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At least 451 records · Page 25Linked to original sources
PubMed1978

Triplo-X constitution of mother explains apparent occurrence of two recombinants in sibship segregating at two closely X-linked loci (G6PD and deutan).

Two male sibs believed to be examples of meiotic recombinants between the closely linked loci for G6PD deficiency of Mediterranean type and severe deutan color blindness proved to be simple segregants of a triplo-X mother of genotype d--GdMediterranean/d+GdMediterranean/d+GdB. This finding suggests that in Sardinia the linkage between the two loci under consideration may be tighter than previously assumed.

Color Vision Defects↗
PubMed1987

Role of G6PD, ABO incompatibility, low birth weight and infection in neonatal hyperbilirubinaemia.

In a random sample of 1,000 neonates from a Delhi Hospital the incidence of jaundice was 53% and of hyperbilirubinaemia (HB) 6%. Rh incompatibility was detected in 4% of the neonates. In 74 cases of HB (excluding those due to Rh incompatibility) collected from the above series and from subsequent hospital admissions, incidences of different factors contributing to HB were: low birth weight in 54%, G6PD deficiency in 35%, ABO incompatibility in 31% and infection in 31%. In 45% of them a single factor was present and in the remaining more than one factor was present.

ABO Blood-Group System↗
PubMed1967

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.

In view of the fact that increased resistance to drugs by malaria parasites in some parts of the world may lead to increasing use of a combination of primaquine with chloroquine for chemotherapy, studies were made on the severity of the haemolytic anaemia induced by 45 mg primaquine in American Negroes with glucose-6-phosphate dehydrogenase deficiency. It was found that twice-weekly administration of primaquine induced more haemolysis than once-weekly administration, and that administration once weekly for 4 weeks and twice weekly thereafter resulted in a degree of anaemia falling between those produced by the other regimens. Anaemia was not induced in controls with no G6PD deficiency. One volunteer developed an intercurrent infection that was treated with salicylates; his haemolysis was markedly intensified, but whether by the infection, the salicylates or both could not be determined.In a conjoint study, the administration of six malaria-suppressive drugs had no detectable effect on the activities of several erythrocyte enzymes or on the levels of adenosine monophosphate, diphosphate or triphosphate.

Black or African American↗
PubMed1983

[Determination of superoxide dismutase (sod) in erythrocytes in glucose-6-phosphate dehydrogenase deficiency (G6PD-deficiency)].

Determining SOD in red blood cells was made in 26 carriers of G6PD defect 9 haemicygotic mark carriers and 16 heterocytic mark carriers had a diminished SOD enzyme activity. This is probably due to an inactivation of SOD by diminished reductive equivalents in the metabolism of defect cells. In this way, more oxidatively effective radicals will appear, even OH. among them. The latter may render the enzyme ineffective by binding it to the imidazol group in the catabolic centre. Consequently, an accumulation of the substrate O2-. may lead to a further cell damage, thus causing an increased haemolysis.

Erythrocytes↗
PubMed1981

Pharmacogenetic interactions in G6PD deficiency and development of an in vitro test to predict a drug's hemolytic potential.

To summarize our results and their implications, by adding induced mouse liver microsomes to an in vitro test for the hemolytic potential of a drug in G6PD deficiency, we found that: 1) Hydroxylation appears to play an important role in activating the hemolytic potential of many drugs. 2) Use of an in vitro test system combining drug, hydroxylation system and red cell, appears to be very reliable in ruling out hemolytic potential, when it is in fact absent, and about 80% effective in identifying hemolytic potential when it is present. 3) Acetylation seems to markedly reduce the hemolytic potential of two drugs studied: promizole and DDS. The genetic polymorphism in acetylation may explain the bimodal response to promizole. 4) These studies suggest that interaction among three pharmacogenetic systems produces a given hemolytic result. Variability of hydroxylation and acetylation rates can be expected to contribute to variability in individual responses to certain hemolytic drugs.

Animals↗
PubMed1996

Sub-Saharan influence on the Canary Islands population deduced from G6PD gene sequence analysis.

In a screening of glucose-6-phosphate dehydrogenase (G6PD) A variants in the Canary Islands and northwest African populations by electrophoresis and posterior gene sequencing, the common A+ 376G and A- 202A/376G and the rare A- 376G/968C mutations were found. In addition, three new silent C-->T transitions have been detected at nucleotides 759 (exon 7), 1338 (exon 11), and 1573 (exon 13). Canary Island and North African samples share sub-Saharan haplotypes with Equatorial Guineans. The slave trade seems the most probable origin of the African haplotypes found in the Canary Islands.

Africa South of the Sahara↗
PubMed1986

T-lymphocyte subpopulation changes during hemolysis in glucose-6-phosphate dehydrogenase (G6PD)-deficient children.

Lymphocyte subpopulations were studied by means of sheep red blood cell (SRC)-rosetting technique and OKT11, OKT3, OKT4, and OKT8 monoclonal antibodies in ten Sicilian glucose-6-phosphate dehydrogenase-deficient children during the hemolytic crisis due to fava bean ingestion. The number of SRC-rosetting lymphocytes was significantly reduced, while the number of OKT3-positive cells was normal. An inversion of the OKT4/OKT8 ratio was observed, due to a decrease of OKT4-positive cells and an increase of OKT8-positive cells. All these abnormalities reverted to normal in the four children studied after recovery.

Antibodies, Monoclonal↗