Prevalence and Pattern of Neonatal Jaundice in Term Male Babies with Glucose-6-Phosphate Dehydrogenase Deficiency in Nigeria

Prevalence and Pattern of Neonatal Jaundice in Term Male Babies with Glucose-6-Phosphate Dehydrogenase Deficiency in Nigeria | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Prevalence and Pattern of Neonatal Jaundice in Term Male Babies with Glucose-6-Phosphate Dehydrogenase Deficiency in Nigeria Tolulope Ogundele, Oluwaseun Terence Bakare, Tina M. Slusher This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6724816/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 14 You are reading this latest preprint version Abstract Background: Neonatal jaundice is one of the major reasons why babies are admitted to neonatal wards worldwide and contributes significantly to neonatal morbidity and mortality. Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is one of the main causes of severe neonatal jaundice. It is inherited as an X-linked recessive disorder and is more common in males. Centers in Nigeria do not routinely screen for G-6-PD deficiency or bilirubin levels in babies, despite the high prevalence of G-6-PD deficiency among Africans. Babies with G-6-PD deficiency often present late, frequently with features of acute bilirubin encephalopathy. This study aimed to determine the prevalence of glucose-6-phosphate dehydrogenase deficiency among male babies and the prevalence and pattern of neonatal jaundice among term male babies with glucose-6-phosphate dehydrogenase deficiency. Study Design: This was a prospective observational study. The G-6-PD status of consecutive term male babies was determined. The babies were classified as G-6-PD-deficient or G-6-PD-normal. The bilirubin and hematocrit levels were monitored for the first seven days of life. The means bilirubin and hematocrit levels of the two groups were compared. Results: A total of 208 term male babies were studied. Seventy-two of the babies were G-6-PD deficient, resulting in an overall prevalence of G-6-PD deficiency of 34.6%. At 48 h of life, 23% of the G-6-PD-deficient were jaundiced. On the 4th day of life, 44 (61.1%) of the babies who were G-6-PD deficient and 16 (11.8%) of the babies who were G-6-PD normal were jaundiced and received phototherapy. The G-6-PD-deficient babies had a greater mean total serum bilirubin (TSB) than did the G-6-PD-normal babies (P<0.001). The TSB level was consistently greater in babies who were glucose-6-phosphate dehydrogenase deficient from the cord blood sample to the 7th day of life sample. The TSB levels peaked on the 4th day of life in both groups. Conclusion: The prevalence of G-6-PD deficiency was very high among males in Southwest, Nigeria. Newborns who were G-6-PD-deficient had a higher prevalence of neonatal jaundice.. Early screening for G-6-PD deficiency, comprehensive educational programs, and follow-up with high-quality neonatal care, including intensive phototherapy, are essential to prevent severe neonatal jaundice. Clinical trial number : Not applicable.’ Neonatal jaundice Glucose-6-phosphate dehydrogenase deficiency Acute bilirubin encephalopathy Term male babies Figures Figure 1 Figure 2 Figure 3 Introduction Neonatal jaundice (NNJ) is one of the significant reasons why term babies are admitted to neonatal wards worldwide. Severe NNJ contributes significantly to neonatal morbidity and mortality in Nigeria and globally. [ 1 – 3 ] Studies have shown that the causes of severe NNJ include glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, blood group incompatibilities, and sepsis. [ 4 , 5 ] Glucose-6-phosphate dehydrogenase deficiency is the most common enzyme defect in humans, affecting approximately 400 million people worldwide. [ 6 ] It is inherited as an X-linked recessive disorder and is more common in males. It is particularly prevalent among individuals of African, Asian, and Mediterranean descent. [ 6 ] Glucose-6-phosphate dehydrogenase deficiency is often associated with severe NNJ, especially in term babies who are exposed to icterogenic substances. Icterogenic substances include menthol, naphthalene balls, camphor and other substances. [ 7 , 8 ] These icterogenic substances are often used in many homes in Nigeria as part of the care for newborns and to preserve their clothes. [ 9 ] Babies are not routinely screened for G-6-PD deficiency in Nigeria and are often discharged early before jaundice is detected. These babies often present late, frequently with features of acute bilirubin encephalopathy (ABE). 10 Severe NNJ often leads to kernicterus spectrum disorder (KSD) with choreoathetoid cerebral palsy, language processing disorders, deafness, and even death. [ 11 , 12 , 20 ] The present study was carried out to determine the prevalence of G-6-PD deficiency in term male babies and the prevalence and pattern of neonatal jaundice among male babies with G-6-PD deficiency at the University of Medical Sciences Teaching Hospital (UNIMEDTH), Ondo-State, Southwest, Nigeria. Methodology Study Area and Design This was a prospective observational study that was conducted in the labor, postnatal and neonatal wards of UNIMEDTH, Ondo, a major referral center for health facilities in Ondo State in southwestern Nigeria. The study was carried out from January to September 2021. Participants and Sampling Method Consecutive term male babies delivered in the hospital during the study period were recruited for the study. Babies that were G-6-PD-deficient were the subjects, whereas the G-6-PD-normal male babies were the controls. Exclusion criteria: 1. Babies whose mothers were rhesus negative 2. Babies with blood group A or B whose mothers’ blood group was O 3. Babies whose mothers/guardians did not give consent Instruments and Data Collection Technique Information, including name, age, home address, last menstrual period, and blood group, was obtained from each mother/guardian before delivery. Gestational age was determined from the first day of the mothers’ last menstrual period (LMP) and/or ultrasound performed in the early stage of pregnancy, as was the standard gestational age scoring chart. After delivery, the Apgar score of each baby was determined at birth, and physical and systemic examinations were also carried out on each baby. The babies were weighed using a Seca digital weighing scale (Hamburg, Germany), model 724, which measured to the nearest 0.1 kilogram. Blood sample collection Immediately after delivery, a cord blood sample was obtained from each baby to determine the G-6-PD status, hematocrit, total serum bilirubin (TSB), and ABO and rhesus blood groups. ABO and rhesus blood groups were also collected from the mothers. Glucose-6-phosphate dehydrogenase status was determined via an Access Bio CareStart TM G-6-PD RDTkit (Access Bio Somerset, NJ, USA). Glucose-6-phosphate dehydrogenase deficiency rapid diagnostic test. CareStart TM is a qualitative enzyme colorimetric test based on the reduction of colorless nitro blue tetrazolium dye to dark-colored formazan. Two microliters (2 μl) of whole blood was added to the sample well, and two drops of buffer were added to the buffer well. This provides the G-6-PD status of an individual, whether deficient or sufficient (normal), within 10 minutes. The samples with normal (sufficient) G-6-PD activity presented a distinct purple background in the result window, whereas no color change was observed for the samples with G-6-PD deficiency. The cutoff value (%) for G-6-PD deficiency was G-6-PD activity less than 30% (3.6 U/g Hb). The sensitivity (95% CI) was 100%, and the specificity (95% CI) was 96.4%. Total serum bilirubin was measured via an Advance Bilirubin 2 Stat Analyzer photometer (Providence, RI, USA). Standard laboratory methods were used for all other laboratory studies. Hematocrit and TSB estimations were repeated at 24 hours of life (HOL), 48 hours of life, and the 4 th and 7 th days of life (DOL) for all the babies. The investigations were repeated as necessary for those with jaundice. Mothers of babies who were G-6-PD deficient were counseled against the use of icterogenic substances. Babies were examined clinically at each visit for jaundice. The degree of jaundice was ascertained by determining the total serum bilirubin (TSB) level. Babies that had TSB levels that required phototherapy were admitted to the newborn unit and managed according to the unit protocol. Phototherapy commenced at these TSB values: cord blood TSB of 5 mg/dl and above, TSB at 24 hours at 7 mg/dl and above, bilirubin of 10 mg/dl and above at 48 hours of life, and bilirubin of 12 mg/dl and above after 48 hours of life. Those that had values very close to 10 mg/dl at 48 hours were repeated the following day and subsequently admitted for phototherapy if indicated above. Other necessary investigations were carried out according to the protocol. Data analysis : The data were analyzed via the Statistical Package for Social Sciences (SPSS) for Windows, version 22.0 (SPSS Inc. Chicago IL, USA).Means and standard deviations (SDs) were determined for continuous variables such as the values of hematocrit and TSB levels, whereas proportions and percentages were determined for discrete variables such as sex and G-6-PD status. Means were compared via Student’s t test. Proportions and ratios were compared via Pearson’s chi-square (χ 2 ) test. The level of statistical significance was set at a p value less than 0.05 in two-tailed tests. Results A total of 208 term male babies were included in the present study. The birth weight ranged from 2.6 to 4.1 kg, with a mean (SD) birth weight of 3.3 (0.37) kg. Table 1 shows the distributions of G-6-PD status and the blood groups of the two hundred and eight term, male babies. Seventy-two of the babies were G-6-PD deficient, and the prevalence of G-6-PD deficiency among term male babies was 34.6%. Table 2 shows the distribution of the mean values of total serum bilirubin as related to the G-6-PD status and timing of sample collection. The differences in the means of TSB in babies who were G-6-PD deficient were greater than those in G-6-PD normal babies from birth until the seventh day of life and statistically significantly higher at 24 hours of life, 48 hours of life and 4 th day of life (p< 0.001). On day 4, the value ranged between 5.7 and 19.1 mg/dl for babies who were G-6-PD deficient, whereas the TSB ranged from 2 to 12.8 mg/dl in babies with normal G-6-PD activity. Figure 1 shows the box-and-whisker plots of total serum bilirubin levels in cord blood, at 24 HOL, 48 HOL, 4 th DOL, and 7 th DOL of babies who were G-6-PD-deficient and those who were G-6-PD-normal. They clearly showed that the median values and two standard deviations of those who were G-6-PD-deficient were greater than those who were G-6-PD-normal. Table 3 shows the presence of jaundice in relation to G-6-PD status. A total serum bilirubin level of 7 mg/dl and above was observed in eight babies in each of the two groups (8/72 = 11.1%) with G-6-PD deficiency and (8/136 = 5.9%) with G-6-PD-normal at 24 HOL, but this difference was not statistically significant (p = 0.178). At 48 hours of life, no baby in the G-6-PD-normal group had a TSB value that defines jaundice, which was 10 mg/dl, although few were clinically jaundiced, while over half (39 (54.2%) of the infants in the G-6-PD-deficient group were clinically jaundiced, but 17 (23.6%) had a TSB value of 10 mg/dl or above. Seventeen babies were admitted and managed appropriately. There was a statistically significant difference in the proportion of babies who were jaundiced between G-6-PD-deficient and G-6-PD-normal babies at the 48 th hour (p< 0.001). At the 4 th DOL, 44 (61.1%) of the babies who were G-6-PD deficient were jaundiced, including the seventeen babies that were jaundiced at 48 hours of life and were admitted and managed as appropriate. Eight babies did not come for day 7 follow-up. All eight babies that did not return on day 7 were G-6-PD-normal babies. The majority of the babies in both groups no longer had elevated TSB values on day 7, but many were still clinically jaundiced. Sixteen (22.2%) babies from the G-6-PD-deficient group were still jaundiced, whereas none were jaundiced in the G-6-PD-normal group, and the difference in the proportions of babies who were jaundiced between the two groups was statistically significant (p < 0.001). Table 4 shows the distributions of the means of hematocrit levels in relation to babies’ age and G-6-PD status. The hematocrit was highest in the cord blood samples and lowest in the day 7 samples. The difference in the means of the values for babies who were G-6-PD-deficent and G-6-PD-normal was statistically significant from the cord blood sample to the sample taken at the 7 th day of life Figure 2 shows the patterns of means of TSB of babies who were G-6-PD-deficient and G-6-PD- normal. The curve of the peaks of the means of values for babies that were G-6-PD-deficient was consistently above the peaks for babies that were G-6-PD normal. The peak mean value for babies that were G-6-PD-deficient was 11.26 mg/dl on day 4 compared with 4. 96 mg/dl on day 4 for babies whose G-6-PD was normal. The peak values occurred on the 4th day of life for both groups. None of the babies in either group required an exchange blood transfusion, and none had features suggestive of acute bilirubin encephalopathy. Figure 3 depicts the graphical representations of the hematocrit levels in babies who were G-6-PD-deficient and those who were G-6-PD-normal. These findings indicate that hematocrit levels decrease in the first week of life. The decrease was very marked on the 4 th day of life, especially in babies who were G-6-PD deficient. Discussion Neonatal jaundice (NNJ) is one of the significant reasons why babies are admitted to newborn units in Nigeria. 1,[13] NNJ affects 60% of full-term and 80% of preterm newborns in the first few days of life. [14] It contributes significantly to neonatal morbidity and mortality in Nigeria. [15] One of the leading causes of severe hyperbilirubinemia and acute bilirubin encephalopathy is G-6-PD deficiency. [5,16-18] In the present study, the prevalence of G-6-PD deficiency and the prevalence and pattern of jaundice in term male babies with G-6-PD deficiency in southwest Nigeria were determined. The highest prevalence of G-6-PD deficiency has been reported across sub-Saharan Africa, ranging from 1.2% in Sudan to 30.7% in the Ivory Coast. [19] A systemic review and meta-analysis of neonates with jaundice in Africa reported the highest prevalence of 49.7% among Nigerian neonates. [20] In Nigeria, the highest prevalence was reported among Yoruba in the southwestern part of Nigeria. [21] Although Yoruba ethnicity made up the most significant proportion of the study population, 77% of the participants in the study group were Yorubas, and the study included individuals aged one to fifteen years. [21] In the present study, the prevalence of G-6-PD deficiency was 34.6%, which was higher than that reported in previous studies in Nigeria, which ranged from 15.3-28.9%. [19, 21, 22] Badejoko et al reported a prevalence of 20%. This study was also performed in southwestern Nigeria, but Badejoko et al. included both sexes, while only males were included in the present study. Therefore, the high prevalence of G-6-PD deficiency in the present study was not unexpected, as males, particularly Yoruba males, have been shown to have a relatively high prevalence of G-6-PD deficiency. [21,23] In Pakistan, Moiz et al. used less than 7.0 U/g Hb and reported a prevalence of 14.8%. [24] The use of different values to define G-6-PD deficiency is one of the reasons for the varied prevalence of G-6-PD deficiency worldwide. Glucose-6-phosphate dehydrogenase deficiency is one of the causes of severe neonatal jaundice, which is often complicated by ABE, especially when a baby is exposed to icterogenic substances. [7,19] The present study demonstrated a significant association between G-6-PD deficiency and neonatal jaundice (p <0.001). However, early diagnosis and treatment of NNJ in the present study prevented the progression of bilirubin to the level that could cause ABE. The present study revealed that babies with G-6-PD- deficiency had higher mean TSB levels and lower hematocrit values, even in the cord blood, than G-6-PD-normal babies did, and this association was maintained until the age of seven days. The hematocrit levels were highest in cord blood for both groups. The higher rate of reduction in hematocrit levels and the higher TSB levels observed among G-6-PD-deficient babies between day 0 and day 7 suggest hemolysis, which has also been shown to occur prenatally. 33 Other studies also suggest that hemolysis plays a significant role in the development of severe NNJ in G-6-PD-deficient neonates. 34, 35 Both groups had similar patterns of TSB increase, with no difference in the age at which TSB levels peaked (day 4). This finding was the same as that of Badejoko et al. and other studies but different from that of Moiz et al., who reported different days in which the bilirubin value peaked in G-6-PD-deficient and G-6-PD-normal babies. [22, 24,29] It is possible that the higher rate of increase in TSB levels among G-6-PD-deficient neonates, despite not being exposed to known icterogenic agents, can be partly explained by the decline in hematocrit during the first seven days of life, along with impaired bilirubin conjugation. [30, 31] This was particularly noteworthy because even a slight decrease in hematocrit can significantly increase bilirubin levels, as each gram of broken-down hemoglobin produces up to 35 mg of bilirubin. [32] In adults, erythrocytes that lack G-6-PD activity have a shorter lifespan, even without any external hemolytic agent. [25, 33], however, this enhanced hemolysis is usually fully compensated for in adults. In fetal life, a similar shortening of the lifespan of red blood cells cannot be fully compensated for, resulting in slightly lower hemoglobin values in cord blood. [25] Additionally, the shorter lifespan of G-6-PD-deficient red blood cells during the fetal and neonatal periods may be even greater than that of adults. [25,34,35] In the present study, there was no significant difference in the number of babies with NNJ in the first 24 hours of life between those who were G-6-PD-deficient and those who were G-6-PD-normal. Although the mean total serum bilirubin level of G-6-PD-deficient babies was greater than that of G-6-PD-normal babies in the first 24 hours of life, there was no statistically significant difference in the proportion of babies that were jaundiced. This finding was different from what was reported by Badejoko et al., who noted a statistically significant difference in the proportion of jaundiced babies who were G-6-PD-deficient and G-6-PD-normal at birth. [30] This difference might be because the majority of the mothers in the present study received antenatal care in health facilities where avoidance of icterogenic substances, such as naphthalene balls, mentholated powders, and mental-containing powders, was emphasized. Icterogenic substances further aggravate hemolysis in babies who are G-6-PD deficient and who have an increased risk of hemolysis. [7, 36] In the present study, no babies who were G-6-PD deficient had exchanged blood transfusions or had any signs of ABE. By the 4th DOL, 44 (61.1%) babies who were G-6-PD-deficient and 16 (11.8%) who were G-6-PD-normal had received phototherapy. This finding was similar to that of the Badejoko study, which reported that 57.4% of G-6-PD-deficient patients received phototherapy and that none had exchanged blood transfusions. [22] This finding was different from that of Mallouh’s study, which reported that 0.7% of G-6-PD-deficient patients underwent blood transfusion, although none had a feature of ABE/kernicterus. [37] This difference might be due to the early screening, comprehensive education, follow-up and timely phototherapy intervention used in the present study. Early screening and the use of phototherapy have been shown to prevent severe neonatal jaundice. [38-40] The most typical variant of G-6-PD in Africa is G-6-PD A–; class III, according to the WHO classification. This variant is less severe than other variants, such as the G-6-PD Mediterranean variant, which is observed among Italian, Grecian, Spanish, Arabic, and Jewish (Kurdish) descendants. [41] Conclusion The present study demonstrated that the prevalence of G-6-PD deficiency is high in our environment and that G-6-PD-deficient newborns have an increased hemolysis rate during both intrauterine and neonatal life, with a higher incidence of NNJ. The pattern shows that the peak value of bilirubin is at the 4th DOL in our population. Therefore, where routine screening for G-6-PD is not possible, babies should be seen in the hospital more frequently in the first week of life, and TSB should be routinely performed on or before the 4th day of life and earlier in clinically jaundiced babies. Early screening, comprehensive educational programs, and follow-ups with high-quality neonatal care are tools to prevent severe neonatal hyperbilirubinemia. Abbreviations G-6-PD: Glucose 6 phosphate dehydrogenase NNJ: Neonatal Jaundice ABE: Acute bilirubin encephalopathy KSD: Kernicterus spectrum disorder UNIMEDTH: University of Medical Science Teaching Hospital LMP: Last menstrual period HOL: Hour of Life DOL: Day of Life TSB: Total serum bilirubin Declarations Ethical Approval: This study was approved by the Health Research and Ethical Committee of the University of Medical science, Ondo, Nigeria, with approval number, Ethics ref: 10-17032020 before the commencement of the study. All methods were performed under the ethical standards as laid down in the Declaration of Helsinki and its later amendments or comparable ethical standards. Written informed consent was obtained from the mother or guardian of each baby before enrollment in the study. Confidentiality and privacy was exercised throughout the study. Consent for publication: Not applicable Clinical trial number :Not applicable.’ Availability of data and materials: The dataset analyzed for the findings of this study is available from the corresponding author and can be accessed upon reasonable request. Competing interests: The authors declare that they have no competing interests. Funding: There was no specific funding for this study. Authors' contributions: T.O. conceptualized and designed the study, coordinated and supervised the data collection, drafted the initial manuscript, and reviewed and revised the manuscript. O.T.B. designed the study, collected data, drafted the initial manuscript, and reviewed and revised the manuscript. T.M.S. conceptualized and designed the study, coordinated and supervised the data collection, drafted the initial manuscript, and reviewed and revised the manuscript. Acknowledgment: The authors wish to thank Prof J.A Owa for reading the manuscript and for his very useful comments. 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Glucose-6-Phosphate Dehydrogenase Deficiency and Neonatal Hyperbilirubinemia: Insights on Pathophysiology, Diagnosis, and Gene Variants in Disease Heterogeneity.Front Pediatr. 2022;10: 875877 doi: 10.3389/fped.2022.875877. Mallouh AA, Imseeh G, Abu-Osba YK, Hamdan JA. Screening for glucose-6-phosphate dehydrogenase deficiency can prevent severe neonatal jaundice. Ann. Trop. Paediatr. 1992;12:391-5 Kaplan M, Hammerman C. The need for neonatal glucose-6-phosphate dehydrogenase screening: a global perspective. J. Perinatol. 2009;29:S46–52 Ibrahim MH, Saeed IM, Hussein SM. G-6-PD Deficiency And Hyperbilirubinemia In Newborn Baby (Prospective Study). J Popul Ther Clin Pharmacol 2023;30:e189–e198 Wennberg RP, Imam ZO, Shwe DD, Hassan L, Farouk ZL, Turner LE et al. Antenatal jaundice instruction and acute bilirubin encephalopathy in Nigeria. Pediatr Res. 2024;95(5):1301-1307. Frank JE. Diagnosis and management of G-6-PD deficiency. Am Fam Physician. 2005;72:1277-82. Tables Table 1: The Distributions G-6-PD Status and Blood Groups of the Babies Parameters of the babies Number, Total = 208 % G-6-PD status Normal 136 65.4 Deficient 72 34.6 Blood group of babies A 8 3.8 B 40 19.2. O 160 76.9 Rhesus Positive 200 96.2 Negative 8 3.8 Table 2: Distribution of Means of TSB Levels as Related to G-6-PD Status and Time of Sample Collection Time TSB Mean (SD) mg/dL t p value G-6-PD deficient (72babies) G-6-PD Normal (136 babies) Cord blood 3.03 (0. 0.81) 2.56 (0.65) 4.522 0.550 24 hours 4.84 (1.56) 3.23 (1.19) 8.300 < 0.001 48hours 7.08 (2.27) 3.69 (1.30) 13.688 <0.001 4 th DOL 11.26 (3.39) 4.96 (3.1) 1.388 <0.001 7 th DOL 8.89 (1.75) 4.24 (1.72) 18.265 0.420 Table 3: Frequency of Neonatal Jaundice (Defined by Bilirubin Values) in Relation to G-6-PD Status and Age Blood Sample NNJ G-6-PD Status Total X 2 p value Normal = 136 Deficient = 72 208 Cord blood Yes 0 (0) 0 (0) 0 (0) - No 136 (100) 72 (100) 208 (100.0) At 24 hours of life Yes= 8 (5.9) 8 (11.1) 16 (7.7) 1.813 0.178 No= 128 (94.1) 64 (88.9) 272?? (92.3) At 48 hour of life Yes= 0 (0) 17 (23.6) 39 (18.8) 90.667 <0.001 No = 136 (100) 55 ( 76.4) 169 (81.2) At 4 th day of life Yes = 16 (11.8.) 44 (61.1) 60 (22.2 ) 55.851 <0.001 No = 120 (88.2) 28 (38.9) 148 (71.2) At 7 th day Yes= 0 (0.0) 16 (22.2) 16 (8.0) 30.918 <0.001 No= 128 (100.0) 56 (77.8) 184 (92.0) Table 4: Mean Hematocrit Levels in Babies with G-6-PD-Normal and G-6-PD-Deficient in Relation to the Age of the Babies Age Hematocrit mean % (SD) t F CI (95%) p value G-6-PD-Normal G-6-PD-Deficient 0h(cord blood) 53.1 (4.1) 49.1 (6.6) 5.359 31.00 2.51-5.43 0.000 24 h 50.8 (3.6) 48.0 (9.0) 3.185 48.11 1.08-4.57 0.000 48h 49.9 (3.6) 44.7 (7.3) 6.976 57.56 3.78-6.77 0.000 Day 4 48.0 (3.6) 41.4 (8.3) 7.913 35.52 4.94-8.22 0.000 Day 7 46.9 (3.3) 41.4 (6.8) 7.641 22.28 4.06- 6.89 0.000 Additional Declarations No competing interests reported. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-6724816","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":464837993,"identity":"b1e6a238-2e42-44a9-9d2e-9b4e292dc1be","order_by":0,"name":"Tolulope Ogundele","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAyUlEQVRIiWNgGAWjYFAC5gYGHiDFD2InFBChgYeBEaJFsgGkxYAULQYHQFxitNizN7ZJvKk4LGd8fnXihwcGDPL8YgcI2MJzsE1yzpnDxmY33m6WADrMcObsBAJaJBLbpHnbDiduu3F2A0hLgsFtIrXUb55xdvMPkrQkGPD3biPSljMHmy3nnEk3nHGDd5tFgoEEYb+wtzcfvPGmwlqev//s5ps/Kmzk+aUJaIGCZgYGCbBKCaKUg0AdMMUcIFr1KBgFo2AUjDAAAOa2RB08ghujAAAAAElFTkSuQmCC","orcid":"","institution":"Obafemi Awolowo University Teaching Hospitals Complex","correspondingAuthor":true,"prefix":"","firstName":"Tolulope","middleName":"","lastName":"Ogundele","suffix":""},{"id":464837994,"identity":"4d47bd62-ee2e-4b9a-b6c3-3488dcc85443","order_by":1,"name":"Oluwaseun Terence Bakare","email":"","orcid":"","institution":"Federal medical centre, Ebute-metta,","correspondingAuthor":false,"prefix":"","firstName":"Oluwaseun","middleName":"Terence","lastName":"Bakare","suffix":""},{"id":464837995,"identity":"70261b4c-e6ca-4489-9513-584d6596d5d5","order_by":2,"name":"Tina M. Slusher","email":"","orcid":"","institution":"University of Minnesota","correspondingAuthor":false,"prefix":"","firstName":"Tina","middleName":"M.","lastName":"Slusher","suffix":""}],"badges":[],"createdAt":"2025-05-22 12:08:21","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-6724816/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6724816/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":83897469,"identity":"5d1a6c06-b368-4a7e-b95c-96d0759a1b93","added_by":"auto","created_at":"2025-06-04 08:58:41","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":52529,"visible":true,"origin":"","legend":"\u003cp\u003eTSB (mg/dL) by G6PD status in the cord blood, 24 HOL, 48HOL, 4th DOL, 7th DOL\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-6724816/v1/b4e8d8a385ea9ee37ad5da48.png"},{"id":83897468,"identity":"0564fc15-533c-4934-9d35-dcde543a041a","added_by":"auto","created_at":"2025-06-04 08:58:41","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":29083,"visible":true,"origin":"","legend":"\u003cp\u003eThe pattern of the means of Total Serum Bilirubin Values in Babies Who Were G-6-PD-Deficient and Those that Were G-6-PD- Normal.\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-6724816/v1/3a341d555801a9a391425d26.png"},{"id":83897472,"identity":"368e5b65-dbed-4f53-9ea9-b8f238ce55ad","added_by":"auto","created_at":"2025-06-04 08:58:41","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":26431,"visible":true,"origin":"","legend":"\u003cp\u003eCurves of the Means of Hematocrit Values in Babies Who Were G-6-PD-Deficient and Those Who Were G-6-PD-normal.\u003c/p\u003e","description":"","filename":"3.png","url":"https://assets-eu.researchsquare.com/files/rs-6724816/v1/2dcec53e7c77c86e49b28d5d.png"},{"id":83897942,"identity":"f1063a48-4797-4d00-9adf-fd61aae8b361","added_by":"auto","created_at":"2025-06-04 09:06:41","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":731438,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6724816/v1/dcdd6347-5ee6-4c32-81e7-bd39d9e146db.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"\u003cp\u003ePrevalence and Pattern of Neonatal Jaundice in Term Male Babies with Glucose-6-Phosphate Dehydrogenase Deficiency in Nigeria\u003c/p\u003e","fulltext":[{"header":"Introduction","content":"\u003cp\u003eNeonatal jaundice (NNJ) is one of the significant reasons why term babies are admitted to neonatal wards worldwide. Severe NNJ contributes significantly to neonatal morbidity and mortality in Nigeria and globally. \u003csup\u003e[\u003cspan additionalcitationids=\"CR2\" citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]\u003c/sup\u003e Studies have shown that the causes of severe NNJ include glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, blood group incompatibilities, and sepsis. \u003csup\u003e[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]\u003c/sup\u003e Glucose-6-phosphate dehydrogenase deficiency is the most common enzyme defect in humans, affecting approximately 400\u0026nbsp;million people worldwide. \u003csup\u003e[\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]\u003c/sup\u003e It is inherited as an X-linked recessive disorder and is more common in males. It is particularly prevalent among individuals of African, Asian, and Mediterranean descent. \u003csup\u003e[\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]\u003c/sup\u003e Glucose-6-phosphate dehydrogenase deficiency is often associated with severe NNJ, especially in term babies who are exposed to icterogenic substances. Icterogenic substances include menthol, naphthalene balls, camphor and other substances. \u003csup\u003e[\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]\u003c/sup\u003e These icterogenic substances are often used in many homes in Nigeria as part of the care for newborns and to preserve their clothes. \u003csup\u003e[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eBabies are not routinely screened for G-6-PD deficiency in Nigeria and are often discharged early before jaundice is detected. These babies often present late, frequently with features of acute bilirubin encephalopathy (ABE).\u003csup\u003e10\u003c/sup\u003e Severe NNJ often leads to kernicterus spectrum disorder (KSD) with choreoathetoid cerebral palsy, language processing disorders, deafness, and even death. \u003csup\u003e[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e, \u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]\u003c/sup\u003e The present study was carried out to determine the prevalence of G-6-PD deficiency in term male babies and the prevalence and pattern of neonatal jaundice among male babies with G-6-PD deficiency at the University of Medical Sciences Teaching Hospital (UNIMEDTH), Ondo-State, Southwest, Nigeria.\u003c/p\u003e"},{"header":"Methodology","content":"\u003cp\u003e\u003cstrong\u003eStudy Area and Design\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis was a prospective observational study that was conducted in the labor, postnatal and neonatal wards of \u003cem\u003eUNIMEDTH, Ondo,\u0026nbsp;\u003c/em\u003ea major referral center for health facilities in Ondo State in southwestern Nigeria. The study was carried out from January to September 2021.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eParticipants and Sampling Method\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eConsecutive term male babies delivered in the hospital during the study period were recruited for the study. Babies that were G-6-PD-deficient were the subjects, whereas the G-6-PD-normal male babies were the controls.\u003c/p\u003e\n\u003cp\u003eExclusion criteria:\u003c/p\u003e\n\u003cp\u003e1. Babies whose mothers were rhesus negative\u003c/p\u003e\n\u003cp\u003e2. Babies with blood group A or B whose mothers’ blood group was O\u003c/p\u003e\n\u003cp\u003e3. Babies whose mothers/guardians did not give consent\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eInstruments and Data Collection Technique\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eInformation, including name, age, home address, last menstrual period, and blood group, was obtained from each mother/guardian before delivery. Gestational age was determined from the first day of the mothers’ last menstrual period (LMP) and/or ultrasound performed in the early stage of pregnancy, as was the standard gestational age scoring chart. After delivery, the Apgar score of each baby was determined at birth, and physical and systemic examinations were also carried out on each baby. The babies were weighed using\u0026nbsp;a Seca digital weighing scale (Hamburg, Germany), model 724, which measured to the nearest 0.1 kilogram.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eBlood sample collection\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eImmediately after delivery, a cord blood sample was obtained from each baby to determine the G-6-PD status, hematocrit, total serum bilirubin (TSB), and ABO and rhesus blood groups. ABO and rhesus blood groups were also collected from the mothers.\u003c/p\u003e\n\u003cp\u003eGlucose-6-phosphate dehydrogenase status was determined via an Access Bio CareStart\u003csup\u003eTM\u003c/sup\u003eG-6-PD RDTkit (Access Bio Somerset, NJ, USA). Glucose-6-phosphate dehydrogenase deficiency rapid diagnostic test. CareStart\u003csup\u003eTM\u003c/sup\u003e is a qualitative enzyme colorimetric test based on the reduction of colorless nitro blue tetrazolium dye to dark-colored formazan. Two microliters (2 μl) of whole blood was added to the sample well, and two drops of buffer were added to the buffer well. This provides the G-6-PD status of an individual, whether deficient or sufficient (normal), within 10 minutes. The samples with normal (sufficient) G-6-PD activity presented a distinct purple background in the result window, whereas no color change was observed for the samples with G-6-PD deficiency. The cutoff value (%) for G-6-PD deficiency was G-6-PD activity less than 30% (3.6 U/g Hb). The sensitivity (95% CI) was 100%, and the specificity (95% CI) was 96.4%.\u003c/p\u003e\n\u003cp\u003eTotal serum bilirubin was measured via an Advance Bilirubin 2 Stat Analyzer photometer (Providence, RI, USA). Standard laboratory methods were used for all other laboratory studies. Hematocrit and TSB estimations were repeated at 24 hours of life (HOL), 48 hours of life, and the 4\u003csup\u003eth\u003c/sup\u003e and 7\u003csup\u003eth\u003c/sup\u003e days of life (DOL) for all the babies. The investigations were repeated as necessary for those with jaundice.\u003c/p\u003e\n\u003cp\u003eMothers of babies who were G-6-PD deficient were counseled against the use of icterogenic substances. Babies were examined clinically at each visit for jaundice. The degree of jaundice was ascertained by determining the total serum bilirubin (TSB) level. Babies that had TSB levels that required phototherapy were admitted to the newborn unit and managed according to the unit protocol. Phototherapy commenced at these TSB values: cord blood TSB of 5 mg/dl and above, TSB at 24 hours at 7 mg/dl and above, bilirubin of 10 mg/dl and above at 48 hours of life, and bilirubin of 12 mg/dl and above after 48 hours of life. Those that had values very close to 10 mg/dl at 48 hours were repeated the following day and subsequently admitted for phototherapy if indicated above. Other necessary investigations were carried out according to the protocol.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eData analysis\u003c/strong\u003e: The data were analyzed via the Statistical Package for Social Sciences (SPSS) for Windows, version 22.0 (SPSS Inc. Chicago IL, USA).Means and standard deviations (SDs) were determined for continuous variables such as the values of hematocrit and TSB levels, whereas proportions and percentages were determined for discrete variables such as sex and G-6-PD status. Means were compared via Student’s t test. Proportions and ratios were compared via Pearson’s chi-square (χ\u003csup\u003e2\u003c/sup\u003e) test. The level of statistical significance was set at a p value less than 0.05 in two-tailed tests.\u003c/p\u003e"},{"header":"Results","content":"\u003cp\u003eA total of 208 term male babies were included in the present study. The birth weight ranged from 2.6 to 4.1 kg, with a mean (SD) birth weight of 3.3 (0.37) kg.\u003c/p\u003e\n\u003cp\u003eTable 1 shows the distributions of G-6-PD status and the blood groups of the two hundred and eight term, male babies. Seventy-two of the babies were G-6-PD deficient, and the prevalence of G-6-PD deficiency among term male babies was 34.6%.\u003c/p\u003e\n\u003cp\u003eTable 2 shows the distribution of the mean values of total serum bilirubin as related to the G-6-PD status and timing of sample collection. The differences in the means of TSB in babies who were G-6-PD deficient were greater than those in G-6-PD normal babies from birth until the seventh day of life and statistically significantly higher at 24 hours of life, 48 hours of life and 4\u003csup\u003eth\u003c/sup\u003e day of life (p\u0026lt; 0.001). On day 4, the value ranged between 5.7 and 19.1 mg/dl for babies who were G-6-PD deficient, whereas the TSB ranged from 2 to 12.8 mg/dl in babies with normal G-6-PD activity.\u003c/p\u003e\n\u003cp\u003eFigure 1 shows the box-and-whisker plots of total serum bilirubin levels in cord blood, at 24 HOL, 48 HOL, 4\u003csup\u003eth\u003c/sup\u003e DOL, and 7\u003csup\u003eth\u003c/sup\u003e DOL of babies who were G-6-PD-deficient and those who were G-6-PD-normal. They clearly showed that the median values and two standard deviations of those who were G-6-PD-deficient were greater than those who were G-6-PD-normal.\u003c/p\u003e\n\u003cp\u003eTable 3 shows the presence of jaundice in relation to G-6-PD status. A total serum bilirubin level of 7 mg/dl and above was observed in eight babies in each of the two groups (8/72 = 11.1%) with G-6-PD deficiency and (8/136 = 5.9%) with G-6-PD-normal at 24 HOL, but this difference was not statistically significant (p = 0.178). At 48 hours of life, no baby in the G-6-PD-normal group had a TSB value that defines jaundice, which was 10 mg/dl, although few were clinically jaundiced, while over half (39 (54.2%) of the infants in the G-6-PD-deficient group were clinically jaundiced, but 17 (23.6%) had a TSB value of 10 mg/dl or above. Seventeen babies were admitted and managed appropriately. There was a statistically significant difference in the proportion of babies who were jaundiced between G-6-PD-deficient and G-6-PD-normal babies at the 48\u003csup\u003eth\u003c/sup\u003e hour (p\u0026lt; 0.001). At the 4\u003csup\u003eth\u003c/sup\u003e DOL, 44 (61.1%) of the babies who were G-6-PD deficient were jaundiced, including the seventeen babies that were jaundiced at 48 hours of life and were admitted and managed as appropriate. Eight babies did not come for day 7 follow-up. All eight babies that did not return on day 7 were G-6-PD-normal babies. The majority of the babies in both groups no longer had elevated TSB values on day 7, but many were still clinically jaundiced. Sixteen (22.2%) babies from the G-6-PD-deficient group were still jaundiced, whereas none were jaundiced in the G-6-PD-normal group, and the difference in the proportions of babies who were jaundiced between the two groups was statistically significant (p \u0026lt; 0.001).\u003c/p\u003e\n\u003cp\u003eTable 4 shows the distributions of the means of hematocrit levels in relation to babies\u0026rsquo; age and G-6-PD status. The hematocrit was highest in the cord blood samples and lowest in the day 7 samples. The difference in the means of the values for babies who were G-6-PD-deficent and G-6-PD-normal was statistically significant from the cord blood sample to the sample taken at the 7\u003csup\u003eth\u003c/sup\u003e day of life\u003c/p\u003e\n\u003cp\u003eFigure 2 shows the patterns of means of TSB of babies who were G-6-PD-deficient and G-6-PD- normal. The curve of the peaks of the means of values for babies that were G-6-PD-deficient was consistently above the peaks for babies that were G-6-PD normal. The peak mean value for babies that were G-6-PD-deficient was 11.26 mg/dl on day 4 compared with 4. 96 mg/dl on day 4 for babies whose G-6-PD was normal. The peak values occurred on the 4th day of life for both groups. None of the babies in either group required an exchange blood transfusion, and none had features suggestive of acute bilirubin encephalopathy.\u003c/p\u003e\n\u003cp\u003eFigure 3 depicts the graphical representations of the hematocrit levels in babies who were G-6-PD-deficient and those who were G-6-PD-normal. These findings indicate that hematocrit levels decrease in the first week of life. The decrease was very marked on the 4\u003csup\u003eth\u003c/sup\u003e day of life, especially in babies who were G-6-PD deficient.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eNeonatal jaundice (NNJ) is one of the significant reasons why babies are admitted to newborn units in Nigeria.\u003csup\u003e1,[13]\u003c/sup\u003e NNJ affects 60% of full-term and 80% of preterm newborns in the first few days of life. \u003csup\u003e[14]\u003c/sup\u003e It contributes significantly to neonatal morbidity and mortality in Nigeria. \u003csup\u003e[15]\u003c/sup\u003e One of the leading causes of severe hyperbilirubinemia and acute bilirubin encephalopathy is G-6-PD deficiency. \u003csup\u003e[5,16-18]\u003c/sup\u003e In the present study, the prevalence of G-6-PD deficiency and the prevalence and pattern of jaundice in term male babies with G-6-PD deficiency in southwest Nigeria were determined.\u003c/p\u003e\n\u003cp\u003eThe highest prevalence of G-6-PD deficiency has been reported across sub-Saharan Africa, ranging from 1.2% in Sudan to 30.7% in the Ivory Coast. \u003csup\u003e[19]\u003c/sup\u003e A systemic review and meta-analysis of neonates with jaundice in Africa reported the highest prevalence of 49.7% among Nigerian neonates.\u003csup\u003e[20]\u0026nbsp;\u003c/sup\u003eIn Nigeria, the highest prevalence was reported among Yoruba in the southwestern part of Nigeria. \u003csup\u003e[21]\u003c/sup\u003e Although Yoruba ethnicity made up the most significant proportion of the study population, 77% of the participants in the study group were Yorubas, and the study included individuals aged one to fifteen years. \u003csup\u003e[21]\u003c/sup\u003e In the present study, the prevalence of G-6-PD deficiency was 34.6%, which was higher than that reported in previous studies in Nigeria, which ranged from 15.3-28.9%. \u003csup\u003e[19, 21, 22]\u003c/sup\u003e Badejoko et al reported a prevalence of 20%. This study was also performed in southwestern Nigeria, but Badejoko et al. included both sexes, while only males were included in the present study. Therefore, the high prevalence of G-6-PD deficiency in the present study was not unexpected, as males, particularly Yoruba males, have been shown to have a relatively high prevalence of G-6-PD deficiency. \u003csup\u003e[21,23]\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; In Pakistan, Moiz et al. used less than 7.0 U/g Hb and reported a prevalence of 14.8%. \u003csup\u003e[24]\u003c/sup\u003e The use of different values to define G-6-PD deficiency is one of the reasons for the varied prevalence of G-6-PD deficiency worldwide.\u003c/p\u003e\n\u003cp\u003eGlucose-6-phosphate dehydrogenase deficiency is one of the causes of severe neonatal jaundice, which is often complicated by ABE, especially when a baby is exposed to icterogenic substances. \u003csup\u003e[7,19]\u003c/sup\u003e The present study demonstrated a significant association between G-6-PD deficiency and neonatal jaundice (p \u0026lt;0.001). However, early diagnosis and treatment of NNJ in the present study prevented the progression of bilirubin to the level that could cause ABE.\u003c/p\u003e\n\u003cp\u003eThe present study \u0026nbsp;revealed that babies with G-6-PD- deficiency had higher mean TSB levels and lower hematocrit values, even in the cord blood, than G-6-PD-normal babies did, and this association was maintained until the age of seven days. The hematocrit levels were highest in cord blood for both groups. The higher rate of reduction in hematocrit levels and the higher TSB levels observed among G-6-PD-deficient babies between day 0 and day 7 suggest hemolysis, which has also been shown to occur prenatally.\u003csup\u003e33\u003c/sup\u003e Other studies also suggest that hemolysis plays a significant role in the development of severe NNJ in G-6-PD-deficient neonates.\u003csup\u003e34, 35\u003c/sup\u003e Both groups had similar patterns of TSB increase, with no difference in the age at which TSB levels peaked (day 4). This finding was the same as that of Badejoko et al. and other studies but different from that of Moiz et al., who reported different days in which the bilirubin value peaked in G-6-PD-deficient and G-6-PD-normal babies. \u003csup\u003e[22, 24,29]\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eIt is possible that the higher rate of increase in TSB levels among G-6-PD-deficient neonates, despite not being exposed to known icterogenic agents, can be partly explained by the decline in hematocrit during the first seven days of life, along with impaired bilirubin conjugation.\u003csup\u003e\u0026nbsp;[30, 31]\u003c/sup\u003e This was particularly noteworthy because even a slight decrease in hematocrit can significantly increase bilirubin levels, as each gram of broken-down hemoglobin produces up to 35 mg of bilirubin.\u003csup\u003e\u0026nbsp;[32]\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eIn adults, erythrocytes that lack G-6-PD activity have a shorter lifespan, even without any external hemolytic agent.\u003csup\u003e\u0026nbsp;[25, 33],\u0026nbsp;\u003c/sup\u003ehowever, this enhanced hemolysis is usually fully compensated for in adults. In fetal life, a similar shortening of the lifespan of red blood cells cannot be fully compensated for, resulting in slightly lower hemoglobin values in cord blood. \u003csup\u003e[25]\u003c/sup\u003e Additionally, the shorter lifespan of G-6-PD-deficient red blood cells during the fetal and neonatal periods may be even greater than that of adults. \u003csup\u003e[25,34,35]\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eIn the present study, there was no significant difference in the number of babies with NNJ in the first 24 hours of life between those who were G-6-PD-deficient and those who were G-6-PD-normal. Although the mean total serum bilirubin level of G-6-PD-deficient babies was greater than that of G-6-PD-normal babies in the first 24 hours of life, there was no statistically significant difference in the proportion of babies that were jaundiced. This finding was different from what was reported by Badejoko et al., who noted a statistically significant difference in the proportion of jaundiced babies who were G-6-PD-deficient and G-6-PD-normal at birth. \u003csup\u003e[30]\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eThis difference might be because the majority of the mothers in the present study received antenatal care in health facilities where avoidance of icterogenic substances, such as naphthalene balls, mentholated powders, and mental-containing powders, was emphasized. Icterogenic substances further aggravate hemolysis in babies who are G-6-PD deficient and who have an increased risk of hemolysis.\u003csup\u003e\u0026nbsp;[7, 36]\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eIn the present study, no babies who were G-6-PD deficient had exchanged blood transfusions or had any signs of ABE. By the 4th DOL, 44 (61.1%) babies who were G-6-PD-deficient and 16 (11.8%) who were G-6-PD-normal had received phototherapy. This finding was similar to that of the Badejoko study, which reported that 57.4% of G-6-PD-deficient patients received phototherapy and that none had exchanged blood transfusions.\u003csup\u003e\u0026nbsp;[22]\u003c/sup\u003e This finding was different from that of Mallouh’s study, which reported that 0.7% of G-6-PD-deficient patients underwent blood transfusion, although none had a feature of ABE/kernicterus.\u003csup\u003e\u0026nbsp;[37]\u003c/sup\u003e This difference might be due to the early screening, comprehensive education, follow-up and timely phototherapy intervention used in the present study. Early screening and the use of phototherapy have been shown to prevent severe neonatal jaundice.\u003csup\u003e\u0026nbsp;[38-40]\u003c/sup\u003e\u003c/p\u003e\n\u003cp\u003eThe most typical variant of G-6-PD in Africa is G-6-PD A–; class III, according to the WHO classification. This variant is less severe than other variants, such as the G-6-PD Mediterranean variant, which is observed among Italian, Grecian, Spanish, Arabic, and Jewish (Kurdish) descendants.\u003csup\u003e\u0026nbsp;[41]\u003c/sup\u003e\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThe present study demonstrated that the prevalence of G-6-PD deficiency is high in our environment and that G-6-PD-deficient newborns have an increased hemolysis rate during both intrauterine and neonatal life, with a higher incidence of NNJ. The pattern shows that the peak value of bilirubin is at the 4th DOL in our population. Therefore, where routine screening for G-6-PD is not possible, babies should be seen in the hospital more frequently in the first week of life, and TSB should be routinely performed on or before the 4th day of life and earlier in clinically jaundiced babies. Early screening, comprehensive educational programs, and follow-ups with high-quality neonatal care are tools to prevent severe neonatal hyperbilirubinemia.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eG-6-PD: Glucose 6 phosphate dehydrogenase\u003c/p\u003e\n\u003cp\u003eNNJ: Neonatal Jaundice\u003c/p\u003e\n\u003cp\u003eABE: Acute bilirubin encephalopathy\u003c/p\u003e\n\u003cp\u003eKSD: Kernicterus spectrum disorder\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eUNIMEDTH: University of Medical Science Teaching Hospital\u003c/p\u003e\n\u003cp\u003eLMP: Last menstrual period\u003c/p\u003e\n\u003cp\u003eHOL: Hour of Life\u003c/p\u003e\n\u003cp\u003eDOL: Day of Life\u003c/p\u003e\n\u003cp\u003eTSB: Total serum bilirubin\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthical Approval:\u0026nbsp;\u003c/strong\u003eThis study was approved by the Health Research and Ethical Committee of the University of Medical science, Ondo, Nigeria, with approval number, Ethics ref: 10-17032020 before the commencement of the study. All methods were performed under the ethical standards as laid down in the Declaration of Helsinki and its later amendments or comparable ethical standards. Written informed consent was obtained from the mother or guardian of each baby before enrollment in the study. Confidentiality and privacy was exercised throughout the study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication: Not applicable\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eClinical trial number\u003c/strong\u003e:Not applicable.’\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials:\u003c/strong\u003e The dataset analyzed for the findings of this study is available from the corresponding author and can be accessed upon reasonable request.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests:\u0026nbsp;\u003c/strong\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding:\u0026nbsp;\u003c/strong\u003eThere was no specific funding for this study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors' contributions:\u0026nbsp;\u003c/strong\u003eT.O. conceptualized and designed the study, coordinated and supervised the data collection, drafted the initial manuscript, and reviewed and revised the manuscript. O.T.B. designed the study, collected data, drafted the initial manuscript, and reviewed and revised the manuscript. T.M.S. conceptualized and designed the study, coordinated and supervised the data collection, drafted the initial manuscript, and reviewed and revised the manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgment:\u003c/strong\u003e The authors wish to thank Prof J.A Owa for reading the manuscript and for his very useful comments.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n \u003cli\u003eEzeaka VC, Ogunbase AO, Awogbemi OT, Grange AO. Why Our Children Die: A review of PediatricsPaediatrics Mortality in A Tertiary Centre in Lagos, Nigeria. Nig. Qt. J. Hosp. Med 2003;13:17-21\u003c/li\u003e\n \u003cli\u003eDiala UM, Usman F, Appiah D, Hassan L, Ogundele T, Abdullahi F et al.. Global Prevalence of Severe Neonatal Jaundice among Hospital Admissions: A Systematic Review and Meta-Analysis. J. Clin. Med. 2023;12:3738.\u003c/li\u003e\n \u003cli\u003eSlusher TM, Day LT, Ogundele T, Woolfield N, Owa JA. Filtered sunlight, solar powered phototherapy and other strategies for managing neonatal jaundice in low-resource settings. Early Hum Dev 2017;114:11-5.\u003c/li\u003e\n \u003cli\u003eOwa JA, Durosinmi MA, Alabi AO. Determinants of severity of neonatal hyperbilirubinaemia in ABO incompatibility in Nigeria. Trop Doct.1991;21:19-22.\u003c/li\u003e\n \u003cli\u003eSlusher TM, Vreman HJ, McLaren DW, Lewinson LJ, Brown AK, Stevenson DK. Glucose-6-phosphate dehydrogenase deficiency and carboxyhemoglobin concentrations associated with bilirubin-related morbidity and death in Nigerian infants. J Pedatr. 1995; 126:102-8.\u003c/li\u003e\n \u003cli\u003eCappellini MD, Fiorelli G. Glucose-6-phosphate dehydrogenase deficiency. Lancet 2008;371:64\u0026ndash;74.\u003c/li\u003e\n \u003cli\u003eOwa JA. Relationship between exposure to icterogenic agents, glucose-6-phosphate dehydrogenase deficiency and neonatal jaundice in Nigeria. Acta Paediatr Scand. 1989;78:848\u0026ndash;52\u003c/li\u003e\n \u003cli\u003eFarouk ZL, Ibrahim M, Ogala WN. Glucose-6-phosphate dehydrogenase deficiency; the single most important cause of neonatal hyperbilirubinaemia in Kano, Nigeria. Niger J Paediatr 2017; 44: 44 \u0026ndash;9.\u003c/li\u003e\n \u003cli\u003eJatau ED, Zakari A, Damulak OD, Toma BO, Egesie O J, Akor EA. Cultural practices and the use of icterogenic agents in glucose-6-phosphate dehydrogenase deficient neonates: any effect? Niger J med 2020;29:120-124\u003c/li\u003e\n \u003cli\u003eOwa J, Taiwo O, Adebiyi J, Dogunro S. Neonatal Jaundice at Wesley Guild Hospital,Ilesa and Ife State Hospital, Ile-Ife. Niger J Paediatr. 1989;16:23\u0026ndash;30.\u003c/li\u003e\n \u003cli\u003eLe Pichon J, Riordan SM, Watchko J, Shapiro SM. The Neurological Sequelae of Neonatal Hyperbilirubinemia: Definitions, Diagnosis and Treatment of the Kernicterus Spectrum Disorders (KSDs). Curr. Pediatr. Rev 2017;13: 199-209.\u003c/li\u003e\n \u003cli\u003eUsman F, Diala UM, Shapiro SM, Le Pichon J, Slusher TM. Res. rep. neonatol 2018; 8: 33\u0026ndash;44.\u003c/li\u003e\n \u003cli\u003eOkagua J, Obikwu U. Morbidity and Mortality Pattern of Neonates admitted into the Special Care Baby Unit of University of Port Harcourt Teaching Hospital, Nigeria. East Afr. Med. J 2017; 94: 259-65\u003c/li\u003e\n \u003cli\u003eKoosha 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\u0026ndash;8.\u003c/li\u003e\n \u003cli\u003eMokuolu OA, Adesiyun OO, Ibrahim OR, Suberu HD, Ibrahim S, Bello SO et al. Appraising Neonatal Morbidity and Mortality in a Developing Country Categorized by Gestational Age Grouping and Implications for Targeted Interventions. Front. Pediatr. 10:899645.doi: 10.3389/fped.2022.899645\u003c/li\u003e\n \u003cli\u003eOgunlesi TA, Dedeke IO, Adekanmbi AF, Fetuga MB, Ogunfowora OB. The incidence and outcome of bilirubin encephalopathy in Nigeria: a bi-centre study. Niger J Med. 2007;16:354\u0026ndash;9.\u003c/li\u003e\n \u003cli\u003eLuzzatto L, Ally M, Notaro R. Glucose-6-phosphate dehydrogenase deficiency. Blood 2020 ;136:1225\u0026ndash;40.\u003c/li\u003e\n \u003cli\u003eOwa J, Dawodu A, Familusi J. Kernicterus in Nigerian infants. West Afr J Med. 1987;6:11\u0026ndash;20\u003c/li\u003e\n \u003cli\u003eNkhoma ET, Poole C, Vannappagari V, Hall SA, Beutler E. The global prevalence of glucose-6-phosphate dehydrogenase deficiency: a systematic review and meta-analysis. Blood Cells Mol Dis.2009;42:267\u0026ndash;78\u003c/li\u003e\n \u003cli\u003eKassahun W, Tunta A, Abera A, Shiferaw M. Glucose-6-phosphate dehydrogenase deficiency among neonates with jaundice in Africa; systematic review and meta-analysis. Heliyon 2023;9:e18437.\u003c/li\u003e\n \u003cli\u003eWilliams O, Gbadero D, Edowhorhu G, Brearley A, Slusher T, Lund TC.Glucose-6-Phosphate Dehydrogenase Deficiency in Nigerian Children. PLoS ONE 2013; 8: e68800.\u003c/li\u003e\n \u003cli\u003eBadejoko BO, Owa JA, Oseni SBA, Badejoko O, Fatusi AO, Adejuyigbe EA. Early Neonatal Bilirubin, Hematocrit, and Glucose-6-Phosphate Dehydrogenase Status. Pediatrics 2014;134:e1082.\u003c/li\u003e\n \u003cli\u003eEyo-Ita EU, Ogunsanya B, Osazee EM, Eyo-Ita IA, Omoigberale A. Glucose-6-Phosphate Dehydrogenase Deficiency in a Nigerian Neonate with Acute bilirubin Encephalopathy triggered by Ciprofloxacin. J Med Case Rep Case Series 2023; 4(13) https://doi.org/10.38\u003c/li\u003e\n \u003cli\u003eMoiz B, Nasir AX, Khan SA, Kherani SA, Qadir M. Neonatal Hyperbilirubinemia in infants with G-6-PD c.563C \u0026gt; T Variant. BMC Pediatr 2012;12:708.\u003c/li\u003e\n \u003cli\u003eChhetri N, Chhetri A. Pattern of glucose 6 phosphate dehydrogenase deficiency in neonates with hyperbilirubinemia in a tertiary care center. Int. J. Med. Health Res 2017; 3: 61-5\u003c/li\u003e\n \u003cli\u003eKaplan M, Herschel M, Hammerman C, Hoyer JD, Stevenson DK. Hyperbilirubinemia among African American, glucose-6-phosphate dehydrogenase-deficient neonates. Pediatrics. 2004;114(2):e213-9.\u003c/li\u003e\n \u003cli\u003eOwa JA, Dawodu AH. Influence of glucose-6- phosphate dehydrogenase status on bilirubin and hematocrit in healthy Nigerian neonates. Niger Med Pract. 1991;22:47\u0026ndash;9\u003c/li\u003e\n \u003cli\u003eGopagondanahalli KR, Mittal RA, Abdul Haium A, Bin Huey Quek BH, Agarwal P,Daniel LM et al. Risk Factors Predicting the Need for Phototherapy in Glucose 6 Phosphate Dehydrogenase-Deficient Infants in a Large Retrospective Cohort Study. Neonatology 2022;119: 494\u0026ndash;500\u003c/li\u003e\n \u003cli\u003eAl-Bedaywi RRR, Salameh KMK, Abedin S, Viswanathan B ,Khedr AA, Habboub LHM. Glucose-6-phosphate dehydrogenase deficiency and neonatal indirect hyperbilirubinemia: a retrospective cohort study among 40,305 consecutively born babies. J Perinatol. 2024;44:1035-1041.\u003c/li\u003e\n \u003cli\u003eKaplan M, Slusher T, Renbaum P. (TA)n UDP-glucuronosyltransferase 1A1 promoter polymorphism in Nigerian neonates. Pediatr Res. 2008; 631:109\u0026ndash;11\u003c/li\u003e\n \u003cli\u003eKaplan M, Muraca M, Hammerman C. Bilirubin conjugation, reflected by conjugated bilirubin fractions, in glucose-6-phosphate dehydrogenase-deficient neonates: a determining factor in the pathogenesis of hyperbilirubinemia. Pediatrics 1998; 102:E37.doi: 10.1542/peds.102.3.e37.\u003c/li\u003e\n \u003cli\u003eMaisels JM. Jaundice. In: MacDonald MG SM, Mullet MD, Seshia MMK, eds. Avery\u0026rsquo;s Neonatology Pathophysiology and Management of the Newborn. 6th ed. Philadelphia: Lippincott Williams \u0026amp; Wilkins; 2005:768\u0026ndash;846\u003c/li\u003e\n \u003cli\u003eGautam K. Glusoce-6-phosphate dehydrogenase- History and diagnosis. J. pathol. Nepal 2016;6:1034- 39\u003c/li\u003e\n \u003cli\u003eUllah S, Rahman K, Hedayati M. Hyperbilirubinemia in Neonates: Types, Causes, Clinical Examinations, Preventive Measures and Treatments: A Narrative Review Article. Iran J Public Health. 2016; 45:558\u0026ndash;68.\u003c/li\u003e\n \u003cli\u003eWaldron PE, Cashore WJ. Hemolytic disease of the fetus and newborn. In: de Alarc\u0026oacute;n PA, Werner EJ eds. Neonatal Hematology. Cambridge University Press; 2005. 91-131\u003c/li\u003e\n \u003cli\u003eLee HY, Ithnin A, Azma RZ, Othman A, Salvador A, Cheah FC. Glucose-6-Phosphate Dehydrogenase Deficiency and Neonatal Hyperbilirubinemia: Insights on Pathophysiology, Diagnosis, and Gene Variants in Disease Heterogeneity.Front Pediatr. 2022;10: 875877 doi: 10.3389/fped.2022.875877.\u003c/li\u003e\n \u003cli\u003eMallouh AA, Imseeh G, Abu-Osba YK, Hamdan JA. Screening for glucose-6-phosphate dehydrogenase deficiency can prevent severe neonatal jaundice. Ann. Trop. Paediatr. 1992;12:391-5\u003c/li\u003e\n \u003cli\u003eKaplan M, Hammerman C. The need for neonatal glucose-6-phosphate dehydrogenase screening: a global perspective. J. Perinatol. 2009;29:S46\u0026ndash;52\u003c/li\u003e\n \u003cli\u003eIbrahim MH, Saeed IM, Hussein SM. G-6-PD Deficiency And Hyperbilirubinemia In Newborn Baby (Prospective Study). J Popul Ther Clin Pharmacol 2023;30:e189\u0026ndash;e198\u003c/li\u003e\n \u003cli\u003eWennberg RP, Imam ZO, Shwe DD, Hassan L, Farouk ZL, Turner LE et al. Antenatal jaundice instruction and acute bilirubin encephalopathy in Nigeria. Pediatr Res. 2024;95(5):1301-1307.\u003c/li\u003e\n \u003cli\u003eFrank JE. Diagnosis and management of G-6-PD deficiency. Am Fam Physician. 2005;72:1277-82.\u003c/li\u003e\n\u003c/ol\u003e"},{"header":"Tables","content":"\u003cp\u003eTable 1: \u0026nbsp; The Distributions G-6-PD Status and Blood Groups of the Babies\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003eParameters of the babies\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003eNumber, Total = 208\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eG-6-PD status\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003eNormal\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e136\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e65.4\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003eDeficient\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e72\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e34.6\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eBlood group of babies\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003eA\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e3.8\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003eB\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e19.2.\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003eO\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e\u0026nbsp;160\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e76.9\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eRhesus\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003ePositive\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e200\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e96.2\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003eNegative\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 208px;\"\u003e\n \u003cp\u003e3.8\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003eTable 2: Distribution of Means of TSB Levels as Related to G-6-PD Status and Time of Sample Collection\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"625\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003eTime\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"2\" valign=\"top\" style=\"width: 402px;\"\u003e\n \u003cp\u003e\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; TSB Mean (SD) mg/dL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003et\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026nbsp; p value\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eG-6-PD deficient (72babies)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 204px;\"\u003e\n \u003cp\u003eG-6-PD Normal (136 babies)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003eCord blood\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003e3.03 (0. 0.81)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 204px;\"\u003e\n \u003cp\u003e2.56 (0.65)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e4.522\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e0.550\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e24 hours\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003e4.84 (1.56)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 204px;\"\u003e\n \u003cp\u003e3.23 (1.19)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e8.300\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026lt; 0.001\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e48hours\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003e7.08 (2.27)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 204px;\"\u003e\n \u003cp\u003e3.69 (1.30)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e13.688\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026lt;0.001\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026nbsp;4\u003csup\u003eth\u003c/sup\u003e DOL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003e11.26 (3.39)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 204px;\"\u003e\n \u003cp\u003e4.96 (3.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e1.388\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026lt;0.001\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026nbsp;7\u003csup\u003eth\u003c/sup\u003e DOL\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003e8.89 (1.75)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 204px;\"\u003e\n \u003cp\u003e4.24 (1.72)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e18.265\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e0.420\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003eTable 3: Frequency of Neonatal Jaundice (Defined by Bilirubin Values) in Relation to G-6-PD Status and Age\u0026nbsp;\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 115px;\"\u003e\n \u003cp\u003eBlood Sample\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003eNNJ\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"2\" valign=\"top\" style=\"width: 246px;\"\u003e\n \u003cp\u003eG-6-PD Status\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003eTotal\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 60px;\"\u003e\n \u003cp\u003e\u003cem\u003eX\u003csup\u003e2\u003c/sup\u003e\u003c/em\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 61px;\"\u003e\n \u003cp\u003ep value\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 115px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003eNormal = 136\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 120px;\"\u003e\n \u003cp\u003eDeficient = 72\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e208\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 60px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 61px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 115px;\"\u003e\n \u003cp\u003eCord blood\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003eYes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e0 (0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 120px;\"\u003e\n \u003cp\u003e0 (0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e0 (0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 60px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 61px;\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003eNo\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e136 (100)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 120px;\"\u003e\n \u003cp\u003e72 (100)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e208 (100.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 115px;\"\u003e\n \u003cp\u003eAt 24 hours of life\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003eYes=\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e8 (5.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 120px;\"\u003e\n \u003cp\u003e8 (11.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e16 (7.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 60px;\"\u003e\n \u003cp\u003e1.813\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 61px;\"\u003e\n \u003cp\u003e0.178\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003eNo=\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e128 (94.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 120px;\"\u003e\n \u003cp\u003e64 (88.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e272?? (92.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 115px;\"\u003e\n \u003cp\u003eAt 48 hour of life\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003eYes=\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e0 (0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 120px;\"\u003e\n \u003cp\u003e17 (23.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e39 (18.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 60px;\"\u003e\n \u003cp\u003e90.667\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 61px;\"\u003e\n \u003cp\u003e\u0026lt;0.001\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003eNo =\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e136 (100)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 120px;\"\u003e\n \u003cp\u003e55 ( 76.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e169 (81.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 115px;\"\u003e\n \u003cp\u003eAt 4\u003csup\u003eth\u003c/sup\u003e day of life\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003eYes =\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e16 (11.8.)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 120px;\"\u003e\n \u003cp\u003e44 (61.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e60 (22.2 )\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 60px;\"\u003e\n \u003cp\u003e55.851\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 61px;\"\u003e\n \u003cp\u003e\u0026lt;0.001\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003eNo =\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e120 (88.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 120px;\"\u003e\n \u003cp\u003e28 (38.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e148 (71.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 115px;\"\u003e\n \u003cp\u003eAt 7\u003csup\u003eth\u003c/sup\u003e day\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003eYes=\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e0 (0.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 120px;\"\u003e\n \u003cp\u003e16 (22.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e16 (8.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 60px;\"\u003e\n \u003cp\u003e30.918\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 61px;\"\u003e\n \u003cp\u003e\u0026lt;0.001\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003eNo=\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e128 (100.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 120px;\"\u003e\n \u003cp\u003e56 (77.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e184 (92.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003eTable 4: Mean Hematocrit Levels in Babies with G-6-PD-Normal and G-6-PD-Deficient in Relation to the Age of the Babies\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" class=\"fr-table-selection-hover\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 121px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003cp\u003eAge\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"2\" valign=\"top\" style=\"width: 258px;\"\u003e\n \u003cp\u003e\u0026nbsp; \u0026nbsp; \u0026nbsp;Hematocrit mean % (SD)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003et\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003eF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003eCI (95%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003ep value\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003eG-6-PD-Normal\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 132px;\"\u003e\n \u003cp\u003eG-6-PD-Deficient\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 121px;\"\u003e\n \u003cp\u003e0h(cord blood)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e53.1 (4.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 132px;\"\u003e\n \u003cp\u003e49.1 (6.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e5.359\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e31.00\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e2.51-5.43\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e0.000\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 121px;\"\u003e\n \u003cp\u003e\u0026nbsp;24 h\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e50.8 (3.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 132px;\"\u003e\n \u003cp\u003e48.0 (9.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e3.185\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e48.11\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e1.08-4.57\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e0.000\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 121px;\"\u003e\n \u003cp\u003e48h\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e49.9 (3.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 132px;\"\u003e\n \u003cp\u003e44.7 (7.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e6.976\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e57.56\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e3.78-6.77\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e0.000\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 121px;\"\u003e\n \u003cp\u003eDay 4\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e48.0 (3.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 132px;\"\u003e\n \u003cp\u003e41.4 (8.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e7.913\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e35.52\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e4.94-8.22\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e0.000\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 121px;\"\u003e\n \u003cp\u003eDay 7\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e46.9 (3.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 132px;\"\u003e\n \u003cp\u003e41.4 (6.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e7.641\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e22.28\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e4.06- 6.89\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e0.000\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-pediatrics","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bped","sideBox":"Learn more about [BMC Pediatrics](http://bmcpediatr.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bped/default.aspx","title":"BMC Pediatrics","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Neonatal jaundice, Glucose-6-phosphate dehydrogenase deficiency, Acute bilirubin encephalopathy, Term male babies","lastPublishedDoi":"10.21203/rs.3.rs-6724816/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6724816/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground:\u003c/strong\u003e Neonatal jaundice is one of the major reasons why babies are admitted to neonatal wards worldwide and contributes significantly to neonatal morbidity and mortality. Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is one of the main causes of severe neonatal jaundice. It is inherited as an X-linked recessive disorder and is more common in males. Centers in Nigeria do not routinely screen for G-6-PD deficiency or bilirubin levels in babies, despite the high prevalence of G-6-PD deficiency among Africans. Babies with G-6-PD deficiency often present late, frequently with features of acute bilirubin encephalopathy.\u003c/p\u003e\n\u003cp\u003eThis study aimed to determine the prevalence of glucose-6-phosphate dehydrogenase deficiency among male babies and the prevalence and pattern of neonatal jaundice among term male babies with glucose-6-phosphate dehydrogenase deficiency.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eStudy Design:\u003c/strong\u003eThis was a prospective observational study. The G-6-PD status of consecutive term male babies was determined. The babies were classified as G-6-PD-deficient or G-6-PD-normal. The bilirubin and hematocrit levels were monitored for the first seven days of life. The means bilirubin and hematocrit levels of the two groups were compared.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eResults:\u003c/strong\u003eA total of 208 term male babies were studied. Seventy-two of the babies were G-6-PD deficient, resulting in an overall prevalence of G-6-PD deficiency of 34.6%. At 48 h of life, 23% of the G-6-PD-deficient were jaundiced. On the 4th day of life, 44 (61.1%) of the babies who were G-6-PD deficient and 16 (11.8%) of the babies who were G-6-PD normal were jaundiced and received phototherapy. The G-6-PD-deficient babies had a greater mean total serum bilirubin (TSB) than did the G-6-PD-normal babies (P\u0026lt;0.001). The TSB level was consistently greater in babies who were glucose-6-phosphate dehydrogenase deficient from the cord blood sample to the 7th day of life sample. The TSB levels peaked on the 4th day of life in both groups.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusion:\u003c/strong\u003eThe prevalence of G-6-PD deficiency was very high among males in Southwest, Nigeria. Newborns who were G-6-PD-deficient had a higher prevalence of neonatal jaundice.. Early screening for G-6-PD deficiency, comprehensive educational programs, and follow-up with high-quality neonatal care, including intensive phototherapy, are essential to prevent severe neonatal jaundice.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eClinical trial number\u003c/strong\u003e: Not applicable.’\u003c/p\u003e","manuscriptTitle":"Prevalence and Pattern of Neonatal Jaundice in Term Male Babies with Glucose-6-Phosphate Dehydrogenase Deficiency in Nigeria","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-06-04 08:58:37","doi":"10.21203/rs.3.rs-6724816/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-01-22T07:00:26+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-06-22T21:52:50+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-06-18T10:14:41+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"226773812906488908002259628314612743177","date":"2025-06-01T10:52:20+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"120794786962813487413265341836667404131","date":"2025-06-01T08:32:32+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-06-01T08:15:06+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"68493647868201363072663079632716310225","date":"2025-06-01T07:13:26+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"282145883701521326020276054486049811046","date":"2025-05-30T17:28:38+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"63415641996428338775164203569426230374","date":"2025-05-30T07:51:45+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-05-30T07:32:13+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2025-05-30T06:56:03+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-05-29T10:53:49+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-05-29T10:53:23+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Pediatrics","date":"2025-05-22T12:00:59+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-pediatrics","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bped","sideBox":"Learn more about [BMC Pediatrics](http://bmcpediatr.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bped/default.aspx","title":"BMC Pediatrics","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"63939af7-4fd5-4c93-9327-23c4976b8385","owner":[],"postedDate":"June 4th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-02-09T08:55:51+00:00","versionOfRecord":[],"versionCreatedAt":"2025-06-04 08:58:37","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-6724816","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6724816","identity":"rs-6724816","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}