{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T06:32:57Z","timestamp":1785306777648,"version":"3.55.0"},"reference-count":26,"publisher":"Springer Science and Business Media LLC","issue":"1","content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Malar J"],"published-print":{"date-parts":[[2013,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n          <jats:sec>\n            <jats:title>Background<\/jats:title>\n            <jats:p>Glucose-6-phosphate dehydrogenase (G6PD) deficiency is particularly prevalent in historically malaria-endemic countries. Although most individuals with G6PD deficiency are asymptomatic, deficiency can result in acute haemolytic anaemia after exposure to oxidative agents. A reliable test is necessary for diagnosing the deficiency to prevent an acute haemolytic crisis following, for example, anti-malarial treatment. The aim of this study was to investigate which method was the best predictor of this disorder.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>The present study investigated four G6PD activity detections (fluorescence spot (FS), methaemoglobin reduction (MR), biochemical and cytochemical test). These methods accompanied with mutation analysis of blood samples were taken from 295 apparently healthy individuals with unknown G6PD deficiency status.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Molecular characterization of 295 Thai adults revealed an overall prevalence of 14.2%. The G6PD Viangchan (871 G&gt;A) was the most common (83.3%), followed by G6PD Mahidol (487G&gt;A) (11.9%), and G6PD Union (1360 C&gt;T) (4.8%). There were two cases of G6PD deficiency carrying the double mutations of Viangchan (871G\u2009&gt;\u2009A)-Mahidol (487G\u2009&gt;\u2009A) and Viangchan (871G\u2009&gt;\u2009A)-Union (1360C\u2009&gt;\u2009T). In comparison, the prevalence of G6PD deficiency was 6.1% by FS test and 7.1% by MR test. G6PD activity was 11 \u00b1 2.5 IU\/gHb in non-deficient females (mean \u00b1 SD), and 10.9 \u00b1 0.6 IU\/gHb in non-deficient males. The upper and lower limit cut-off points for partial and severe deficiency in adults were 5.7 IU\/gHb (60% of the normal mean) and 0.95 IU\/gHb (10% of the normal mean), respectively. All hemizygote, homozygote and double mutations were associated with severe enzyme deficiency (the residual enzyme activity &lt;10% of the normal mean), whereas only 14.3% of the heterozygote mutations showed severe enzyme deficiency. Based on the cut-off value &lt;5.7 IU\/gHb, the quantitative G6PD assay diagnosed 83% of cases as G6PD-deficient. Using a cut-off number of negative cell &gt;20% in the cytochemical assay to define G6PD deficiency, the prevalence of G6PD deficiency was closest to the molecular analysis (12.9% G6PD-deficient) compared to the others methods.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>The cytochemical method is a significant predictor of this disease, while FS and MR test are recommended for the detection of severe G6PD deficiency in developing countries.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1475-2875-12-289","type":"journal-article","created":{"date-parts":[[2013,8,21]],"date-time":"2013-08-21T14:14:27Z","timestamp":1377094467000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":50,"title":["Evaluation of the phenotypic test and genetic analysis in the detection of glucose-6-phosphate dehydrogenase deficiency"],"prefix":"10.1186","volume":"12","author":[{"given":"Duangdao","family":"Nantakomol","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rick","family":"Paul","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Attakorn","family":"Palasuwan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas PJ","family":"Day","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas J","family":"White","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mallika","family":"Imwong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2013,8,21]]},"reference":[{"key":"2902_CR1","doi-asserted-by":"crossref","first-page":"3613","DOI":"10.1182\/blood.V84.11.3613.bloodjournal84113613","volume":"84","author":"E Beutler","year":"1994","unstructured":"Beutler E: G6PD deficiency. Blood. 1994, 84: 3613-3636.","journal-title":"Blood"},{"key":"2902_CR2","first-page":"193","volume":"35","author":"AM Salvati","year":"1999","unstructured":"Salvati AM, Maffi D, Caprari P, Pasquino MT, Caforio MP, Tarzia A: Glucose-6-phosphate dehydrogenase deficiency and hereditary hemolytic anemia. Ann Ist Super Sanita. 1999, 35: 193-203.","journal-title":"Ann Ist Super Sanita"},{"key":"2902_CR3","doi-asserted-by":"publisher","first-page":"e7246","DOI":"10.1371\/journal.pone.0007246","volume":"4","author":"MK Johnson","year":"2009","unstructured":"Johnson MK, Clark TD, Njama-Meya D, Rosenthal DPJ, Parikh S: Impact of the method of G6PD deficiency assessment on genetic association studies of malaria susceptibility. PLoS One. 2009, 4: e7246-10.1371\/journal.pone.0007246.","journal-title":"PLoS One"},{"key":"2902_CR4","doi-asserted-by":"publisher","first-page":"220","DOI":"10.1016\/0035-9203(94)90306-9","volume":"88","author":"KN Bangchang","year":"1994","unstructured":"Bangchang KN, Songsaeng KNW, Thanavibul A, Choroenlarp P, Karbwang J: Pharmacokinetics of primaquine in G6PD deficient and G6PD normal patients with vivax malaria. Trans R Soc Trop Med Hyg. 1994, 88: 220-222. 10.1016\/0035-9203(94)90306-9.","journal-title":"Trans R Soc Trop Med Hyg"},{"key":"2902_CR5","first-page":"303","volume":"36","author":"GJ Brewer","year":"1967","unstructured":"Brewer GJ, Zarafonetis CJ: The haemolytic effect of various regimens of primaquine with chloroquine in American Negroes with G6PD deficiency and the lack of an effect of various antimalarial suppressive agents on erythrocyte metabolism. Bull World Health Organ. 1967, 36: 303-308.","journal-title":"Bull World Health Organ"},{"key":"2902_CR6","first-page":"710","volume":"25","author":"K Myat Phone","year":"1994","unstructured":"Myat Phone K, Myint O, Aung N, Aye Lwin H: The use of primaquine in malaria infected patients with red cell glucose-6-phosphate dehydrogenase (G6PD) deficiency in Myanmar. Southeast Asian J Trop Med Public Health. 1994, 25: 710-713.","journal-title":"Southeast Asian J Trop Med Public Health"},{"key":"2902_CR7","first-page":"177","volume":"36","author":"CE Amiwero","year":"2007","unstructured":"Amiwero CE, Olatunji PO: Re-evaluation of methaemoglobin reduction as a screening procedure for glucose-6-phosphate dehydrogenase (G6PD). Afr J Med Med Sci. 2007, 36: 177-181.","journal-title":"Afr J Med Med Sci"},{"issue":"Suppl 1","key":"2902_CR8","first-page":"S91","volume":"84","author":"S Sanpavat","year":"2001","unstructured":"Sanpavat S, Nuchprayoon I, Kittikalayawong A, Ungbumnet W: The value of methemoglobin reduction test as a screening test for neonatal glucose 6-phosphate dehydrogenase deficiency. J Med Assoc Thai. 2001, 84 (Suppl 1): S91-S98.","journal-title":"J Med Assoc Thai"},{"key":"2902_CR9","doi-asserted-by":"publisher","first-page":"46","DOI":"10.1136\/jms.7.1.46","volume":"7","author":"GJ Reclos","year":"2000","unstructured":"Reclos GJ, Hatzidakis CJ, Schulpis KH: Glucose-6-phosphate dehydrogenase deficiency neonatal screening: preliminary evidence that a high percentage of partially deficient female neonates are missed during routine screening. J Med Screen. 2000, 7: 46-51. 10.1136\/jms.7.1.46.","journal-title":"J Med Screen"},{"key":"2902_CR10","doi-asserted-by":"publisher","first-page":"493","DOI":"10.1007\/BF00640601","volume":"75","author":"CJ van Noorden","year":"1982","unstructured":"van Noorden CJ, Vogels IM, James J, Tas J: A sensitive cytochemical staining method for glucose-6-phosphate dehydrogenase activity in individual erythrocytes. I. Optimalization of the staining procedure. Histochemistry. 1982, 75: 493-506.","journal-title":"Histochemistry"},{"key":"2902_CR11","first-page":"405","volume":"34","author":"OA Ainoon","year":"2003","unstructured":"Ainoon OA, Alawiyah A, Yu YH, Cheong SK, Hamidah NH, Boo NY, Zaleha M: Semiquantitative screening test for G6PD deficiency detects severe deficiency but misses a substantial proportion of partially-deficient females. Southeast Asian J Trop Med Public Health. 2003, 34: 405-414.","journal-title":"Southeast Asian J Trop Med Public Health"},{"key":"2902_CR12","doi-asserted-by":"publisher","first-page":"445","DOI":"10.1007\/s004390100527","volume":"108","author":"K Iwai","year":"2001","unstructured":"Iwai K, Hirono A, Matsuoka H, Kawamoto F, Horie T, Lin K, Tantular IS, Dachlan YP, Notopuro H, Hidayah NI, Salim AM, Fujii H, Miwa S, Ishii A: Distribution of glucose-6-phosphate dehydrogenase mutations in Southeast Asia. Hum Genet. 2001, 108: 445-449. 10.1007\/s004390100527.","journal-title":"Hum Genet"},{"key":"2902_CR13","doi-asserted-by":"publisher","first-page":"448","DOI":"10.1007\/s10038-005-0276-2","volume":"50","author":"C Louicharoen","year":"2005","unstructured":"Louicharoen C, Nuchprayoon I: G6PD Viangchan (871G\u2009>\u2009A) is the most common G6PD-deficient variant in the Cambodian population. J Hum Genet. 2005, 50: 448-452. 10.1007\/s10038-005-0276-2.","journal-title":"J Hum Genet"},{"key":"2902_CR14","doi-asserted-by":"publisher","first-page":"544","DOI":"10.1007\/s10038-004-0187-7","volume":"49","author":"H Matsuoka","year":"2004","unstructured":"Matsuoka H, Wang J, Hirai M, Arai M, Yoshida S, Kobayashi T, Jalloh A, Lin K, Kawamoto F: Glucose-6-phosphate dehydrogenase (G6PD) mutations in Myanmar: G6PD Mahidol (487G\u2009>\u2009A) is the most common variant in the Myanmar population. J Hum Genet. 2004, 49: 544-547. 10.1007\/s10038-004-0187-7.","journal-title":"J Hum Genet"},{"key":"2902_CR15","doi-asserted-by":"publisher","first-page":"468","DOI":"10.1007\/s10038-005-0279-z","volume":"50","author":"H Matsuoka","year":"2005","unstructured":"Matsuoka H, Nguon C, Kanbe T, Jalloh A, Sato H, Yoshida S, Hirai M, Arai M, Socheat D, Kawamoto F: Glucose-6-phosphate dehydrogenase (G6PD) mutations in Cambodia: G6PD Viangchan (871G\u2009>\u2009A) is the most common variant in the Cambodian population. J Hum Genet. 2005, 50: 468-472. 10.1007\/s10038-005-0279-z.","journal-title":"J Hum Genet"},{"key":"2902_CR16","doi-asserted-by":"publisher","first-page":"185","DOI":"10.1002\/humu.9010","volume":"19","author":"I Nuchprayoon","year":"2002","unstructured":"Nuchprayoon I, Sanpavat S, Nuchprayoon S: Glucose-6-phosphate dehydrogenase (G6PD) mutations in Thailand: G6PD Viangchan (871G\u2009>\u2009A) is the most common deficiency variant in the Thai population. Hum Mutat. 2002, 19: 185-","journal-title":"Hum Mutat"},{"key":"2902_CR17","doi-asserted-by":"publisher","first-page":"48","DOI":"10.1007\/s10038-007-0217-3","volume":"53","author":"I Nuchprayoon","year":"2008","unstructured":"Nuchprayoon I, Louicharoen C, Charoenwej W: Glucose-6-phosphate dehydrogenase mutations in Mon and Burmese of southern Myanmar. J Hum Genet. 2008, 53: 48-54. 10.1007\/s10038-007-0217-3.","journal-title":"J Hum Genet"},{"key":"2902_CR18","unstructured":"Primer3.http:\/\/frodo.wi.mit.edu\/cgi-in\/primer3\/primer3,"},{"key":"2902_CR19","unstructured":"Life technologies.http:\/\/resource.lifetechnologies.com\/pages\/WE28396\/,"},{"key":"2902_CR20","doi-asserted-by":"publisher","first-page":"386","DOI":"10.1001\/jama.1962.03050180032008","volume":"180","author":"GJ Brewer","year":"1962","unstructured":"Brewer GJ, Tarlov AR, Alving AS: The methemoglobin reduction test for primaquine-type sensitivity of erythrocytes. A simplified procedure for detecting a specific hypersusceptibility to drug hemolysis. JAMA. 1962, 180: 386-388. 10.1001\/jama.1962.03050180032008.","journal-title":"JAMA"},{"key":"2902_CR21","doi-asserted-by":"publisher","first-page":"1313","DOI":"10.1177\/37.9.2768805","volume":"37","author":"CJ Van Noorden","year":"1989","unstructured":"Van Noorden CJ, Dolbeare F, Aten J: Flow cytofluorometric analysis of enzyme reactions based on quenching of fluorescence by the final reaction product: detection of glucose-6-phosphate dehydrogenase deficiency in human erythrocytes. J Histochem Cytochem. 1989, 37: 1313-1318. 10.1177\/37.9.2768805.","journal-title":"J Histochem Cytochem"},{"key":"2902_CR22","first-page":"601","volume":"67","author":"WHO","year":"1989","unstructured":"WHO: Glucose\u20136 - phosphate dehydrogenase deficiency. Bull World Health Organ. 1989, 67: 601-611.","journal-title":"Bull World Health Organ"},{"key":"2902_CR23","first-page":"576","volume":"55","author":"V Panich","year":"1972","unstructured":"Panich V, Sungnate T, Wasi P, Na-Nakorn S: G-6-PD Mahidol. The most common glucose-6-phosphate dehydrogenase variant in Thailand. J Med Assoc Thai. 1972, 55: 576-585.","journal-title":"J Med Assoc Thai"},{"key":"2902_CR24","doi-asserted-by":"publisher","first-page":"1546","DOI":"10.1126\/science.1178849","volume":"326","author":"C Louicharoen","year":"2009","unstructured":"Louicharoen C, Patin E, Paul R, Nuchprayoon I, Witoonpanich B, Peerapittayamongkol C, Casademont I, Sura T, Laird NM, Singhasivanon P, Quintana-Murci L, Sakuntabhai A: Positively selected G6PD-Mahidol mutation reduces Plasmodium vivax density in Southeast Asians. Science. 2009, 326: 1546-1549. 10.1126\/science.1178849.","journal-title":"Science"},{"issue":"Suppl 1","key":"2902_CR25","doi-asserted-by":"publisher","first-page":"S8","DOI":"10.1186\/1475-2875-7-S1-S8","volume":"7","author":"NJ White","year":"2008","unstructured":"White NJ: The role of anti-malarial drugs in eliminating malaria. Malar J. 2008, 7 (Suppl 1): S8-10.1186\/1475-2875-7-S1-S8.","journal-title":"Malar J"},{"key":"2902_CR26","doi-asserted-by":"publisher","first-page":"376","DOI":"10.1186\/1475-2875-9-376","volume":"9","author":"KL Burgoine","year":"2010","unstructured":"Burgoine KL, Bancone G, Nosten F: The reality of using primaquine. Malar J. 2010, 9: 376-10.1186\/1475-2875-9-376.","journal-title":"Malar J"}],"container-title":["Malaria Journal"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/link.springer.com\/content\/pdf\/10.1186\/1475-2875-12-289.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,9,2]],"date-time":"2021-09-02T01:07:04Z","timestamp":1630544824000},"score":1,"resource":{"primary":{"URL":"https:\/\/malariajournal.biomedcentral.com\/articles\/10.1186\/1475-2875-12-289"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2013,8,21]]},"references-count":26,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2013,12]]}},"alternative-id":["2902"],"URL":"https:\/\/doi.org\/10.1186\/1475-2875-12-289","relation":{},"ISSN":["1475-2875"],"issn-type":[{"value":"1475-2875","type":"electronic"}],"subject":[],"published":{"date-parts":[[2013,8,21]]},"assertion":[{"value":"22 May 2013","order":1,"name":"received","label":"Received","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"18 August 2013","order":2,"name":"accepted","label":"Accepted","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"21 August 2013","order":3,"name":"first_online","label":"First Online","group":{"name":"ArticleHistory","label":"Article History"}}],"article-number":"289"}}