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Region (year)
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Findings
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Reference
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Oriximiná, in the northeast of the state of Pará, Brazilian Amazon (2011)
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In an Afro-descendant population, molecular genotyping revealed the presence of G6PD variants in 24% (126/522) of the individuals studied (5% male and 19% female). The G6PD*A– variant was identified in 10 (1.9%) hemizygous males and in 36 (6.5%) females (32 heterozygous and 4 homozygous). The Mediterranean variant was not detected
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Oliveira, et al. Genet Mol BIol 2018;41:758–765.
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Alto do Juruá valley, Acre, western Brazilian Amazon (2016)
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A survey of healthy males using the fluorescent spot test found a G6PD deficiency prevalence of 4.7% (20/423) in those of non-European descent and 4.3% (3/70) of those of European descent. 22/23 of the G6PD-deficient individuals had the G6PD*A− variant and one was G6PD*A
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Dombrowski, et al. Malar J 2017;16:253.
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Manaus (2013–2014)
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In suspected malaria cases in males, the spectrophotometric assay indicated a G6PD deficiency prevalence of 13.6% (92/674) using <60% enzyme activity to define G6PD-deficienc y. Of five genotypic variants investigated, only African variants G6PD*A− and G6PD*A were identified
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Peixoto, et al. Trop Med Int Health 2017;22:21–31.
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Minas Gerais (before 2016)
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In children with sickle-cell anaemia, the prevalence of G6PD deficiency assessed using an enzymatic-colorimetric assay was 4.3% (17/395)
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Belisário, et al. Pediatr Blood Cancer 2016;63:1046–9.
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Manaus (2011–2012)
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Using the spectrophotometric test, 2.9% (1/35) of males and 0% (0/7) females were G6PD deficient
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Osorio, et al. Am J Trop Med Hyg 2015;92:22–7.
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Meta-analysis (data published before 2014)
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A meta-analysis indicated a prevalence of G6PD deficiency of 0–12.9% in males (n=28,617) and 0–13.6% in females (n=6,709) with a range of prevalence of 1.1–13.3%
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Monteiro et al. Mem Inst Oswaldo Cruz 2014;109:553–68.
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Manaus (2009–2010)
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In a survey of randomly selected males, 4.5% (66/1478) were G6PD deficient. 84.8% (56/66) had the G6PD*A− variant, and 15.2% (10/66) had Mediterranean variant
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Santana, et al. Am J Trop Med Hyg 2014;91:74–6.
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Acrelândia, northwest Brazil (2007)
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In a community survey in children, 8.9% (7.2–10.8) (n=1104) were G6PD-deficient
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Cardoso, et al. PLoS One 2012;7:e36341.
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Porto Alegre (2007)
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In a survey of newborns admitted to hospital for phototherapy, sixteen (6.2%, 16/258) boys and 6 (2.7%, 6/222) girls had G6PD deficiency. By ethnic group, 15 (4%, 15/368) were white, 4 (7%, 4/56) were black and 3 (5.4%, 3/56) were mulatto. All cases with an identified genotype were G6PD*A−, there were no cases with G6PD Mediterranean
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Carvalho, et al. Asian Pac J Trop Biomed 2011;1:110–3.
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São Paulo (2008)
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In a survey of newborns using Brewer’s test, G6PD deficiency was present in 6.1% (37/571). 19 (3.1% of the total sample) had a very low enzyme activity (18 male hemizygotes and one female heterozygote. All cases were G6PD*A− and G6PD Mediterranean was not detected
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Mezzacappa, et al. J Perinatol 2010;30:819–26.
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Ismail Aziz Community, on the outskirts of Manaus, Brazilian Amazon (2006)
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In a survey of men in a malaria endemic area, 3% (6/200) were G6PD deficient using the qualitative Brewer's test. Gel electrophoresis showed that five of these subjects were G6PD*A–
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Santana, et al. PLoS One 2009;4:e5259.
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São Paulo State (before 2009)
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In a survey in healthy adult men using a red-cell G6PD activity assay, 4.0% (15/373) were G6PD deficient. In children admitted to hospital for suspected enzymopathies, 12/21 (57%) were G6PD deficient. Twelve G6PD*A– and two G6PD Seattle, as well as a new variant identified as G6PD São Paulo, were detected among adults, and 11 G6PD*A− and one G6PD Seattle were found among children
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Oliveria, et al. Genet Mol Biol 2009;32:251–4.
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Rio Grande do Sul, southern Brazil (2003)
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A survey of newborn blood samples using quantitative measurement of G6PD found1.4% (39/2799) were fully G6PD deficient and 6.4% (178/2799) had partial deficiency, for an overall prevalence of 7.9%. The overall prevalence of G6PD-deficiency in males was 8.7% (124/1433) and in females was 7.0% (94/1339)
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Castro, et al. J Med Screen 2006;13:85–86.
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Belém (before 2002)
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Genetic analysis of G6PD-deficient male blood donors, showed that 82% (161/196) were G6PD*A− (202G>A, 376A>G) and 7.1% (14/196) had G6PD*A– (968T>C, 376A>G). Other variants identified were: G6PD Seattle in 4.6%, G6PD Santamaria in 2.5%, and G6PD Tokyo in one. Four novel variants were also identified: G6PD Belém, G6PD Ananindeua, G6PD Crispim and G6PD Amazonia
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Hamel, et al. Blood Cells Mol Dis 2002;28:399–406.
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Bragança Paulista, São Paulo State (1995–1998)
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In male blood donors, the prevalence of G6PD deficiency was 1.7% (80/4621) using Brewer’s method confirmed with enzymatic assay. Of these 80 subjects, 69 were G6PD*A− (86%). G6PD Mediterranean was not found but a probable Chatham variant was detected
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Compri, et al. Cad Saude Publica 2000;16:335–42.
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Nationwide (before 1998)
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In a large survey of 4,558 European-derived, 2,484 mixed with black heritage, and 10,298 Amerindian subjects the overall prevalence was 0.6% (98/17340). There were no G6PD-deficient genotypes found in Amerindians. Seven different types (besides the most common Gd*B, Gd*A, Gd*A– and Gd*Med) were observed among the Europeans, including G6PD Seattle, plus two new mutations G6PD Farroupilhaand and G6PD Lages
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Weimer, et al. Hum Hered 1998;48:92–6.
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Campinas, southeastern Brazil (before 1997)
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In 150 unrelated G6PD-deficient blood donors, 146 (97.3%) were G6PD*A−. G6PD Mediterranean was present in three individuals and one had G6PD Chatham
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Saad, et al. Hum Hered 1997;47:17–21.
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Campinas, southeastern Brazil (before 1995)
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In individuals with sickle cell anaemia 16% (6/37) of males and 16% (9/55) of females had the G6PD*A− genotype; values for controls were 9% (3/37) for males and 24% (6/25) for females (one homozygote)
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Saad, et al. Blood 1995;85;601–2.
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Nationwide (before 1993)
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Electrophoretic surveys of 7794 individuals from different regions of Brazil and a study of subjects with haemolytic anaemia disclosed 9 putative G6PD variants in addition to the B, A, A–, and Mediterranean types. Four variants underwent DNA analysis. Three were identified as G6PD Mediterranean, Seattle, and Anaheim, but the fourth variant was novel (G6PD São Borja). No variants were found among the 3739 Brazilian Amerindians tested.
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Weimer, et al. 1993;65:41–47.
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Campinas, southeastern Brazil (before 1992)
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In male patients with sickle cell diseases G6PD deficiency prevalence was 13% (7/54); all were G6PD*A−
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Saad, et al. Hum Hered 1992;42:125–8.
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