Displaying publications 61 - 80 of 83 in total

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  1. The treatment of malaria in glucose-6-phosphate dehydrogenase deficient patients in Sabah
    Khoo KK
    Ann Trop Med Parasitol, 1981 Dec;75(6):591-5.
    PMID: 7325735 DOI: 10.1080/00034983.1981.11687489
    One hundred and nine (9·8%) out of 1103 malaria patients examined in Sabah were deficient in glucose-6-phosphate dehydrogenase (G6PD). Sixty-nine of these G6PD-deficient patients were randomly allocated to one of three treatment regimes with (a) chloroquine, (b) chloroquine and primaquine or (c) sulfadoxine-pyrimethamine (Fansidar). No haemolysis was observed in group (a); except for a single mild case, no haemolysis was seen in group (c). However, in the primaquine group (23 patients), haemolysis occurred in seven of the 16 patients who had complete G6PD deficiency. Of these seven, five required blood transfusion and the other two developed acute renal failure, one requiring peritoneal dialysis. In the Fansidar group (c), four of the 22 patients took more than 15 days to clear the parasitaemia. Chloroquine resistance to falciparum infection was common in the patients given this anti-malarial.
    Study site: Queen Elizabeth Hospital, Kola Kinabalu, Sabah, Malaysia
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/complications*
  2. Red cell metabolism and severe neonatal jaundice in West Malaysia
    Lie-Injo LE, Virik HK, Lim PW, Lie AK, Ganesan J
    Acta Haematol., 1977;58(3):152-60.
    PMID: 409030 DOI: 10.1159/000207822
    A study was carried out of 332 babies suffering from severe neonatal jaundice who were admitted to the General Hospital, Kuala Lumpar, Malaysia. Of the 332 neonates, 51 were premature and 281 were full-term babies, 178 (110 Chinese, 58 Malay, 9 Indian and 1 European-Pakistani) had bilirubin levels of 20 mg% or higher, requiring exchange blood transfusion. Of the Chinese neonates, 23 (20.9%) had G6PD deficiency, 9 (8.2%) had Hb Bart's and 2 (1.8%) had an abnormal haemoglobin, one Hb Q and one fetal variant. Among the Malay infants, 10 (17.2%) had G6PD deficiency, 7 (12.1%) had Hb Bart's and 10 (17.2%) had abnormal haemoglobins (four had Hb E trait, one had Hb K and Bart's in addition to Hb E, three had Hb CoSp with Hb Bart's, one had Hb Q and one Hb Tak). One of the nine Indian neonates had G6PD deficiency and one had Hb S trait. The one European-Pakistani baby was a carrier of Hb D Punjab. In addition to G6PD deficiency, abnormal haemoglobins seem to have contributed to the high incidence of severe neonatal jaundice in Malaysia. The mean activities of GP, GR and GR after stimulation with FAD were higher, while the mean activity of PK and mean level of reduced glutathione were lower than in normal cord bloods. The percent increase of GR after FAD stimulation was significantly lower; fewer in this group had increases above 20% than in normal cord blood. The possible significance of the findings is discussed.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/complications
  3. Fulltext Challenges for achieving safe and effective radical cure of Plasmodium vivax: a round table discussion of the APMEN Vivax Working Group
    Thriemer K, Ley B, Bobogare A, Dysoley L, Alam MS, Pasaribu AP, et al.
    Malar J, 2017 04 05;16(1):141.
    PMID: 28381261 DOI: 10.1186/s12936-017-1784-1
    The delivery of safe and effective radical cure for Plasmodium vivax is one of the greatest challenges for achieving malaria elimination from the Asia-Pacific by 2030. During the annual meeting of the Asia Pacific Malaria Elimination Network Vivax Working Group in October 2016, a round table discussion was held to discuss the programmatic issues hindering the widespread use of primaquine (PQ) radical cure. Participants included 73 representatives from 16 partner countries and 33 institutional partners and other research institutes. In this meeting report, the key discussion points are presented and grouped into five themes: (i) current barriers for glucose-6-phosphate deficiency (G6PD) testing prior to PQ radical cure, (ii) necessary properties of G6PD tests for wide scale deployment, (iii) the promotion of G6PD testing, (iv) improving adherence to PQ regimens and (v) the challenges for future tafenoquine (TQ) roll out. Robust point of care (PoC) G6PD tests are needed, which are suitable and cost-effective for clinical settings with limited infrastructure. An affordable and competitive test price is needed, accompanied by sustainable funding for the product with appropriate training of healthcare staff, and robust quality control and assurance processes. In the absence of quantitative PoC G6PD tests, G6PD status can be gauged with qualitative diagnostics, however none of the available tests is currently sensitive enough to guide TQ treatment. TQ introduction will require overcoming additional challenges including the management of severely and intermediately G6PD deficient individuals. Robust strategies are needed to ensure that effective treatment practices can be deployed widely, and these should ensure that the caveats are outweighed by  the benefits of radical cure for both the patients and the community. Widespread access to quality controlled G6PD testing will be critical.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/diagnosis
  4. Genetic factors and malaria in the Temuan
    Baer A, Lie-Injo LE, Welch QB, Lewis AN
    Am J Hum Genet, 1976 Mar;28(2):179-88.
    PMID: 817597
    The jungle habitat of the Temuan aborigines harbors a variety of infectious diseases, the most notable being malaria. Our study of 15 genetic systems in the Temuan revealed substantial polymorphism and within-population genetic diversity. The polymorphisms for Hb beta, G6PD, and El are of interest in regard to genetic adaptation to malaria. Among the polymorphisms investigated we conclude that G6PD deficiency and elliptocytosis are likely to have malaria-resistant effects as evidenced by their low association with malarial parasitemia or their higher frequency in adults than in children. These findings suggest that the malarial habitat of the Temuans is livable in the long range sense for them because of the cluster of malaria-resistant alleles in their gene pool (G6PD)-, El, and possibly, but not tested here because of its low frequency, Hb beta E). The same condition probably holds for the Semai, the nearest aborigine neighbors of the Temuan (although the Semai have not been tested for malarial parasitemia and for these polymorphisms simultaneously), since the Semai have substantial Hb betaE, G6PD-, and El. The Temuan have a cultural identity system of rituals, beliefs, and certain aspects of language which effectively isolates them genetically from Malays and other nonaborigines. This system hinders the dilution of the malaria-resistant alleles of the Temuan gene pool with the malaria-susceptible alleles of the nonaborigine gene pools.
    Matched MeSH terms: Glucosephosphate Dehydrogenase/blood
  5. Homozygous state for Hb Constant Spring (slow-moving Hb X components)
    Lie-Injo LE, Ganesan J, Clegg JB, Weatherall DJ
    Blood, 1974 Feb;43(2):251-9.
    PMID: 4810076
    Matched MeSH terms: Glucosephosphate Dehydrogenase/metabolism
  6. Fulltext Increased basal oxidation of peroxiredoxin 2 and limited peroxiredoxin recycling in glucose-6-phosphate dehydrogenase-deficient erythrocytes from newborn infants
    Cheah FC, Peskin AV, Wong FL, Ithnin A, Othman A, Winterbourn CC
    FASEB J, 2014 Jul;28(7):3205-10.
    PMID: 24636884 DOI: 10.1096/fj.14-250050
    Erythrocytes require glucose-6-phosphate dehydrogenase (G6PD) to generate NADPH and protect themselves against hemolytic anemia induced by oxidative stress. Peroxiredoxin 2 (Prx2) is a major antioxidant enzyme that requires NADPH to recycle its oxidized (disulfide-bonded) form. Our aims were to determine whether Prx2 is more highly oxidized in G6PD-deficient erythrocytes and whether these cells are able to recycle oxidized Prx2 after oxidant challenge. Blood was obtained from 61 Malaysian neonates with G6PD deficiency (average 33% normal activity) and 86 controls. Prx2 redox state was analyzed by Western blotting under nonreducing conditions. Prx2 in freshly isolated blood was predominantly reduced in both groups, but the median level of oxidation was significantly higher (8 vs 3%) and the range greater for the G6PD-deficient population. When treated with reagent H2O2, the G6PD-deficient erythrocytes were severely compromised in their ability to recycle oxidized Prx2, with only 27 or 4% reduction after 1 h treatment with 0.1 or 1 mM H2O2 respectively, compared with >97% reduction in control erythrocytes. The accumulation of oxidized Prx2 in oxidatively stressed erythrocytes with common G6PD variants suggests that impaired antioxidant activity of Prx2 could contribute to the hemolysis and other complications associated with the condition.-Cheah, F.-C., Peskin, A. V., Wong, F.-L., Ithnin, A., Othman, A., Winterbourn, C. C. Increased basal oxidation of peroxiredoxin 2 and limited peroxiredoxin recycling in glucose-6-phosphate dehydrogenase deficient erythrocytes from newborn infants.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/metabolism*
  7. Fulltext Audit of birth defects in 34,109 deliveries in a tertiary referral center
    Noraihan MN, See MH, Raja R, Baskaran TP, Symonds EM
    Med J Malaysia, 2005 Oct;60(4):460-8.
    PMID: 16570708
    The objective of the study is to determine the proportion and different types of birth defects among the children born in Hospital Kuala Lumpur. A cross-sectional study was conducted for a period of 18 months where all consecutively born infants, dead or alive were included. There were total of 34,109 births recorded during this period. The proportion of birth defects in Hospital Kuala Lumpur was 3.1% (n = 1056). The commonest involved were the hematology system, (157.7 per 10,000 births), the central nervous system, genitourinary system and chromosomal anomalies. The proportion was significantly higher in males and in the Chinese (p < 0.001). The commonest abnormalities are Glucose 6 Phosphate Deficiency (157.7/10000), Down's syndrome (12.6/10000), thalassaemia (8.8/10000), cleft lip and/or palate (7.6/10000) and anencephaly (7.3/10000). Neural tube defect is common and ranked second after G6PD deficiency. There is a need for a birth defect registry to assess the extent of the problem in Malaysia.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/epidemiology
  8. Fulltext G6PD Viangchan and G6PD Mediterranean are the main variants in G6PD deficiency in the Malay population of Malaysia
    Mohd Yusoff N, Shirakawa T, Nishiyama K, Choo KE, Isa MN, Matsuo M
    Southeast Asian J Trop Med Public Health, 2003;34 Suppl 3:135-7.
    PMID: 15906717
    Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked red blood cell enzymopathy common in malaria endemic areas. Individuals affected by this disease show a wide variety of clinical signs of acute hemolytic anemia. Mutations of the G6PD gene in the Malay population with G6PD deficiency in Kelantan, a state in North East Malaysia were studied. Ninety-three individuals with G6PD deficiency were subjected to mutation analysis of the G6PD gene using polymerase chain reaction based techniques of multiplex PCR. Of the ninety-three DNA samples studied, molecular defects were identified in 80 cases (86%). Variants were heterogeneous - 28.7% were found to have a G to A nucleotide change at nucleotide 871 of the G6PD gene (G871A), corresponding to G6PD Viangchan. The other major mutations were G6PD Mediterranean, G6PD Vanua Lava, G6PD Coimbra, G6PD Kaiping, G6PD Orissa, G6PD Mahidol, G6PD Canton and G6PD Chatham. These results showed that there are heterogeneous mutations of the G6PD gene associated with G6PD deficiency and that G6PD Viangchan and G6PD Mediterranean account for the main variants in G6PD deficiency among the Malay population in Malaysia.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/genetics*
  9. Goniothalamin enhances the ATPase activity of the molecular chaperone Hsp90 but inhibits its chaperone activity
    Yokoyama Y, Ohtaki A, Jantan I, Yohda M, Nakamoto H
    J. Biochem., 2015 Mar;157(3):161-8.
    PMID: 25294885 DOI: 10.1093/jb/mvu061
    Hsp90 is an ATP-dependent molecular chaperone that is involved in important cellular pathways such as signal transduction pathways. It is a potential cancer drug target because it plays a critical role for stabilization and activation of oncoproteins. Thus, small molecule compounds that control the Hsp90 function are useful to elucidate potential lead compounds against cancer. We studied effect of a naturally occurring styryl-lactone goniothalamin on the activity of Hsp90. Although many drugs targeting Hsp90 inhibit the ATPase activity of Hsp90, goniothalamin enhanced rather than inhibited the ATPase activity of a cyanobacterial Hsp90 (HtpG) and a yeast Hsp90. It increased both K(m) and k(cat) of the Hsp90s. Domain competition assays and tryptophan fluorescence measurements with various truncated derivatives of HtpG indicated that goniothalamin binds to the N-terminal domain of HtpG. Goniothalamin did not influence on the interaction of HtpG with a non-native protein or the anti-aggregation activity of HtpG significantly. However, it inhibited the activity of HtpG that assists refolding of a non-native protein in cooperation with the Hsp70 chaperone system. This is the first report to show that a small molecule that binds to the N-terminal domain of Hsp90 activates its ATPase activity, while inhibiting the chaperone function of Hsp90.
    Matched MeSH terms: Glucosephosphate Dehydrogenase/chemistry
  10. 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: Glucosephosphate Dehydrogenase/genetics*
  11. Fulltext Adverse effects of herbal or dietary supplements in G6PD deficiency: a systematic review
    Lee SW, Lai NM, Chaiyakunapruk N, Chong DW
    Br J Clin Pharmacol, 2017 01;83(1):172-179.
    PMID: 27081765 DOI: 10.1111/bcp.12976
    AIM: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common genetic disorder, affecting nearly 400 million individuals worldwide. Whilst it is known that a number of drugs, foods and chemicals can trigger haemolysis in G6PD deficient individuals, the association between herbal and dietary supplements and haemolysis is less clear. The objective of this study was to evaluate the association between herbal or dietary supplements and adverse events in G6PD deficient individuals.

    METHODS: We searched 14 electronic databases from their inception until November 2015 for articles describing the use of herbal or dietary supplements in G6PD deficient individuals. Additional publications were identified from manually searching textbooks, conference abstracts and the grey literature. All study designs were included as long as they contained clinical information. These gathered findings were summarized narratively.

    RESULTS: Thirty-two publications met inclusion criteria. These reported on 10 herbal and dietary supplements. Overall evidence linking haemolysis to a herbal/dietary supplement was only found for henna. No evidence of harm was observed for vitamin C, vitamin E, vitamin K, Gingko biloba and α-lipoic acid.

    CONCLUSIONS: The review showed that there was insufficient evidence to contravene the use of most herbal or dietary products at therapeutic doses in G6PD deficient subjects.

    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/blood*
  12. Isozymes of a rattan species and their genetic interpretation
    Bon MC
    Electrophoresis, 1996 Jul;17(7):1248-52.
    PMID: 8855412
    A combination of a modified Feret' (Silvae Genet. 1971, 20, 46-50) extraction buffer and two types of electrophoresis with acrylamide and starch gels were used to characterize allozymes in mature vegetative tissue of a commercially high value species of rattans (Calamus subinermis). From the analysis of allelic segregation from single maternal rattans and their offspring, genetic control of the 16 observed banding zones, which were consistently scorable, was assumed. Seventeen gene loci were identified. The percentage of polymorphic loci within Calamus subinermis was much higher (70.5%) than expected levels of genetic diversity for tropical woody and non-woody species. It is thought that the protocol described may be applied to the analysis of the genetic diversity of all the endangered Calamus species.
    Matched MeSH terms: Glucosephosphate Dehydrogenase/analysis; Glucosephosphate Dehydrogenase/genetics
  13. Fulltext Vernonia amygdalina simultaneously suppresses gluconeogenesis and potentiates glucose oxidation via the pentose phosphate pathway in streptozotocin-induced diabetic rats
    Atangwho IJ, Yin KB, Umar MI, Ahmad M, Asmawi MZ
    BMC Complement Altern Med, 2014;14:426.
    PMID: 25358757 DOI: 10.1186/1472-6882-14-426
    This study evaluated the impact of Vernonia amygdalina (VA) on the transcription of key enzymes involved in cellular modulation of glucose in streptozotocin-induced diabetic rats in a bid to understand the possible anti-diabetic mechanism of VA.
    Matched MeSH terms: Glucosephosphate Dehydrogenase/genetics; Glucosephosphate Dehydrogenase/metabolism
  14. Effect of dietary ascorbate on lipogenesis and lipolysis activities in black sea bream, Acanthopagrus schlegelii
    Ji H, Om AD, Yoshimatsu T, Umino T, Nakagawa H, Sakamoto S
    Fish Physiol Biochem, 2010 Sep;36(3):749-755.
    PMID: 19685218 DOI: 10.1007/s10695-009-9349-z
    To assess the effect of dietary ascorbate on lipid metabolism, 1-year black sea bream (Acanthopagrus schlegelii) were reared on a casein-based purified diet and an ascorbate fortified diet (1,100 mg of L: -ascorbyl-2- monophosphate-Mg/kg diet). The fortified ascorbate was effectively incorporated into the fish body and elevated muscle carnitine content. Fortifications of dietary ascorbate depressed activities of glucose-6-phosphate dehydrogenase and NADP-isocitrate dehydrogenase as lipogenic enzymes in the hepatopancreas and intraperitoneal fat body. Starvation after feeding experiment activated carnitine palmitoyltransferase as a lipolysis enzyme in the hepatopancreas in both control and vitamin C(VC) groups, while the lipolysis activity was significantly higher in VC group. These results confirmed that dietary ascorbate depressed lipogenesis and activated lipolysis, i.e., influenced the lipid metabolism of black sea bream.
    Matched MeSH terms: Glucosephosphate Dehydrogenase/analysis
  15. Fulltext Unstable haemoglobin Köln disease in members of a Malay family
    Eng LL, Lopez CG, Eapen JS, Eravelly J, Wiltshire BG, Lehmann H
    J Med Genet, 1972 Sep;9(3):340-3.
    PMID: 5079107 DOI: 10.1136/jmg.9.3.340
    Matched MeSH terms: Glucosephosphate Dehydrogenase/analysis
  16. The distribution of blood genetic markers in immigrant Chinese populations
    Hawkins BR
    Acta Genet Med Gemellol (Roma), 1973;22:139-66.
    PMID: 4790793
    Matched MeSH terms: Glucosephosphate Dehydrogenase/blood
  17. Fulltext Dengue virus type 2 (DENV2)-induced oxidative responses in monocytes from glucose-6-phosphate dehydrogenase (G6PD)-deficient and G6PD normal subjects
    Al-Alimi AA, Ali SA, Al-Hassan FM, Idris FM, Teow SY, Mohd Yusoff N
    PLoS Negl Trop Dis, 2014 Mar;8(3):e2711.
    PMID: 24625456 DOI: 10.1371/journal.pntd.0002711
    Dengue virus is endemic in peninsular Malaysia. The clinical manifestations vary depending on the incubation period of the virus as well as the immunity of the patients. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is prevalent in Malaysia where the incidence is 3.2%. It has been noted that some G6PD-deficient individuals suffer from more severe clinical presentation of dengue infection. In this study, we aim to investigate the oxidative responses of DENV2-infected monocytes from G6PD-deficient individuals.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency*
  18. Fulltext Factors Affecting Primaquine Combination Treatment in Malaria Patients in Selangor, Malaysia
    Ariffin NM, Islahudin F, Makmor-Bakry M, Kumolosasi E, Hamid MHA
    J Pharm Bioallied Sci, 2017 Oct-Dec;9(4):239-245.
    PMID: 29456374 DOI: 10.4103/jpbs.JPBS_48_17
    Introduction: Primaquine is vital for the management of liver-stagePlasmodium vivaxandPlasmodium ovalemalaria. However, primaquine effectiveness is dependent on various factors and differs between populations. Therefore, this study was conducted to identify factors that affect the length of stay and relapse during primaquine combination treatment in malaria-infected patients in the local setting.

    Materials and Methods: A retrospective study on the use of primaquine combination amongP. vivaxandP. ovaleinfected patients in Selangor, Malaysia within a 5-year period from 2011 to 2015 was obtained from the National Malaria Case Registry, Malaysia. Data collected were patient characteristics (age, gender, nationality, glucose-6-phosphate dehydrogenase, pregnancy); disease characteristics (survival, past malaria infection, parasite type, presence of gametocyte, parasite count, week onset, severity, transmission type); and treatment characteristics (type of antimalarial, treatment completion). Outcome measures were length of stay and relapse during a 1-year follow-up.

    Results: A total of 635 patients were included in the study. Based on a multivariate logistic regression analysis, the significant predictors for length of stay were gender (P= 0.009) and indigenous transmission (P< 0.001). Male patients had a shorter length of stay than females by 0.868 days (P= 0.009), and indigenous transmission took 1.82 days more compared to nonindigenous transmission (P< 0.001). Predictors for relapse were indigenous transmission of malaria (P= 0.019), which was 15.83 times more likely to relapse than nonindigenous transmission (P< 0.01).

    Conclusions: This study reveals that the effectiveness of primaquine was clinically associated with gender and indigenous transmission. To that end, vigilant monitoring of primaquine use is required to reduce relapse and future transmission.
    Matched MeSH terms: Glucosephosphate Dehydrogenase
  19. Fulltext Data on PCR primer design for glucose 6-phosphate dehydrogenase gene and the effects of dietary carbohydrate levels on its expression in the liver of Malaysian mahseer (Tor tambroides)
    Ishak SD, Razali SA, Kamarudin MS, Abol-Munafi AB
    Data Brief, 2020 Aug;31:105916.
    PMID: 32642522 DOI: 10.1016/j.dib.2020.105916
    The enzyme glucose-6-phosphate dehydrogenase (G6PD) catalyses the metabolite glucose-6-phosphate in producing NADPH during the first phase of pentose-phosphate pathway thus provides reducing power to all cells for cellular growth, antioxidant defence, and biosynthetic reactions in all living organism. The deliberate inclusion of starch as carbohydrate source in commercial feed however may affect the G6PD hepatic activity in cultured fish. We designed a set of primers to target G6PD gene in the popular Malaysian aquaculture species, Tor tambroides. For this dataset, the molecular characteristics of obtained T. tambroides G6PD (TtG6PD) nucleotide sequence was analysed using multiple alignments and phylogenetic analyses of the deduced amino acids. The set of primers obtained were then used in a study to evaluate the effect of different dietary carbohydrate inclusion levels on the hepatic TtG6PD mRNA expression of the T. tambroides fingerlings. Four groups of fish were given a dietary treatment of 15%, 20%, 25% and 30% starch at the optimal inclusion level of 23.4% for 10 weeks. The TtG6PD mRNA transcripts were measured using real-time-PCR assays and its expression normalized against β-actin, which acts as the internal control gene. This article provides supportive data in relation between hepatic TtG6PD mRNA gene expression in T. tambroides and how it is influenced by its dietary carbohydrate intake. These data will also assist in further nutritional genomic studies of carbohydrate and energy utilization for all species in the mahseer family.
    Matched MeSH terms: Glucosephosphate Dehydrogenase
  20. Exchange transfusion for neonatal hyperbilirubinaemia: experience in an inborn neonatal intensive care unit
    Lim, N.L., Boo, N.Y., Nur Atiqah, N.A., Padma Soosai, A., Musa Mohd Nordin, M Sham. Kasim
    Malaysian Journal of Child Health, 1998;10(1):46-51.
    MyJurnal
    Severe jaundice (serum bilirubin level > 340 gmol/L) occurred in 81 infants admitted to the Neonatal Intensive Care Unit (NICU) of the Maternity Hospital Kuala Lumpur (MHKL) in 1993. Of these 46 (56.8%) underwent 53 exchange transfusions. In-patient case notes were available for study on 41 of them. Two infants had no cause identified while 12 were associated with prematurity, 13 ABO incompatibility, 8 G6PD deficiency, 6 sepsis 2 Rh isoimmunisation and 6 miscellaneous causes. In 14 infants it was felt that exchange transfusions might have been avoided if they were detected earlier and phototherapy instituted promptly. Twenty six (26) infants were deemed to have been given phototherapy at the appropriate time but jaundice increased to exchange transfusion levels, threshold values depending on the unit in charge. Use of higher intensity phototherapy might have been more effective in some of the cases. Available data showed similar outcomes in both groups.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency
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