males in the United States. [4] In India, there are 13 biochemical variants of G6PD being reported so far, out of which G6PD Mediterranean is most common in the caste groups; whereas G6PD Orissa is most prevalent in the tribals of India. The 3 rd most common variant seen in India is G6PD Kerala-Kalyan. [3] In West Bengal, there is dearth of research on G6PD deficiency. With this perspective, the present study was undertaken among the newborns in the department of Neonatology and Labor room of the Institute of Post-graduate Medical Education and Research, Kolkata, West Bengal.

The study was a descriptive observational type with a longitudinal design undertaken among all the babies born in the labor room of IPGME and R, Kolkata during the period from June to August 2009, including those who developed jaundice and admitted to neonatology ward for treatment. The stillborns were excluded. A total of 109 such live newborns were included in the study. An objective of the study was to find out the occurrence of G6PD deficiency and its association with relevant clinical, socio-demographic and gestational factors. Necessary ethical permission for the study was taken from the respective ethical committee of IPGME and R, Kolkata. Information was collected by interviewing the mothers after taking consent in prescribed proforma, with the help of a pre-designed and pre-tested schedule and also by record analysis of bed-head tickets. Cord blood of all the babies were collected in heparin containing vials, immediately after birth. Blood was tested for its G6PD status by semi-quantitative method, by using prepared reagent for it (Screening for Glucose-6-Phosphate Dehydrogenase deficiency by 8 Dichlorophenol-Indophenol (DPIP) Screening Test -semi-quantitative assay).[5] All the babies were followed up for a period of at least 3 days. Those who developed jaundice were followed up for at least 1 week in the neonatology ward, because these babies were transferred to this unit for treatment of jaundice. By using the standard method of estimation of bilirubin (van den Bergh reaction) in the laboratory of neonatology unit, the incidence of severe jaundice (serum total bilirubin > 15 mg/dl) in them was documented. Analysis of data was done by standard methods of descriptive statistics. Pearson's Chi-square test of independence with Yates' correction, whenever required, was employed for categorical variables to see the statistical significance.

Criteria for some of the variables are: Blood of individuals having G6PD activity below 7.24 eu / gm of Hb (Normal 8.83 ± 1.59 eu / gm of Hb) were considered G6PD deficient.[6] Preterm babies had been defined as thoseneonate having gestational age of < 37 weeks, and low birth weight (LBW) babies were those whose birth weight was < 2.5 kg. [7] Total serum bilirubin > 15 mg/dl [7] was considered as having significant jaundice.

In the present study, the G6PD deficient neonates comprises 16 (14.68%) out of 109 newborns, that was much higher than the study conducted on 5140 neonates in Karnataka (7.8%). [8] In North-Eastern India, a study conducted on the Mizo population of Mizoram showed that out of the 490 study subjects, 17.5% were found to be G6PD deficient. [9] The ratio of male and female G6PD deficient neonates in our study was 1:1 (15.8%: 15%), whereas in a similar study, conducted in the Vataliya Prajapati Community in Western India, the ratio was 3:1. [10] A study conducted on molecular variants of G6PD deficiency among certain tribal communities of Orissa revealed that, 6.4% of males were G6PD deficient. [11] In the present study, 13.13% Hindu babies and 16.66% Muslim babies were found G6PD deficient. Considering ethnicity, G6PD deficiency was found among 13.04% Bengalee babies and 17.5% among non-Bengalees. Both of these differences were statistically not significant (P > 0.05) [Table 1].{Table 1}

In this study, it was observed that only 5 (4.58%) babies had parents of consanguineous marriage. Out of those 5 babies, 1 (20%) was G6PD deficient. However, the percentage of G6PD deficiency among other babies with no such parentage was 14.42%. But this difference was statistically insignificant. The maturity of the newborn was determined by its gestational age. Most (78.9%) of the babies were term babies. Among the preterm babies, 26.08% were found to be G6PD deficient, whereas it was 11.6% among the term babies. This difference of gestational age and G6PD deficiency was not statistically significant. In a study in Jerusalem, Israel, it shows that G6PD activity is higher in preterm than in term and near-term neonates, but this increase is limited to the 29 - 32 weeks gestational age range. [12] In our study, 24.13% among 26.6% low birth weight (LBW) babies were found to be G6PD deficient and among the normal birth weight (NBW) babies, it was 11.25%. This difference is statistically not significant. In a study, conducted in Iran, no significant relationship was observed between G6PD deficiency with birth weight and gestational age, but it is related to consanguinity (P < 0.05). [13]

In the present series, 5 (31.25%) of the 16 G6PD deficient babies developed severe jaundice as compared to the 16 (17.2%) of the 93 non-G6PD deficient babies developing the same. 23.8% of the babies who developed severe jaundice were G6PD deficient, but 12.5% of babies who did not develop severe jaundice were also G6PD deficient. This difference was not statistically significant (P > 0.05).

G6PD deficiency detection by neonatal screening is feasible and cost-effective. It also allows the early preventive measures against severe hemolysis, jaundice, kernicterus etc. to be implemented in neonatal life, as well as other preventive measures in later life. Some practical guidance to the family members of the G6PD deficient babies regarding the food items, herbs, chemicals and drugs to be avoided will be beneficial, if we diagnose the condition at the first opportunity.


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