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  1. Fulltext Management of late-preterm and term infants with hyperbilirubinaemia in resource-constrained settings
    Olusanya BO, Ogunlesi TA, Kumar P, Boo NY, Iskander IF, de Almeida MF, et al.
    BMC Pediatr, 2015 Apr 12;15:39.
    PMID: 25884679 DOI: 10.1186/s12887-015-0358-z
    Hyperbilirubinaemia is a ubiquitous transitional morbidity in the vast majority of newborns and a leading cause of hospitalisation in the first week of life worldwide. While timely and effective phototherapy and exchange transfusion are well proven treatments for severe neonatal hyperbilirubinaemia, inappropriate or ineffective treatment of hyperbilirubinaemia, at secondary and tertiary hospitals, still prevails in many poorly-resourced countries accounting for a disproportionately high burden of bilirubin-induced mortality and long-term morbidity. As part of the efforts to curtail the widely reported risks of frequent but avoidable bilirubin-induced neurologic dysfunction (acute bilirubin encephalopathy (ABE) and kernicterus) in low and middle-income countries (LMICs) with significant resource constraints, this article presents a practical framework for the management of late-preterm and term infants (≥ 35 weeks of gestation) with clinically significant hyperbilirubinaemia in these countries particularly where local practice guidelines are lacking. Standard and validated protocols were followed in adapting available evidence-based national guidelines on the management of hyperbilirubinaemia through a collaboration among clinicians and experts on newborn jaundice from different world regions. Tasks and resources required for the comprehensive management of infants with or at risk of severe hyperbilirubinaemia at all levels of healthcare delivery are proposed, covering primary prevention, early detection, diagnosis, monitoring, treatment, and follow-up. Additionally, actionable treatment or referral levels for phototherapy and exchange transfusion are proposed within the context of several confounding factors such as widespread exclusive breastfeeding, infections, blood group incompatibilities and G6PD deficiency, which place infants at high risk of severe hyperbilirubinaemia and bilirubin-induced neurologic dysfunction in LMICs, as well as the limited facilities for clinical investigations and inconsistent functionality of available phototherapy devices. The need to adjust these levels as appropriate depending on the available facilities in each clinical setting and the risk profile of the infant is emphasised with a view to avoiding over-treatment or under-treatment. These recommendations should serve as a valuable reference material for health workers, guide the development of contextually-relevant national guidelines in each LMIC, as well as facilitate effective advocacy and mobilisation of requisite resources for the optimal care of infants with hyperbilirubinaemia at all levels.
    Matched MeSH terms: Hyperbilirubinemia, Neonatal/complications; Hyperbilirubinemia, Neonatal/diagnosis; Hyperbilirubinemia, Neonatal/therapy*
  2. Randomised controlled trial of single phototherapy with reflecting curtains versus double phototherapy in term newborns with hyperbilirubinaemia
    Abd Hamid IJ, M Iyen MI, Ibrahim NR, Abd Majid N, Ramli N, Van Rostenberghe H
    J Paediatr Child Health, 2013 May;49(5):375-9.
    PMID: 23573836 DOI: 10.1111/jpc.12192
    The use of reflecting curtains with single phototherapy has not yet been directly compared with double phototherapy (DP). The objective of this study is to compare the efficacy of single phototherapy with reflecting curtains (SPRC) and DP in treating neonatal jaundice.
    Matched MeSH terms: Hyperbilirubinemia, Neonatal/therapy*
  3. Fulltext Effectiveness of home versus hospital phototherapy for term infants with uncomplicated hyperbilirubinemia: a pilot study in Pahang, Malaysia
    Zainab K, Adlina S
    Med J Malaysia, 2004 Aug;59(3):395-401.
    PMID: 15727387 MyJurnal
    A comparative pilot study was conducted to determine the difference in the reduction of total serum bilirubin in a group of infants who had phototherapy at home compared to an in-patient group on hospital phototherapy. Eighteen infants with unconjugated hyperbilirubinaemia who fitted the selection criteria were put under the mobile home unit (Bluelite Portable Light) placed in the home. A control group of 18 infants with the same matching characteristics had intense phototherapy in the hospital using a unit with top and bottom light sources. The infants were matched for race, starting total serum bilirubin level, birth weight (up to 250 grams) and age of baby at initiation of phototherapy (up to one-day difference). It was observed that the mean daily decrease in serum bilirubin concentration was significantly more in the home group as compared to the hospital group (t=2.95, df=17, P<0.05). The mean duration of treatment was significantly less for the home group as compared to the hospital group (t=2.84, df=17, P<0.05). None of the infants who had home phototherapy were re-hospitalized. Phototherapy related complications were mild and comparable in both groups. The result suggests that home phototherapy is safe and effective in bringing down the concentration of serum bilirubin for term babies with uncomplicated hyperbilirubinaemia.
    Matched MeSH terms: Hyperbilirubinemia/therapy*
  4. Risk factors associated with hearing loss in term neonates with hyperbilirubinaemia
    Boo NY, Oakes M, Lye MS, Said H
    J Trop Pediatr, 1994 Aug;40(4):194-7.
    PMID: 7932930
    A study of 128 jaundiced term neonates showed that 28 (22 per cent) had hearing loss based on brain stem-evoked response. There was no significant difference in the percentage of neonates with hearing loss between those with peak serum bilirubin levels of less than 340 mumol/l (16 per cent) and those with hyperbilirubinaemia > 339 mumol/l (33 per cent) (P = 0.11). Logistic regression analysis showed that severe jaundice which required exchange transfusion and earlier age of onset of hyperbilirubinaemia were statistically significant risk factors associated with hearing loss (P = 0.038 and P = 0.012, respectively).
    Matched MeSH terms: Hyperbilirubinemia/complications*; Hyperbilirubinemia/therapy
  5. Fulltext Hyperbilirubinaemia and erythrocytic glucose 6 phosphate dehydrogenase deficiency in Malaysian children
    Hon AT, Balakrishnan S, Ahmad Z
    Med J Malaysia, 1989 Mar;44(1):30-4.
    PMID: 2626111
    Cord blood from 8,975 babies delivered in Hospital Sultanah Aminah Johor Bahru over a period of eight months (1st August 1985 to 31st March 1986) were screened for G6PD deficiency. The overall incidence was 4.5% in Chinese, 3.5% in Malays and 1.5% in Indian babies. One hundred of these babies were observed in the nursery for seven days and their daily serum bilirubin recorded. The serum bilirubin peaked at 96 hours to a value of 12mg%. None of the babies in the nursery developed a serum bilirubin level of more than 15mg%. Six of the babies with G6PD deficiency that were sent home were readmitted with hyperbilirubinaemia that needed exchange transfusion.
    Matched MeSH terms: Hyperbilirubinemia/ethnology; Hyperbilirubinemia/epidemiology*
  6. Fulltext Comparison of detection of glucose-6-phosphate dehydrogenase deficiency using fluorescent spot test, enzyme assay and molecular method for prediction of severe neonatal hyperbilirubinaemia
    Wang FL, Boo NY, Ainoon O, Wong MK
    Singapore Med J, 2009 Jan;50(1):62-7.
    PMID: 19224086
    INTRODUCTION:
    This study aimed to compare the detection rates of glucose-6-phosphate dehydrogenase (G6PD) deficiency in neonates by fluorescent spot test (FST), enzyme assay and molecular methods, and to identify which method was a significant predictor of severe hyperbilirubinaemia.
    METHODS:
    74 term infants of Chinese descent admitted with severe hyperbilirubinaemia (total serum bilirubin equal or greater than 300 micromol/L) and 125 healthy term infants born in the hospital without severe hyperbilirubinaemia were recruited into the study. Specimens of blood were collected from each infant for FST, G6PD enzyme assay and TaqMan minor groove binder single nucleotide polymorphism genotyping assay.
    RESULTS:
    26 (13.1 percent) infants were diagnosed to have G6PD deficiency by FST. They had significantly lower median enzyme levels (0.8 IU/g Hb, interquartile range [IQR] 0.4-4.3) than those diagnosed to be normal (12.0 IU/g Hb, IQR 10.3-15.8) (p-value is less than 0.0001). Based on the enzyme assay, 39 (19.6 percent) infants had G6PD deficiency at an enzyme cut-off level of less than 8.5 IU/g Hb. G6PD mutation was detected in 27 (13.6 percent) infants. Logistic regression analysis showed that the only significant predictors of severe hyperbilirubinaemia were G6PD deficiency based on a cut-off level of less than 8.5 IU/g Hb (adjusted odds ratio [OR] 5.3, 95 percent confidence interval [CI] 2.4-11.4; p-value is less than 0.0001) and exclusive breast-feeding (adjusted OR 11.4, 95 percent CI 3.1-42.4; p-value is less than 0.0001). The gender and birth weight of infants, FST results, G6PD mutation and the actual G6PD enzyme levels were not significant predictors.
    CONCLUSION:
    A G6PD enzyme level of less than 8.5 IU/g Hb is a significant predictor of severe hyperbilirubinaemia
    Matched MeSH terms: Hyperbilirubinemia, Neonatal/enzymology*; Hyperbilirubinemia, Neonatal/epidemiology
  7. Fulltext Subaponeurotic haemorrhage in Malaysian neonates
    Boo NY
    Singapore Med J, 1990 Jun;31(3):207-10.
    PMID: 2392696
    In a 30-month prospective study, between January 1987 and June 1989, 101 of 64,424 Malaysian neonates (1.6 per 1000 livebirths) born in the Maternity Hospital, Kuala Lumpur were found to have subaponeurotic haemorrhage shortly after delivery. The incidence was highest in neonates weighting 4000 gm or more. There was no significant difference in incidence of this condition in neonates of different ethnic origins. Hypoprothrombinemia was present in only 5/101 (5.0%) of the affected neonates. Sixty seven (66.3%) of the neonates with subaponeurotic haemorrhage had history of trial of vacuum extraction. The incidence of subaponeurotic haemorrhage was significantly higher in neonates delivered by vacuum extraction than by other modes of delivery in this hospital (41.4 per 1000 livebirths in neonates delivered by vacuum extraction versus 1.0 per 1000 livebirths in neonates delivered by other modes). Those neonates who developed subaponeurotic haemorrhage without trial of vacuum extraction had a history of either prolonged labour or difficult delivery. Thirty-three (32.7%) of the neonates with subaponeurotic haemorrhage developed anaemia which required blood transfusion and 3/33 (9.1%) were in shock. Fifty seven (56.4%) of the neonates with subaponeurotic haemorrhage developed hyperbilirubinemia due to the haemorrhage. Four (7.0%) of them had severe unconjugated hyperbilirubinemia which required exchange transfusion. The results of this study suggest that subaponeurotic haemorrhage in Malaysian neonates was commonly associated with vacuum extraction and was not a benign condition.
    Matched MeSH terms: Hyperbilirubinemia/etiology; Hyperbilirubinemia/epidemiology
  8. Risk factors associated with unconjugated neonatal hyperbilirubinemia in Malaysian neonates
    Wong F, Boo N, Othman A
    J Trop Pediatr, 2013 Aug;59(4):280-5.
    PMID: 23640907 DOI: 10.1093/tropej/fmt023
    To investigate the risk factors associated with neonatal hyperbilirubinemia in Malaysian neonates.
    Matched MeSH terms: Hyperbilirubinemia, Neonatal/ethnology*; Hyperbilirubinemia, Neonatal/genetics
  9. Fulltext Variants of organic anion transporter polypeptide 2 gene are not risk factors associated with severe neonatal hyperbilirubinemia
    Wong FL, Boo NY, Ainoon O, Wang MK
    Malays J Pathol, 2009 Dec;31(2):99-104.
    PMID: 20514852 MyJurnal
    This study aimed to determine the prevalence of four variants of organic anion transporter polypeptide 2 (OATP2) gene, and their association with severe hyperbilirubinemia.
    Matched MeSH terms: Hyperbilirubinemia, Neonatal/genetics*; Hyperbilirubinemia, Neonatal/metabolism
  10. Fulltext Detection of sensorineural hearing loss using automated auditory brainstem-evoked response and transient-evoked otoacoustic emission in term neonates with severe hyperbilirubinaemia
    Boo NY, Rohani AJ, Asma A
    Singapore Med J, 2008 Mar;49(3):209-14.
    PMID: 18363002
    This study was designed to compare the sensitivity and specificity of detecting sensorineural hearing loss (SNHL) using the transient-evoked otoacoustic emissions (OAE) machine (the Madsen TE Echoscreen) and automated auditory brainstem response (AABR) machine (the Sabre Compac portable AABR) in term neonates exposed to severe hyperbilirubinaemia.
    Matched MeSH terms: Hyperbilirubinemia/complications*; Hyperbilirubinemia/diagnosis
  11. Rapid detection of the UGT1A1 single nucleotide polymorphism G211A using real-time PCR with Taqman minor groove binder probes
    Wong FL, Wang MK, Boo NY, Hamidah NH, Ainoon BO
    J Clin Lab Anal, 2007;21(3):167-72.
    PMID: 17506482
    The UGT1A1 Taqman MGB probe single nucleotide polymorphism (SNP) genotyping assay was developed to detect nucleotide 211 of the UDP-glucoronocyltransferase 1A1 (UGT1A1) gene. Defects in this enzyme interfere with process of conjugation of bilirubin and cause unconjugated hyperbilirubinemia. Variation at nucleotide 211 in the coding region of the UGT1A1 gene has been shown to be prevalent in Japanese and Chinese. Using an ABI sequence detection system (SDS) 7000, an allele-specific real-time PCR-based genotyping method was established to detect nucleotide G211A. Cord blood from 125 infants without hyperbilirubinemia (controls) were compared with cord blood from 74 infants (cases) with severe hyperbilirubinemia (total serum bilirubin > 300 micromol/L). Homozygous variation of the UGT1A1 gene at nucleotide 211(A/A) is significantly more common in cases (14.9%) than in controls (0.8%) (P<0.001). Direct sequencing from 20 randomly selected samples showed eight samples with homozygous wild type, seven with homozygous variant, and five samples were heterozygous. The result from this assay was in complete concordance with the DNA sequencing result and clearly discriminate wild-type (G/G), homozygous variant (A/A), and heterozygous (G/A). This assay is rapid and robust for screening of SNP G211A to determine if this polymorphism plays a role in causing severe neonatal jaundice in the local context.
    Matched MeSH terms: Hyperbilirubinemia, Neonatal/blood; Hyperbilirubinemia, Neonatal/diagnosis; Hyperbilirubinemia, Neonatal/enzymology*
  12. Fulltext Occurrence of Recurrent Aphthous Stomatitis (RAS) as a Rare Oral Manifestation in a Patient with Gilbert's Syndrome
    Heboyan A, Avetisyan A, Skallevold HE, Rokaya D, Marla V, Vardanyan A
    Case Rep Dent, 2021;2021:6648729.
    PMID: 33953989 DOI: 10.1155/2021/6648729
    Recurrent aphthous stomatitis is an ulcerative disease of the oral cavity and can occur in isolation or as a manifestation of many systemic diseases. It is a quite common entity and may hence often be overlooked as an isolated lesion. Gilbert's syndrome is a genetic disorder where a deficiency of an enzyme associated with the conjugation of bilirubin results in unconjugated hyperbilirubinemia. The disease is generally asymptomatic and is aggravated by certain trigger factors. No associated oral manifestations are known. In this case report, we discuss the concomitant presence of recurrent aphthous stomatitis in a patient of Gilbert's syndrome. The presence of such recurrent stomatitis may represent as an oral manifestation of Gilbert's syndrome. Early identification of these entities may improve the overall quality of life of the patient.
    Matched MeSH terms: Hyperbilirubinemia
  13. Genetic Factors and Delayed TSB Monitoring and Treatment as Risk Factors Associated with Severe Hyperbilirubinemia in Term Neonates Admitted for Phototherapy
    Boo NY, Sin S, Chee SC, Mohamed M, Ahluwalia AK, Ling MM, et al.
    J Trop Pediatr, 2020 12 01;66(6):569-582.
    PMID: 32577754 DOI: 10.1093/tropej/fmaa016
    OBJECTIVES: This study aimed to determine whether maternal-fetal blood group isoimmunization, breastfeeding, birth trauma, age when first total serum bilirubin (TSB) was measured, age of admission, and genetic predispositions to hemolysis [due to genetic variants of glucose-6-phosphate dehydrogenase (G6PD) enzyme], and reduced hepatic uptake and/or conjugation of serum bilirubin [due to genetic variants of solute carrier organic anion transporter protein family member 1B1 (SLCO1B1) and uridine diphosphate glucuronosyltransferase family 1 member A1 (UGT1A1)] were significant risk factors associated with severe neonatal hyperbilirubinemia (SNH, TSB ≥ 342µmol/l) in jaundiced term neonates admitted for phototherapy.

    METHODS: The inclusion criteria were normal term neonates (gestation ≥ 37 weeks). Parents/care-givers were interviewed to obtain data on demography, clinical problems, feeding practice and age when first TSB was measured. Polymerase chain reaction-restriction fragment length polymorphism method was used to detect common G6PD, UGT1A1 and SLCO1B1 variants on each neonate's dry blood specimens.

    RESULTS: Of 1121 jaundiced neonates recruited, 232 had SNH. Logistic regression analysis showed that age (in days) when first TSB was measured [adjusted odds ratio (aOR) = 1.395; 95% confidence interval (CI) 1.094-1.779], age (in days) of admission (aOR = 1.127; 95% CI 1.007-1.260) and genetic mutant UGT1A1 promoter A(TA)7TAA (aOR = 4.900; 95% CI 3.103-7.739), UGT1A1 c.686C>A (aOR = 6.095; 95% CI 1.549-23.985), SLCO1B1 c.388G>A (aOR = 1.807; 95% CI 1.242-2.629) and G6PD variants and/or abnormal G6PD screening test (aOR = 2.077; 95% CI 1.025-4.209) were significantly associated with SNH.

    CONCLUSION: Genetic predisposition, and delayed measuring first TSB and commencing phototherapy increased risk of SNH.

    Matched MeSH terms: Hyperbilirubinemia, Neonatal/diagnosis; Hyperbilirubinemia, Neonatal/genetics*; Hyperbilirubinemia, Neonatal/therapy
  14. Fulltext Adrenal haemorrhage in a newborn
    Shalini, N., Rohani, A.J., Neoh, S.H., Cheah, I.G.S., Che Zubaidah
    Malaysian Journal of Paediatrics and Child Health, 2016;22(101):0-0.
    MyJurnal
    Adrenal hemorrhage (AH) is a relatively uncommon condition (0.55-1.9%) during the neonatal period [1]. The adrenal gland is vulnerable to haemorrhage because of its large size and high vascularity. Clinical features of AH are variable and nonspecific. AH in a newborn can present as anemia, hyperbilirubinemia, abdominal mass, painful swelling or hematoma of the scrotum, acute adrenal crisis or shock [2]. We report such a case of adrenal haemorrhage in a newborn.(Copied from article)
    Matched MeSH terms: Hyperbilirubinemia
  15. Fulltext Prevalence of uridine glucuronosyl transferase 1A1 (UGT1A1) mutations in Malay neonates with severe jaundice
    Azlin I, Wong FL, Ezham M, Hafiza A, Ainoon O
    Malays J Pathol, 2011 Dec;33(2):95-100.
    PMID: 22299209 MyJurnal
    A number of genetic risk factors have been implicated in the development of neonatal severe hyperbilirubinaemia. This includes mutations in the uridine glucoronosyl transferase 1A1 (UGT1A1) gene which is responsible for unconjugated hyperbilirubinemia in Gilbert's Syndrome. We studied the prevalence of UGT1A1 gene mutations in a group of Malay neonates to determine whether they are risk factors to severe neonatal jaundice. One hundred and twenty-five Malay neonates with severe hyperbilirubinemia were studied. Ninety-eight infants without severe hyperbilirubinaemia were randomly selected from healthy Malay term infants (controls). DNA from EDTA cord blood samples were examined for UGT1A1 mutations nt211G > A and nt247T > C using established Taqman SNP genotyping assays and the UGT1A1*28 variant was detected by the Agilent 2100 bioanalyzer. All samples were also screened for common Malay G6PD variants using established techniques. The frequency of UGT1A1 211G > A mutation is significantly higher in the severely hyperbilirubinemic group (13%) than the control group (4%; p = 0.015) and all the positive cases were heterozygous for the mutation. There was no significant difference in the frequency of UGT1A1*28 mutation between the severely hyperbilirubinemic (3.5%) and the control group (0.01%; p = 0.09). None of the neonates in both groups carried the nt247 T > C mutation. The prevalence of G6PD mutation was significantly higher in the severely jaundiced group than control (9% vs 4%; p = 0.04). In conclusion, nt 211 G > A alleles constitute at least 12% of UGT1A1 mutations underlying unconjugated hyperbilirubinemia and appears to be a significant independent risk factor associated with severe neonatal hyperbilirubinemia in the Malay newborns.
    Matched MeSH terms: Hyperbilirubinemia, Neonatal/genetics*
  16. Homozygous variant of UGT1A1 gene mutation and severe neonatal hyperbilirubinemia
    Boo NY, Wong FL, Wang MK, Othman A
    Pediatr Int, 2009 Aug;51(4):488-93.
    PMID: 19674361 DOI: 10.1111/j.1442-200X.2008.02798.x
    The aim of the present study was to compare, in a case-control study, the prevalence of nucleotide 211 guanine to adenine (G-->A) mutation of uridine diphosphoglucuronosyl transferase (UGT1A1) gene in Malaysian Chinese newborns with and without severe hyperbilirubinemia (total serum bilirubin >250 micromol/L during first 48 h of life or > or =300 micromol/L thereafter), and to determine whether this mutation was a significant risk factor associated with severe hyperbilirubinemia.
    Matched MeSH terms: Hyperbilirubinemia, Neonatal/genetics*
  17. Prediction of severe hyperbilirubinaemia using the Bilicheck transcutaneous bilirubinometer
    Boo NY, Ishak S
    J Paediatr Child Health, 2007 Apr;43(4):297-302.
    PMID: 17444833
    To determine the sensitivity and specificity of different levels of bilirubin measured by the transcutaneous bilirubinometer Bilicheck on forehead and sternum for predicting severe hyperbilirubinaemia of total serum bilirubin (TSB)>or=300 micromol/L in Malay, Chinese and Indian infants.
    Matched MeSH terms: Hyperbilirubinemia, Neonatal/diagnosis*
  18. Frequencies of A(TA)7TAA, G71R, and G493R mutations of the UGT1A1 gene in the Malaysian population
    Yusoff S, Van Rostenberghe H, Yusoff NM, Talib NA, Ramli N, Ismail NZ, et al.
    Biol. Neonate, 2006;89(3):171-6.
    PMID: 16210851
    Gilbert syndrome is caused by defects in the uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene. These mutations differ among different populations and many of them have been found to be genetic risk factors for the development of neonatal jaundice.
    Matched MeSH terms: Hyperbilirubinemia, Neonatal/genetics
  19. Fulltext High resolution melting analysis of the NR1I3 genetic variants: Is there an association with neonatal hyperbilirubinemia?
    Cheung TP, Van Rostenberghe H, Ismail R, Nawawi NN, Abdullah NA, Ramli N, et al.
    Gene, 2015 Dec 1;573(2):198-204.
    PMID: 26188155 DOI: 10.1016/j.gene.2015.07.045
    Constitutive androstane receptor (CAR) encoded by the nuclear receptor subfamily 1, group I, member 3 (NR1I3) gene regulates the elimination of bilirubin through activating the components of the bilirubin clearance pathway. Hence, NR1I3 genetic variants may affect bilirubin metabolism and result in neonatal hyperbilirubinemia. Thus far, research which investigates the association between NR1I3 variants and neonatal hyperbilirubinemia has not been undertaken in any population. The present study aimed to evaluate the influence of MPJ6_1I3008 (rs10157822), IVS8+116T>G (rs4073054) and 540A>G (rs2307424) on neonatal hyperbilirubinemia development in the Malay population. Buccal swabs were collected from 232 hyperbilirubinemia and 277 control term newborns with gestational age ≥37weeks and birth weight ≥2500g. The NR1I3 variants were genotyped by using high resolution melting (HRM) assays and verified by DNA sequencing. Gender, mode of delivery and birth weight did not differ between hyperbilirubinemia and control groups. The genotypic and allelic frequencies of MPJ6_1I3008, IVS8+116T>G and 540A>G were not significantly different between the groups. However, stratification by gender revealed a significant inverse association between homozygous variant genotype of MPJ6_1I3008 and risk of neonatal hyperbilirubinemia in the females (OR, 0.44; 95% CI, 0.20-0.95; p=0.034). This study demonstrates that the homozygous variant genotype of MPJ6_1I3008 was associated with a significant reduced risk of neonatal hyperbilirubinemia in the females.
    Matched MeSH terms: Hyperbilirubinemia, Neonatal/genetics*
  20. Neonatal hyperbilirubinaemia
    Sinniah D
    Med J Malaya, 1971 Mar;25(3):211-4.
    PMID: 4253249
    Matched MeSH terms: Hyperbilirubinemia/epidemiology*
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