Molecular genetics of glucose-6-phosphate dehydrogenase deficiency in a population of newborns from Ivory Coast

Coulibaly, Foungotin H; Koffi, Gustave; Touré, H; Bouanga, Jean-Claude; Allangba, Olivier; Tolo, A.; Sawadogo, Duni; Sanogo, Ibrahim; Konaté, Seïdou; Préhu, Claude; Sangaré, A.; Galactéros, Frédéric

doi:10.1016/s0009-9120(00)00078-3

Cited by 7 publications

(7 citation statements)

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“…In our cohort of patients with SCA diagnosed at birth, the prevalence of G6PD deficiency was almost 10% overall and 16% in males. This frequency and the genotype distribution were in accordance with the geographic origin of the parents (Vulliamy et al, 1991;Bouanga et al, 1998;Coulibaly et al, 2000;De Araujo et al, 2006;Nkhoma et al, 2009).…”

Section: Discussionsupporting

confidence: 66%

Impact of glucose‐6‐phosphate dehydrogenase deficiency on sickle cell anaemia expression in infancy and early childhood: a prospective study

et al. 2013

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Summary In patients with sickle cell anaemia (SCA), concomitant glucose‐6‐phosphate dehydrogenase (G6PD) deficiency is usually described as having no effect and only occasionally as increasing severity. We analysed sequential clinical and biological data for the first 42 months of life in SCA patients diagnosed by neonatal screening, including 27 G6PD‐deficient patients, who were matched on sex, age and parents' geographic origin to 81 randomly selected patients with normal G6PD activity. In the G6PD‐deficient group, steady‐state haemoglobin was lower (−6·2 g/l, 95% confidence interval (CI), [−10·1; −2·3]) and reticulocyte count higher (247 × 109/l, 95%CI, [97; 397]). The acute anaemic event rate was 3 times higher in the G6PD‐deficient group (P < 10−3). A higher proportion of G6PD‐deficient patients required blood transfusion (20/27 [74%] vs. 37/81 [46%], P < 10−3), for acute anaemic events, and also vaso‐occlusive and infectious events. No significant between‐group differences were found regarding the rates of vaso‐occlusive, infectious, or cerebrovascular events. G6PD deficiency in babies with SCA worsens anaemia and increases blood transfusion requirements in the first years of life. These effects decrease after 2 years of age, presumably as the decline in fetal haemoglobin levels leads to increased sickle cell haemolysis and younger red blood cells with higher G6PD activity.

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Section: Discussionsupporting

confidence: 66%

Impact of glucose‐6‐phosphate dehydrogenase deficiency on sickle cell anaemia expression in infancy and early childhood: a prospective study

et al. 2013

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“…Metabolism of these HIV and antimalarial agents occurs primarily via cytochrome P450 (CYP) enzymes. Artemether is metabolized to an active metabolite, dihydroartemisinin (DHA), predominately by CYP3A4/5 and to a lesser extent by CYP2B6, CYP2C9, and CYP2C19 (4). DHA undergoes glucuronidation by uridine diphosphoglucuronosyltransferases.…”

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confidence: 99%

“…DHA undergoes glucuronidation by uridine diphosphoglucuronosyltransferases. Lumefantrine is metabolized by CYP3A4 into active desbutyl-lumefantrine (2,4,5). Nevirapine is metabolized by CYP3A4 and CYP2B6 while inducing CYP3A4 (6,7).…”

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confidence: 99%

“…The control group received artemether-lumefantrine alone, following the same schedule but with food provided immediately postdose (16). Blood samples for quantification of artemether, DHA, lumefantrine, and nevirapine were collected around the sixth (last) dose on day 3, predose and 0.5, 1, 1.5, 2, 3, 4,6,8,10,12,24,48,72, and 96 h postdose. Pharmacokinetic sampling was identical for the control group, although samples were collected through 296 h. Plasma was stored at Ϫ80°C within 30 min after collection.…”

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confidence: 99%

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Artemether-Lumefantrine Exposure in HIV-Infected Nigerian Subjects on Nevirapine-Containing Antiretroviral Therapy

Parikh

Fehintola

Huang

et al. 2015

Antimicrob Agents Chemother

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i Coadministration of nevirapine-based antiretroviral therapy (ART) and artemether-lumefantrine is reported to result in variable changes in lumefantrine exposure. We conducted an intensive pharmacokinetic study with 11 HIV-infected adults who were receiving artemether-lumefantrine plus nevirapine-based ART, and we compared the results with those for 16 HIV-negative adult historical controls. Exposure to artemether and lumefantrine was significantly lower and dihydroartemisinin exposure was unchanged in subjects receiving nevirapine-based ART, compared with controls. Nevirapine exposure was unchanged before and after artemether-lumefantrine administration. Malaria and HIV affect millions of children and adults in subSaharan Africa, and drug-drug interactions between antiretroviral therapy (ART) and antimalarial agents are clinically important to characterize. Nevirapine-based ART represents 50% of first-line ART in regions where malaria coinfection occurs (1). Artemether-lumefantrine, an artemisinin derivative combined with a longer-acting partner drug, represents the most common antimalarial therapy (2, 3). Metabolism of these HIV and antimalarial agents occurs primarily via cytochrome P450 (CYP) enzymes. Artemether is metabolized to an active metabolite, dihydroartemisinin (DHA), predominately by CYP3A4/5 and to a lesser extent by CYP2B6, CYP2C9, and CYP2C19 (4). DHA undergoes glucuronidation by uridine diphosphoglucuronosyltransferases. Lumefantrine is metabolized by CYP3A4 into active desbutyl-lumefantrine (2, 4, 5). Nevirapine is metabolized by CYP3A4 and CYP2B6 while inducing CYP3A4 (6, 7). Studies report reduced artemisinin exposure in the presence of nevirapinebased ART, but the effects on lumefantrine concentrations are variable, with studies showing increased, decreased, or unchanged concentrations (8)(9)(10)(11)(12)(13)(14). Importantly, reduced antimalarial levels have been associated with therapeutic failure (12,13,15). The primary objective of this study was to evaluate the pharmacokinetics of artemether, DHA, and lumefantrine in HIV-infected Nigerian adults without clinical malaria who were receiving nevirapine-based ART.(Data were presented at the 15th International Workshop on Clinical Pharmacology of HIV and Hepatitis Therapy, Washington, DC, 19 May 2014.) HIV-infected subjects (Ն18 years of age) who had been receiving nevirapine-based ART for Ն4 weeks (nevirapine-based ART group) were eligible after informed consent was obtained. Exclusion criteria were current pregnancy; intolerance to study drugs; use of antimalarials or CYP substrates, inducers, or inhibitors within 4 weeks; and clinical symptoms of malaria. The historical control group included healthy adults (n ϭ 16). The same laboratory analyzed all plasma drug concentrations (16). The University College Hospital Ethics Committee approved this study (protocol NHREC/05/01/2008a).Participants received coformulated nevirapine-zidovudinelamivudine (200/300/150 mg; Aurobindo Pharma, India) twice daily. On day 0, participants underwent venou...

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“…Le gène de cette enzyme est localisé sur le chromosome X, ce qui explique le mode de transmission du déficit, lié au sexe, avec des sujets mâles hémizygotes pour l'anomalie et des femmes, transmettant l'anomalie mais, habituellement, cliniquement indemnes. Toutefois de nombreuses femmes sont homozygotes dans les populations où la fréquence génique est élevée, par exemple elles sont près de 3 % en Côte-d'Ivoire [6] et de 5 % en république du Congo.…”

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Le déficit en glucose-6 phosphate déshydrogénase : protection contre le paludisme et risque d'accidents hémolytiques

Wajcman

Galactéros

2004

Comptes Rendus. Biologies

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La glucose 6-phosphate déshydrogénase (G6PD) catalyse la première étape de la voie des pentoses et permet, dans le globule rouge, la réduction du NADP en NADPH, coenzyme essentiel à la lutte contre les agressions oxydantes. À travers le monde, le déficit en G6PD concerne plus de 400 millions de personnes, de sexe masculin pour plus de 90 %. Il se superpose à la carte de l'endémie palustre et se retrouve, bien entendu, dans toutes les populations originaires de ces régions. Les globules rouges déficitaires sont particulièrement sensibles aux stress oxydants. Ce déficit protège contre les formes graves de paludisme en offrant un milieu défavorable au développement d'un parasite, lui-même très sensible aux oxydants. La contrepartie de cet avantage est un risque hémolytique accru en réponse à de multiples agents oxydo-réducteurs. Parmi ces derniers, citons les glycosides contenus dans les fèves (favisme) et certains médicaments (sulfamides, anti-paludéens, etc.). La coexistence, dans une même région géographique, d'une parasitose, d'une mutation protectrice, et de traditions (alimentaires ou culturelles) pose le problème d'évolutions convergentes. On connaît aujourd'hui environ 150 variantes de G6PD classées en quatre types selon leurs effets cliniques. Un petit nombre d'entre elles, comme la G6PD A-en Afrique ou la variante méditerranéenne sont de véritables polymorphismes dans les régions impaludées. La connaissance de la structure tridimensionnelle de la protéine permet de formuler des hypothèses expliquant les déficits en termes de relations structure-fonction.

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Molecular genetics of glucose-6-phosphate dehydrogenase deficiency in a population of newborns from Ivory Coast

Cited by 7 publications

References 13 publications

Impact of glucose‐6‐phosphate dehydrogenase deficiency on sickle cell anaemia expression in infancy and early childhood: a prospective study

Impact of glucose‐6‐phosphate dehydrogenase deficiency on sickle cell anaemia expression in infancy and early childhood: a prospective study

Artemether-Lumefantrine Exposure in HIV-Infected Nigerian Subjects on Nevirapine-Containing Antiretroviral Therapy

Le déficit en glucose-6 phosphate déshydrogénase : protection contre le paludisme et risque d'accidents hémolytiques

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