Displaying publications 41 - 60 of 83 in total

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  1. Jalloh S, Van Rostenberghe H, Yusoff NM, Ghazali S, Nik Ismail NZ, Matsuo M, et al.
    Pediatr Int, 2005 Jun;47(3):258-61.
    PMID: 15910447
    The role of hemolysis in the pathophysiology of neonatal jaundice (NNJ) in patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency has been questioned recently. The aim of the present study was to determine the contribution of hemolysis to the pathophysiology of jaundice in Malay neonates with G6PD deficiency and NNJ.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/blood; Glucosephosphate Dehydrogenase Deficiency/physiopathology*
  2. Saha N, Mak JW, Tay JS, Liu Y, Tan JA, Low PS, et al.
    Hum Biol, 1995 Feb;67(1):37-57.
    PMID: 7721278
    A population genetic study was undertaken to provide gene frequency data on the additional blood genetic markers in the Semai and to estimate the genetic relations between the Semai and their neighboring and linguistically related populations by genetic distance and principal components analyses. Altogether 10 polymorphic and 7 monomorphic blood genetic markers (plasma proteins and red cell enzymes) were studied in a group of 349 Senoi Semai from 11 aboriginal settlements (villages) in the Pahang State of western Malaysia. Both the red cell glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (PGD) loci reveal the presence of polymorphic frequencies of a nondeficient slow allele at the G6PD locus and a fast allele at the PGD locus. The Semai are characterized by high prevalences of ahaptoglobinemia and G6PD deficiency, high frequencies of HP*1, HB*E, RH*R1, ACP*C, GLO1*1, PGM1*2+, and GC*1F and corresponding low frequencies of ABO*A, HbCoSp, HB*B0, TF*D, CHI, and GC*2. Genetic distance analyses by both cluster and principal components models were performed between the Semai and 14 other populations (Malay; Javanese; Khmer; Veddah; Tamils of Malaysia, Sri Lanka, and India; Sinhalese; Oraon; Toda and Irula of India; Chinese; Japanese; Koreans) on the basis of 30 alleles at 7 polymorphic loci. A more detailed analysis using 53 alleles at 13 polymorphic loci with 10 populations was carried out. Both analyses give genetic evidence of a close relationship between the Semai and the Khmer of Cambodia. Furthermore, the Semai are more closely related to the Javanese than to their close neighbors--the Malay, Chinese, and Tamil Indians. There is no evidence for close genetic relationship between the Semai and the Veddah or other Indian tribes. The evidence fits well with the linguistic relationship of the Semai with the Mon-Khmer branch of the Austro-Asiatic language family.
    Matched MeSH terms: Glucosephosphate Dehydrogenase/blood; Glucosephosphate Dehydrogenase/genetics*
  3. Kandasamy Y, Somasundram P
    Singapore Med J, 2007 Oct;48(10):926-8.
    PMID: 17909678
    The Orang Asli are the indigenous population in peninsular Malaysia and are in fact a diverse sub-ethnic group with different languages. Our aim was to collect data on Orang Asli newborns, from western and central Pahang, that were admitted to a general hospital with paediatric specialist services.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/ethnology*; Glucosephosphate Dehydrogenase Deficiency/epidemiology
  4. Lee SW, Chaiyakunapruk N, Lai NM
    Br J Clin Pharmacol, 2017 01;83(1):211-212.
    PMID: 27650490 DOI: 10.1111/bcp.13091
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/blood; Glucosephosphate Dehydrogenase Deficiency/complications; Glucosephosphate Dehydrogenase Deficiency/diet therapy*
  5. Lie-Injo LE, Ng T, Balakrishnan S
    Clin Chim Acta, 1974 Jan 19;50(1):77-83.
    PMID: 4856203 DOI: 10.1016/0009-8981(74)90079-5
    Matched MeSH terms: Glucosephosphate Dehydrogenase/blood; Glucosephosphate Dehydrogenase Deficiency/blood
  6. Saha N, Toh CC, Ghosh MB
    J Med Genet, 1973 Dec;10(4):340-5.
    PMID: 4204387
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/complications; Glucosephosphate Dehydrogenase Deficiency/genetics*; Glucosephosphate Dehydrogenase Deficiency/epidemiology
  7. Suria AA, Nurasyikin Y, Adibah AG, Cheah FC, Leong CF
    Clin Ter, 2014;165(3):151-4.
    PMID: 24999569 DOI: 10.7417/CT.2014.1714
    ABO incompatibility and glucose-6-phosphate dehydrogenase deficiency G6PD are common haematological problems affecting the newborn. The resulting haemolytic disease of foetus and newborn (HDFN) caused by either of these pathologies generally follows a benign course. It is typically characterized by mild jaundice without significant anaemia. ABO incompatibility alone as a cause of foetal hydrops is extremely rare. We report a case of a newborn baby girl with an anti-B isoimmunisation and G6PD deficiency manifesting with hydrops foetalis, anaemia and hyperbilirubinaemia, born to a mother with blood group O.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency
  8. Boo NY, Ainoon BO, Ooi LH, Cheong SK, Haliza BM
    J Paediatr Child Health, 1994 Jun;30(3):273-4.
    PMID: 8074916
    The cord blood glucose-6-phosphate dehydrogenase (G6PD) enzyme activity of 262 normal term Malaysian neonates (92 Malays, 96 Chinese and 74 Indians) was quantitatively determined by the World Health Organisation method. Analysis of variance for the levels of G6PD enzyme activity by ethnic origin and sex showed that there was a significant difference between mean levels of enzyme activity in the three ethnic groups (P = 0.03) but no difference between the sexes (P = 0.36). Multiple range analysis showed that Malays had significantly higher mean levels of G6PD enzyme activity than those of Chinese (P = 0.01). There was no significant difference between the mean levels of G6PD enzyme activity of Chinese and Indians (P = 0.52), nor was there any difference between those of Malays and Indians (P = 0.08). The difference in levels of G6PD enzyme activity among the different ethnic groups could be due to the existence of different G6PD variants.
    Matched MeSH terms: Glucosephosphate Dehydrogenase/blood*
  9. George E
    Ann Acad Med Singap, 1994 Jan;23(1):89-93.
    PMID: 7514384
    The clinical severity of the mutations causing beta-thalassaemia in West Malaysia is presented. Thalassaemia clinical scores (Thal CS), a scoring system, has been formulated to predict clinical severity. It is the type of beta-thalassaemia mutation present that decides on the clinical phenotype. The most severe beta-thalassaemia mutation is assigned a score of 4. A score of 8 indicates a severe thalassaemia phenotype. Alpha-thalassaemia, increased synthesis of Hb F, and glucose-6-phosphate deficiency may ameliorate the clinical condition at phenotype level, and the co-inheritance of hereditary ovalocytosis aggravates it.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/complications
  10. Saha N, Banerjee B
    Trop Geogr Med, 1971 Jun;23(2):141-4.
    PMID: 5568538
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/epidemiology*
  11. Lie-Injo Luan Eng, Pillay RP, Virik HK
    Trans R Soc Trop Med Hyg, 1966;60(2):262-6.
    PMID: 5922616 DOI: 10.1016/0035-9203(66)90039-3
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/epidemiology*
  12. Hayati Mansor, Eusni Rahayu Mohd. Tohit, Faridah Idris, Alawiyah Abdul Rahman
    MyJurnal
    Introduction: Glucose-6-phosphate dehydrogenase (G6PD) deficiency causes red blood cell destruction due to oxi- dative stress. G6PD is essential for NADPH conversion; which is critical for glutathione reductase to prevent damage to cellular structures. In Malaysia, blood donors are not routinely screened for G6PD deficiency. We hypothesise that G6PD-deficient red blood cells are more likely to haemolyse during storage due to increased oxidative molecules. The objectives of this study were to determine the prevalence of G6PD deficiency among blood donors, describe their characteristics and to evaluate the effects of storage on G6PD-deficient donated blood. Methods: This study was conducted at selected mobile donation centres in Terengganu. Consented blood donors were screened for G6PD sta- tus using fluorescent spot tests (FST). G6PD enzyme activities were measured for donors who were G6PD deficient. Effects of storage on haemolysis from G6PD-deficient donors were compared with non G6PD-deficient group. Sixty ml of blood was collected from blood unit to transfer pouch for estimation of haemoglobin (Hb), plasma Hb, per- centage of haemolysis and plasma potassium. Serial sampling with a 7-day interval was done from Day 1 to Day 35. Statistical analysis was considered significant if p 0.05. Results: A total of 440 blood donors were screened and 12 male donors were found to be G6PD deficient by FST. Enzymatic activities were measured in 11 donors as one donor sample failed to be sent to the centre due to logistic problem. Their enzymatic activities ranged from 1.66-2.93 U/g Hb whereby 6 have severe deficiency and the other 5 were categorised as partial deficiency. Donors were asymp- tomatic for haemolytic episode. Serial sampling showed there was no significant difference of haemolytic parameters in blood units of G6PD-deficient donors as compared to control (p>0.05). Conclusion: Prevalence of G6PD blood donors in Terengganu mobile centres was 2.7%. G6PD enzyme activities did not correlate with clinical symptoms. Haemolytic parameters were not affected in blood units which were G6PD-deficient.
    Matched MeSH terms: Glucosephosphate Dehydrogenase; Glucosephosphate Dehydrogenase Deficiency
  13. Azma RZ, Hidayati N, Farisah NR, Hamidah NH, Ainoon O
    PMID: 21073074
    Glucose-6-phosphate dehydrogenase (G6PD) deficiency is one of the commonest causes of neonatal jaundice in Malaysia. Screening of cord blood for G6PD deficiency by the semiquantitative fluorescent spot test (FST) is performed in Malaysia but this test can miss cases of partial G6PD deficiency. The OSMMR-D kit assay measures G6PD activity and hemoglobin (Hb) concentration, allowing direct expression of results in U/gHb. We evaluated this method and established the normal range for G6PD activity in normal term neonates and adults. EDTA blood from 94 neonates and 295 adults (age 15-59 years old) with normal Hb and FST were selected. The normal means for G6PD activity for neonates and adults were 12.43 +/- 2.28 U/gHb and 9.21 +/- 2.6 U/gHb, respectively; the reference ranges for normal G6PD activity in neonates and adults were 10.15-14.71 U/gHb and 6.61-11.81 U/gHb respectively. There were no significant differences in mean normal G6PD activity between the Malays and Chinese racial groups or between genders. The upper and lower limit cut-off points for partial deficiency in neonates were 7.4 U/gHb (60% of the normal mean) and 2.5 U/gHb (20% of the normal mean), respectively. For adults, the upper and lower limit cut-off points for partial deficiency in adults were 5.52 U/gHb (60% of the normal mean) and 1.84 U/gHb (20% of the normal mean), respectively. The quantitation of G6PD enzymes using this OSMMR-D kit with Hb normalization was simple since the Hb was analyzed simultaneously and the results were reproducible with a CV of less than 5%.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/diagnosis*
  14. Matsuo M, Nishiyama K, Shirakawa T, Padilla CD, San LP, Suryantoro P, et al.
    PMID: 15906715
    Glucose-6-phosphate dehydrogenase (G6PD) deficiency is common in malaria endemic regions and is estimated to affect more than 400 million people worldwide. Deficient subjects are mostly asymptomatic but clinical manifestations range from neonatal jaundice due to acute hemolytic anemia to chronic non-spherocytic hemolytic anemia. To date, biochemical parameters allowed more than 400 different G6PD variants to be distinguished thereby suggesting a vast genetic heterogeneity. So far, only a small portion of this heterogeneity has been confirmed at the DNA level with the identification of about 90 different point mutations in the G6PD coding sequence. To determine the molecular background of G6PD deficiency in Southeast Asian countries, we conducted molecular analyses of G6PD patients from the Philippines, Malaysia, Singapore, Vietnam and Indonesia. The most prevalent mutation identified differs from country to country, thus suggesting independent mutational events of the G6PD gene.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/genetics*
  15. Commons RJ, Simpson JA, Thriemer K, Chu CS, Douglas NM, Abreha T, et al.
    BMC Med, 2019 08 01;17(1):151.
    PMID: 31366382 DOI: 10.1186/s12916-019-1386-6
    BACKGROUND: Malaria causes a reduction in haemoglobin that is compounded by primaquine, particularly in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency. The aim of this study was to determine the relative contributions to red cell loss of malaria and primaquine in patients with uncomplicated Plasmodium vivax.

    METHODS: A systematic review identified P. vivax efficacy studies of chloroquine with or without primaquine published between January 2000 and March 2017. Individual patient data were pooled using standardised methodology, and the haematological response versus time was quantified using a multivariable linear mixed effects model with non-linear terms for time. Mean differences in haemoglobin between treatment groups at day of nadir and day 42 were estimated from this model.

    RESULTS: In total, 3421 patients from 29 studies were included: 1692 (49.5%) with normal G6PD status, 1701 (49.7%) with unknown status and 28 (0.8%) deficient or borderline individuals. Of 1975 patients treated with chloroquine alone, the mean haemoglobin fell from 12.22 g/dL [95% CI 11.93, 12.50] on day 0 to a nadir of 11.64 g/dL [11.36, 11.93] on day 2, before rising to 12.88 g/dL [12.60, 13.17] on day 42. In comparison to chloroquine alone, the mean haemoglobin in 1446 patients treated with chloroquine plus primaquine was - 0.13 g/dL [- 0.27, 0.01] lower at day of nadir (p = 0.072), but 0.49 g/dL [0.28, 0.69] higher by day 42 (p  25% to  5 g/dL.

    CONCLUSIONS: Primaquine has the potential to reduce malaria-related anaemia at day 42 and beyond by preventing recurrent parasitaemia. Its widespread implementation will require accurate diagnosis of G6PD deficiency to reduce the risk of drug-induced haemolysis in vulnerable individuals.

    TRIAL REGISTRATION: This trial was registered with PROSPERO: CRD42016053312. The date of the first registration was 23 December 2016.

    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/complications; Glucosephosphate Dehydrogenase Deficiency/diagnosis
  16. 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: Glucosephosphate Dehydrogenase/genetics*; Glucosephosphate Dehydrogenase/metabolism
  17. Wu S, Gu W, Huang A, Li Y, Kumar M, Lim PE, et al.
    Microb Cell Fact, 2019 Sep 23;18(1):161.
    PMID: 31547820 DOI: 10.1186/s12934-019-1214-x
    BACKGROUND: Numerous studies have shown that stress induction and genetic engineering can effectively increase lipid accumulation, but lead to a decrease of growth in the majority of microalgae. We previously found that elevated CO2 concentration increased lipid productivity as well as growth in Phaeodactylum tricornutum, along with an enhancement of the oxidative pentose phosphate pathway (OPPP) activity. The purpose of this work directed toward the verification of the critical role of glucose-6-phosphate dehydrogenase (G6PDH), the rate-limiting enzyme in the OPPP, in lipid accumulation in P. tricornutum and its simultaneous rapid growth rate under high-CO2 (0.15%) cultivation.

    RESULTS: In this study, G6PDH was identified as a target for algal strain improvement, wherein G6PDH gene was successfully overexpressed and antisense knockdown in P. tricornutum, and systematic comparisons of the photosynthesis performance, algal growth, lipid content, fatty acid profiles, NADPH production, G6PDH activity and transcriptional abundance were performed. The results showed that, due to the enhanced G6PDH activity, transcriptional abundance and NAPDH production, overexpression of G6PDH accompanied by high-CO2 cultivation resulted in a much higher of both lipid content and growth in P. tricornutum, while knockdown of G6PDH greatly decreased algal growth as well as lipid accumulation. In addition, the total proportions of saturated and unsaturated fatty acid, especially the polyunsaturated fatty acid eicosapentaenoic acid (EPA; C20:5, n-3), were highly increased in high-CO2 cultivated G6PDH overexpressed strains.

    CONCLUSIONS: The successful of overexpression and antisense knockdown of G6PDH well demonstrated the positive influence of G6PDH on algal growth and lipid accumulation in P. tricornutum. The improvement of algal growth, lipid content as well as polyunsaturated fatty acids in high-CO2 cultivated G6PDH overexpressed P. tricornutum suggested this G6PDH overexpression-high CO2 cultivation pattern provides an efficient and economical route for algal strain improvement to develop algal-based biodiesel production.

    Matched MeSH terms: Glucosephosphate Dehydrogenase
  18. Wan Ya, W. N., Mohsin, H. F., Abdul Wahab, I.
    MyJurnal
    Introduction: Acalypha indica is commonly referred to as “pokok kucing galak”. It is an herbaceous species that grow along the earth’s equator line, including the wet, temperate and tropical regions. Domestic cats experience the effect of this plant by reacting very favorably to the root. The first compilation of the ethnopharmacology and phytochemistry of the Acalypha plants was published. This genus is the fourth largest genus of the Euphorbiaceae family, with about 500 species. However, the review only represents about one third of the species from the Acalypha genus. Methods: Hence, this study is performed to obtain updates on the biochemistry of this plant, via literature search. Results: From the articles, almost every part of the plant, including the leaves, stems and roots, are used as traditional remedies. Local people consume the plant for therapeutic purposes such as anthelminthic, anti-ulcer, anti-bacteria, anti-microbial and wound healing. In homeopathy practice, it is used for asthma and bronchitis. Nevertheless,
    there is still a potential risk of using A. indica. It was reported that this traditional medicine could induce Intravascular haemolysis in patients with a glucose-6-phosphate-dehydrogenase (G6PD) deficiency. Clinical evaluations of Acalypha extract could be utilized to justify the ethnomedicinal claims and for the safety of its therapeutic applications. Meanwhile, there is an increase in the phytochemical and chromatographic experiments of A. indica that could introduce the extract’s role in pharmaceutical, nutraceutical, zoology and veterinary fields. It contains secondary metabolites, including dihydroactinidiolide; a terpenoid, alkaloids, flavonoids and steroids, for example, brassicasterol. Conclusion: The finding of this review concludes that Acalypha is a natural source, worth to be further investigated. It is hoped that new biologically active constituents could be discovered, since only few Acalypha species were comprehensively studied.
    Matched MeSH terms: Glucosephosphate Dehydrogenase
  19. Jalil N, Azma RZ, Mohamed E, Ithnin A, Alauddin H, Baya SN, et al.
    EXCLI J, 2016;15:155-62.
    PMID: 27103895 DOI: 10.17179/excli2015-604
    Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is the commonest cause of neonatal jaundice in Malaysia. Recently, OSMMR2000-D G6PD Assay Kit has been introduced to quantitate the level of G6PD activity in newborns delivered in Universiti Kebangsaan Malaysia Medical Centre (UKMMC). As duration of sample storage prior to analysis is one of the matters of concern, this study was conducted to identify the stability of G6PD enzyme during storage. A total of 188 cord blood samples from normal term newborns delivered at UKMMC were selected for this study. The cord bloods samples were collected in ethylene-diamine-tetra-acetic acid (EDTA) tubes and refrigerated at 2-8 °C. In addition, 32 out of 188 cord blood samples were spotted on chromatography paper, air-dried and stored at room temperature. G6PD enzyme activities were measured daily for 7 days using the OSMMR2000-D G6PD Assay Kit on both the EDTA blood and dried blood samples. The mean value for G6PD activity was compared between days of analysis using Student Paired T-Test. In this study, 172 out of 188 cord blood samples showed normal enzyme levels while 16 had levels corresponding to severe enzyme deficiency. The daily mean G6PD activity for EDTA blood samples of newborns with normal G6PD activity showed a significant drop on the fourth day of storage (p < 0.005) while for samples with severely deficient G6PD activity, significant drop was seen on third day of storage (p = 0.002). Analysis of dried cord blood showed a significant reduction in enzyme activity as early as the second day of storage (p = 0.001). It was also noted that mean G6PD activity for spotted blood samples were lower compared to those in EDTA tubes for all days (p = 0.001). Thus, EDTA blood samples stored at 2-8 °C appeared to have better stability in terms of their G6PD enzyme level as compared to dried blood samples on filter paper, giving a storage time of up to 3 days.
    Matched MeSH terms: Glucosephosphate Dehydrogenase
  20. Ley B, Thriemer K, Jaswal J, Poirot E, Alam MS, Phru CS, et al.
    Malar J, 2017 08 10;16(1):329.
    PMID: 28797255 DOI: 10.1186/s12936-017-1981-y
    BACKGROUND: Primaquine is essential for the radical cure of vivax malaria, however its broad application is hindered by the risk of drug-induced haemolysis in individuals with glucose-6-phosphate-dehydrogenase (G6PD) deficiency. Rapid diagnostic tests capable of diagnosing G6PD deficiency are now available, but these are not used widely.

    METHODS: A series of qualitative interviews were conducted with policy makers and healthcare providers in four vivax-endemic countries. Routine G6PD testing is not part of current policy in Bangladesh, Cambodia or China, but it is in Malaysia. The interviews were analysed with regard to respondents perceptions of vivax malaria, -primaquine based treatment for malaria and the complexities of G6PD deficiency.

    RESULTS: Three barriers to the roll-out of routine G6PD testing were identified in all sites: (a) a perceived low risk of drug-induced haemolysis; (b) the perception that vivax malaria was benign and accordingly treatment with primaquine was not regarded as a priority; and, (c) the additional costs of introducing routine testing. In Malaysia, respondents considered the current test and treat algorithm suitable and the need for an alternative approach was only considered relevant in highly mobile and hard to reach populations.

    CONCLUSIONS: Greater efforts are needed to increase awareness of the benefits of the radical cure of Plasmodium vivax and this should be supported by economic analyses exploring the cost effectiveness of routine G6PD testing.

    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/diagnosis*
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