Is Testing for Glucose-6-Phosphate Dehydrogenase Deficiency Before Starting Sulfa Useful In HIV-Infected Male Patients Originating From Sub-Saharan Africa?

2011 ◽  
Vol 56 (2) ◽  
pp. e60-e63 ◽  
Author(s):  
Pierre O Sellier ◽  
Nathalie Mario ◽  
Agathe Rami ◽  
Annalisa Andreoli ◽  
Beda M Choho ◽  
...  
Keyword(s):  
Dehydrogenase Deficiency ◽  
Sub Saharan Africa ◽  
Infected Male ◽  
Male Patients ◽  
Sub Saharan ◽  
Glucose 6 Phosphate Dehydrogenase

scholarly journals Malaria in Tunisian Military Personnel after Returning from External Operation

2013 ◽  
Vol 2013 ◽  
pp. 1-3
Author(s):  
Faïda Ajili ◽  
Riadh Battikh ◽  
Janet Laabidi ◽  
Rim Abid ◽  
Najeh Bousetta ◽  
...  
Keyword(s):  
Military Personnel ◽  
Malaria Infection ◽  
Imported Malaria ◽  
Sub Saharan Africa ◽  
Military Hospital ◽  
Imported Cases ◽  
Male Patients ◽  
Sub Saharan ◽  
The Military

Introduction. Malaria had been eliminated in Tunisia since 1979, but there are currently 40 to 50 imported cases annually. Soldiers are no exception as the incidence of imported malaria is increasing in Tunisian military personnel after returning from malaria-endemic area, often in Sub-Saharan Africa. Methods. We retrospectively analyzed the clinical and biological presentations, treatment, and outcomes of 37 Tunisian military personnel hospitalized at the Department of Internal Medicine, the Military Hospital of Tunis, between January 1993 and January 2011, for imported malaria. The clinical and laboratory features were obtained from the medical records and a questionnaire was filled by the patients about the compliance of malaria prophylaxis. Results. Thirty-seven male patients, with a mean age of 41 years, were treated for malaria infection. Twenty-two were due to Plasmodium falciparum. The outcome was favourable for all patients, despite two severe access. The long-term use of chemoprophylaxis has been adopted by only 21 (51%) of expatriate military for daily stresses. Moreover, poor adherence was found in 32 patients. Conclusion. The risk of acquiring malaria infection in Tunisian military personnel can largely be prevented by the regular use of chemoprophylactic drugs combined with protective measures against mosquito bites.

scholarly journals Glucose-6-Phosphate Dehydrogenase Deficiency in Greece

Blood ◽  
1961 ◽  
Vol 18 (1) ◽  
pp. 34-47 ◽  
Author(s):  
LEDA ZANNOS-MARIOLEA ◽  
CHRISTOS KATTAMIS
Keyword(s):  
Individual Differences ◽  
Dehydrogenase Deficiency ◽  
Normal Limit ◽  
Red Cells ◽  
Female Patients ◽  
Male Patients ◽  
Stability Method ◽  
Fava Beans ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Genetic Hypothesis

Abstract The glutathione stability of red cells was estimated in 40 patients during acute hemolysis induced by fava beans. There were wide individual differences but in all cases except one (Case 18) the post-incubation GSH fell to levels below 40 mg. per cent packed RBC which is the lower normal limit. The GSH stability on 44 mothers and 37 fathers gave results consistent with the genetic hypothesis that in male patients the mother is the carrier of the biochemical defect, while in female patients both parents are carriers, since, as a rule, only female homozygotes suffer from hemolytic episodes. However, in only 77.7 per cent of the mothers could the biochemical defect be proved by this method. The Motulsky test was performed in 30 of the 40 patients. It gave abnormal decolorization times in 25 or 83 per cent of the cases. This test is therefore valuable for diagnosing "sensitivity" during a hemolytic episode; it is, nevertheless, less sensitive than the GSH stability method. The Motulsky test was also performed on 31 mothers, 18 fathers and 8 siblings. It proved to be unreliable in the detection of female heterozygotes. G-6-PD deficiency is widely disseminated in Greece; it is, however, not evenly distributed throughout the country. The highest frequency of G-6-PD deficiency found so far in males was about 3 per cent; the lowest was 0.7 per cent.

scholarly journals G6PD variant distribution in sub-Saharan Africa and potential risks of using chloroquine/hydroxychloroquine based treatments for COVID-19

2020 ◽  
Author(s):  
Jorge da Rocha ◽  
Houcemeddine Othman ◽  
Caroline T. Tiemessen ◽  
Gerrit Botha ◽  
Michèle Ramsay ◽  
...  
Keyword(s):  
Allele Frequency ◽  
G6pd Deficiency ◽  
Sequence Data ◽  
Sub Saharan Africa ◽  
Whole Genome Sequence ◽  
Interaction Factor ◽  
High Prevalence ◽  
Potential Risks ◽  
Sub Saharan ◽  
Glucose 6 Phosphate Dehydrogenase

AbstractChloroquine/hydroxychloroquine have been proposed as potential treatments for COVID-19. These drugs have warning labels for use in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency. Analysis of whole-genome sequence data of 458 individuals from sub-Saharan Africa showed significant G6PD variation across the continent. We identified nine variants, of which four are potentially deleterious to G6PD function, and one (rs1050828) that is known to cause G6PD deficiency. We supplemented data for the rs1050828 variant with genotype array data from over 11,000 Africans. Although this variant is common in Africans overall, large allele frequency differences exist between sub-populations. African sub-populations in the same country can show significant differences in allele frequency (e.g. 16.0% in Tsonga vs 0.8% in Xhosa, both in South Africa, p = 2.4 × 10−3). The high prevalence of variants in the G6PD gene found in this analysis suggests that it may be a significant interaction factor in clinical trials of chloroquine and hydrochloroquine for treatment of COVID-19 in Africans.

scholarly journals Glucose 6-phosphate dehydrogenase deficiency and sickle cell anemia: frequency and features of the association in an African community

Blood ◽  
1975 ◽  
Vol 46 (4) ◽  
pp. 591-597 ◽  
Author(s):  
U Bienzle ◽  
O Sodeinde ◽  
CE Effiong ◽  
L Luzzatto
Keyword(s):  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Dehydrogenase Deficiency ◽  
Clinical Course ◽  
Normal Subjects ◽  
Starch Gel Electrophoresis ◽  
African Community ◽  
Starch Gel ◽  
Male Patients ◽  
Glucose 6 Phosphate Dehydrogenase

Abstract The glucose 6-phosphate dehydrogenase (G6PD) genotype was determined in 100 male patients with homozygous sickle cell anemia (SS) by a combination of quantitative assay, cytochemical testing, and starch-gel electrophoresis. Of the 100 patients tested, 16 were found to be G6PD deficient (GdA-), AND 84 G6PD normal (22GsA and 62 GdB). This distribution of G6PD genotypes did not differ significantly from that observed in the general population. The level of G6PD activity in GdA- SS patients was nearly always higher than in G6PD-deficient subjects who did not have an associated hemolytic state, but it was nearly always lower than in G6PD-normal subjects. The clinical course of sickle cell disease, including the degree of anemia, was not milder in GdA- than in G6PD-normal patients but could not be proved to be significantly more severe. It was concluded that in this community the incidence of G6PD deficiency in sickle cell anemia was not greater than would be expected by chance, and there was no evidence that the coexistence of the GdA- gene in SS patients ameliorated their disease.

scholarly journals Glucose 6-phosphate dehydrogenase deficiency and sickle cell anemia: frequency and features of the association in an African community

Blood ◽  
1975 ◽  
Vol 46 (4) ◽  
pp. 591-597
Author(s):  
U Bienzle ◽  
O Sodeinde ◽  
CE Effiong ◽  
L Luzzatto
Keyword(s):  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Dehydrogenase Deficiency ◽  
Clinical Course ◽  
Normal Subjects ◽  
Starch Gel Electrophoresis ◽  
African Community ◽  
Starch Gel ◽  
Male Patients ◽  
Glucose 6 Phosphate Dehydrogenase

The glucose 6-phosphate dehydrogenase (G6PD) genotype was determined in 100 male patients with homozygous sickle cell anemia (SS) by a combination of quantitative assay, cytochemical testing, and starch-gel electrophoresis. Of the 100 patients tested, 16 were found to be G6PD deficient (GdA-), AND 84 G6PD normal (22GsA and 62 GdB). This distribution of G6PD genotypes did not differ significantly from that observed in the general population. The level of G6PD activity in GdA- SS patients was nearly always higher than in G6PD-deficient subjects who did not have an associated hemolytic state, but it was nearly always lower than in G6PD-normal subjects. The clinical course of sickle cell disease, including the degree of anemia, was not milder in GdA- than in G6PD-normal patients but could not be proved to be significantly more severe. It was concluded that in this community the incidence of G6PD deficiency in sickle cell anemia was not greater than would be expected by chance, and there was no evidence that the coexistence of the GdA- gene in SS patients ameliorated their disease.

scholarly journals Prevalence of neonatal hyperbilirubinaemia and its association with glucose-6-phosphate dehydrogenase deficiency and blood-type incompatibility in sub-Saharan Africa: a systematic review and meta-analysis

2020 ◽  
Vol 4 (1) ◽  
pp. e000750
Author(s):  
Yared Asmare Aynalem ◽  
Getaneh Baye Mulu ◽  
Tadesse Yirga Akalu ◽  
Wondimeneh Shibabaw Shiferaw
Keyword(s):  
G6pd Deficiency ◽  
Meta Analysis ◽  
Random Effect ◽  
Cochrane Review ◽  
Random Effect Model ◽  
Blood Type ◽  
Sub Saharan Africa ◽  
Inconsistency Index ◽  
Sub Saharan ◽  
Glucose 6 Phosphate Dehydrogenase

BackgroundHyperbilirubinaemia is a silent cause of newborn disease and death worldwide. However, studies of the disease in sub-Saharan Africa are highly variable with respect to its prevalence. Hence, this study aimed to estimate the overall magnitude of neonatal hyperbilirubinaemia and its association with glucose-6-phosphate dehydrogenase (G6PD) deficiency and blood-type incompatibility in sub-Saharan Africa.MethodsPubMed, Scopus, Google Scholar and the Cochrane Review were systematically searched online to retrieve hyperbilirubinaemia-related articles. All observational studies reported the prevalence of hyperbilirubinaemia in sub-Saharan Africa were included for analysis and excluded if the study failed to determine the desired outcome. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were followed. Heterogeneity across the included studies was evaluated using the inconsistency index (I2). Subgroup and meta- regression analysis were also done. Publication bias was examined by funnel plot and the Egger’s regression test. The random-effect model was fitted to estimate the pooled prevalence of neonatal hyperbilirubinaemia. The meta-analysis was performed using the STATA V.14 software.ResultsA total of 30 486 studies were collected from the different databases and 10 articles were included for the final analysis. The overall magnitude of neonatal hyperbilirubinaemia was 28.08% (95% CI20.23 to 35.94, I2=83.2) in sub-Saharan Africa. Neonates with G6PD deficiency (OR 2.42, 95% CI 1.64 to 3.56, I2=37%) and neonates that had a blood type that was incompatible with their mother’s (OR 3.3, (95% CI 1.96 to 5.72, I2=84%) were more likely to develop hyperbilirubinaemia.ConclusionThe failure to prevent and screen G6PD deficiency and blood-type incompatibility with their mother’s results in high burden of neonatal hyperbilirubinaemia in sub-Saharan Africa. Therefore, early identification and care strategies should be developed to the affected neonates with G6PD deficiency and blood-type incompatibility with their mother’s to address long-term medical and scholastic damages among those exposed to hyperbilirubinaemia

scholarly journals Porphyrin metabolism in secondary hepatic porphyria in patients with hereditary deficiency of glucose-6-phosphate dehydrogenase

2012 ◽  
Vol 93 (3) ◽  
pp. 451-455
Author(s):  
D A Baytaeva ◽  
S S Bessmel’tsev
Keyword(s):  
Quantitative Methods ◽  
Dehydrogenase Deficiency ◽  
Early Stage ◽  
Diagnostic Feature ◽  
High Concentration ◽  
Qualitative And Quantitative Methods ◽  
Porphyrin Metabolism ◽  
Endogenous Intoxication ◽  
Male Patients ◽  
Glucose 6 Phosphate Dehydrogenase

Aim. The study the porphyrin metabolism during the development of secondary hepatic porphyria in patients with glucose-6-phosphate dehydrogenase deficiency. Methods. Examined were 148 male patients aged 5-19 years (median 12 years) with impaired activity of glucose-6-phosphate dehydrogenase in combination with β-thalassemia and without it. Qualitative and quantitative methods of examining the activity of this enzyme were used in order to verify the diagnosis. Taking into account the varying degree of glucose-6-phosphate dehydrogenase deficiency, the indices of metabolism of the enzyme and of the porphyrins were correlated with the severity of anemia, functional liver capacities, with parameters reflecting iron content in blood serum, bone marrow, liver and urine. The markers of intoxication were also taken into account in the development of secondary hepatic porphyria and endotoxemia. Therapeutic plasmapheresis was used to correct the revealed disorders. Results. The influence of glucose-6-phosphate dehydrogenase deficiency on the metabolism of porphyrins and liver functional status has been shown, which leads to the development of anemia and endogenous intoxication. With the help of parameters, which characterize the porphyrin metabolism in patients, secondary hepatic porphyria was revealed. It was established that determination of the content of glucose-6-phosphate dehydrogenase and porphyrins makes it possible to detect disturbances in heme synthesis at an early stage and to evaluate the compensatory abilities of the liver. An important diagnostic feature for glucose-6-phosphate dehydrogenase deficiency, regardless of severity, is the impaired synthesis of the end products of metabolism of porphyrins - uro-, copro- and protoporphyrin. The effectiveness of therapeutic plasmapheresis for hemolysis, secondary hepatic porphyria and endogenous intoxication has been shown. Conclusion. Increased excretion of uro-and coproporphyrin with urine reflects the severity of endotoxemia, and is an alternative to markers of intoxication; high concentration of free protoporphyrin and low concentration of uro- and coproporphyrin in erythrocytes is an important diagnostic sign of impaired activity of glucose-6-phosphate dehydrogenase in patients.

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