{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T09:40:41Z","timestamp":1793353241211,"version":"4.5.0"},"reference-count":134,"publisher":"American Society of Hematology","issue":"11","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2020,9,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Glucose 6-phosphate dehydrogenase (G6PD) deficiency is 1 of the commonest human enzymopathies, caused by inherited mutations of the X-linked gene G6PD. G6PD deficiency makes red cells highly vulnerable to oxidative damage, and therefore susceptible to hemolysis. Over 200 G6PD mutations are known: approximately one-half are polymorphic and therefore common in various populations. Some 500 million persons with any of these mutations are mostly asymptomatic throughout their lifetime; however, any of them may develop acute and sometimes very severe hemolytic anemia when triggered by ingestion of fava beans, by any of a number of drugs (for example, primaquine, rasburicase), or, more rarely, by infection. Approximately one-half of the G6PD mutations are instead sporadic: rare patients with these mutations present with chronic nonspherocytic hemolytic anemia. Almost all G6PD mutations are missense mutations, causing amino acid replacements that entail deficiency of G6PD enzyme activity: they compromise the stability of the protein, the catalytic activity is decreased, or a combination of both mechanisms occurs. Thus, genotype-phenotype correlations have been reasonably well clarified in many cases. G6PD deficiency correlates remarkably, in its geographic distribution, with past\/present malaria endemicity: indeed, it is a unique example of an X-linked human polymorphism balanced through protection of heterozygotes from malaria mortality. Acute hemolytic anemia can be managed effectively provided it is promptly diagnosed. Reliable diagnostic procedures are available, with point-of-care tests becoming increasingly important where primaquine and its recently introduced analog tafenoquine are required for the elimination of malaria.<\/jats:p>","DOI":"10.1182\/blood.2019000944","type":"journal-article","created":{"date-parts":[[2020,7,23]],"date-time":"2020-07-23T21:57:35Z","timestamp":1595541455000},"page":"1225-1240","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":396,"title":["Glucose-6-phosphate dehydrogenase deficiency"],"prefix":"10.1182","volume":"136","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4663-8790","authenticated-orcid":false,"given":"Lucio","family":"Luzzatto","sequence":"first","affiliation":[{"name":"Department of Haematology and Blood Transfusion, Muhimbili University of Health and Allied Sciences, Dar es Salaam, United Republic of Tanzania;"},{"name":"Department of Hematology, University of Florence, Florence, Italy; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mwashungi","family":"Ally","sequence":"additional","affiliation":[{"name":"Department of Haematology and Blood Transfusion, Muhimbili University of Health and Allied Sciences, Dar es Salaam, United Republic of Tanzania;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9087-9404","authenticated-orcid":false,"given":"Rosario","family":"Notaro","sequence":"additional","affiliation":[{"name":"Laboratory of Cancer Genetics and Gene Transfer, Core Research Laboratory, Institute for Cancer Research, Prevention and Clinical Network (ISPRO), Florence, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"234","reference":[{"key":"2020091011284456400_B1","first-page":"438","article-title":"Uber ein neues oxydationsferment und sein absorptionsspektrum","volume":"254","author":"Warburg","year":"1932","journal-title":"Biochem Z"},{"issue":"3220","key":"2020091011284456400_B2","doi-asserted-by":"crossref","first-page":"484","DOI":"10.1126\/science.124.3220.484-a","article-title":"Enzymatic deficiency in primaquine-sensitive erythrocytes","volume":"124","author":"Alving","year":"1956","journal-title":"Science"},{"issue":"7","key":"2020091011284456400_B3","first-page":"327","article-title":"New aspects of the biochemical alterations in the erythrocytes of patients with favism; almost complete absence of glucose-6-phosphate dehydrogenase [in Italian]","volume":"34","author":"Sansone","year":"1958","journal-title":"Boll Soc Ital Biol Sper"},{"issue":"4618","key":"2020091011284456400_B4","doi-asserted-by":"crossref","first-page":"1256","DOI":"10.1038\/1811256a0","article-title":"Enzymatic abnormality in erythrocytes of a population sensitive to Vicia faba or haemolytic anemia induced by drugs","volume":"181","author":"Szeinberg","year":"1958","journal-title":"Nature"},{"issue":"7159","key":"2020091011284456400_B5","doi-asserted-by":"crossref","first-page":"1093","DOI":"10.1016\/S0140-6736(60)92177-2","article-title":"Erythrocyte enzyme deficiency in unexplained kernicterus [letter]","volume":"2","author":"Panizon","year":"1960","journal-title":"Lancet"},{"issue":"7172","key":"2020091011284456400_B6","doi-asserted-by":"crossref","first-page":"297","DOI":"10.1016\/S0140-6736(61)91476-3","article-title":"Glucose-6-phosphate dehydrogenase deficiency. 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