Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID: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. 486 52

One hundred and twenty-three cases of sickle-cell trait (122 negro immigrants) are studied in a department of internal medicine. The frequencies of G6PD deficiency, anemia, splenomegaly and tuberculosis are neighbouring at the negro without hemoglobinopathy. The relationship between the sickle-cell trait and the reason of admission of the final diagnosis il likely in 2,4 % of the cases, doubtfully in 15,4 %, null in the other cases. The occasional (hemolytic, thrombotic, painful, visceral, osseous) manifestations of the sickle-cell trait (apart from the constant hyposthenuria) and their mechanism are summarized and discussed.
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PMID:[One hundred and twenty-three cases of sickle-cell trait (author's transl)]. 625 31

A 6-year-old boy with chronic haemolytic anaemia was found to have glucose 6-phosphate dehydrogenase (G6PD) deficiency and the morphological, ultrastructural and serological features of congenital dyserythropoietic anaemia (CDA) type II. The patient's mother was heterozygous for G6PD deficiency. G6PD from the patient's red cells, upon partial purification and full characterization, was found to be a new variant designated G6PD Gabrovizza. We conclude that two distinct genetic abnormalities coexisted in this patient. We suggest that CDA type II may become clinically more expressed when another abnormality of the erythrocytes coexists.
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PMID:Congenital dyserythropoietic anaemia type II associated with a new type of G6PD deficiency (G6PD Gabrovizza). 642 35

A child suffering from G6PD deficiency developed a severe haemolytic crisis without an apparent trigger. The possible pathogenetic role of the ingestion of unripe peaches was studied biochemically in this anaemia. We show that an extract from the unripe peach exerts an oxidative challenge on normal as well as on asymptomatic G6PD-deficient erythrocytes. This effect is analogous to that of the favism-inducing agents. The effect of the extract on the patient's red blood cells was more pronounced than on other asymptomatic G6PD-deficient erythrocytes, particularly during his haemolytic crisis. The chemical nature of the deleterious component was not identified. It is suggested that unripe peaches be added to the list of hazards for G6PD-deficient subjects in combination with other factors.
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PMID:Haemolysis in a G6PD-deficient child induced by eating unripe peaches. 650 33

HbE, beta thalassemia, and G6PD deficiency were demonstrated in a 6-year-old Mexican-American child with anemia, jaundice, and delayed growth. The father was heterozygous for HbE, and the mother for beta-thalassemia and G6PD deficiency. The association of these three diseases should be included in the differential diagnosis of anemia in childhood, particularly after the recent influx of people form Southeast Asia into the United States.
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PMID:HbE-beta-thalassemia associated with G6PD deficiency. 736 46

Thirty-five children with G6PD deficiency, who presented with acute intravascular haemolysis, were evaluated to define its aetiology, clinical features and ultimate outcome. All were boys with ages ranging from 6 months to 12 years. Pallor of abrupt onset and passage of cola-coloured urine were universal presenting symptoms. Incriminating factors responsible for haemolysis include hepatitis (7), malaria (4), bacterial sepsis (3) and drug intake (24), with more than one predisposing condition existing in some children. Marked elevations in serum bilirubin, coinciding with intravascular haemolysis, was a feature in all the seven children with hepatitis. Azotaemia was noted in 20 patients, of whom 14 did not have oliguria. All four children with malaria presented with protracted renal failure. Therapy focused on maintaining a high urine output in those without oliguria. A total of 15 peritoneal dialyses and five haemodialyses were required in six patients with acute renal failure, all of whom were oliguric. Supportive therapy consisted of blood transfusions and treatment of the predisposing diseases. Thirty-two children recovered completely while three died, the cause of death being severe anaemia and congestive cardiac failure, malaria with oliguric renal failure and hepatic encephalopathy, respectively.
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PMID:Acute intravascular haemolysis in glucose-6-phosphate dehydrogenase deficiency. 750 89

We have studied the prevalence and molecular nature of hereditary anaemias (abnormal haemoglobins, beta-thalassaemia, alpha-thalassaemia, and Glucose 6 phosphate dehydrogenase (G6PD) deficiency) in a primitive central Indian tribe, the Baiga. 43% of the population appear to be iron-deficient. Hereditary anaemia gene frequencies are, sickle cell 0.0824, G6PD deficiency (in males) 0.0457, beta-thalassaemia 0.0057, and deletional alpha-plus thalassaemia 0.65. Both -alpha 3.7 and -alpha 4.2 deletions were observed and non-deletional alpha-thalassaemia was suspected. The overall gene frequency of Xmn I+polymorphism (C-->T - 158 cap site; upstream of G gamma region) is 0.35. This polymorphism is preferentially linked to beta s genes. It appears that sickle cell disease covers a wide range of severity in the Baiga tribe based on higher mortality in the offspring of AS x AS parents (2.5/couple) compared to AA x AS (0.75/couple) and AA x AA (0.76/couple) parents. This is compatible with the high frequency of genetic modifying factors, i.e., the Xmn I polymorphism and alpha-thalassaemia. The results also indicate that "normal" red cell values must be defined for each population where thalassaemias, G6PD deficiency and iron deficiency are common.
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PMID:Hereditary anaemias and iron deficiency in a tribal population (the Baiga) of central India. 762 84

Between 1986 and 1990, 107,397 National Servicemen between the ages of 17 to 18 years were screened on enlistment for Glucose-6-Phosphate Dehydrogenase (G6PD) enzyme activity by fluorescent spot test. The overall prevalence rate was 1.6% with ethnic differences as follows: 1.62% for Chinese, 1.80% for Malay, 0.76% for Indian and 0.68% for other races. The majority had no prior knowledge of their G6PD deficiency status (89.9%), or of any significant haemolytic episode (93.3%). The rest gave a history of neonatal jaundice, non-neonatal jaundice, anaemia and haemoglobinuria. Maloprim, fava beans, sulphur drugs and aspirin were cited as triggering factors.
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PMID:Prevalence of G6PD deficiency among recruits in the Singapore Armed Forces. 765 79

Anemia is the most common hematologic complication of pregnancy and is associated with increased rates of premature birth, low birth weight and perinatal mortality. Iron deficiency is the most common cause of anemia, and most pregnant women benefit from daily supplementation of 30 to 60 mg of elemental iron. Folic acid deficiency, the most common cause of megaloblastic anemia in pregnancy, is associated with open neural tube defects and other complications. It is recommended that daily supplementation with 4 mg of folic acid be started at least one month before conception and continued through the first trimester. Other less common causes of anemia include glucose-6-phosphate dehydrogenase deficiency, sickle cell trait and disease, and the thalassemias. The primary care provider should emphasize risk evaluation, dietary and preconceptual counseling, testing and appropriate treatment.
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PMID:Anemia in pregnancy. 770 94

Man evolved as a hunter-gatherer, and the invention and spread of agriculture was followed by changes in diet, the environment and population densities which have resulted in globally high prevalences of anaemias due to nutritional deficiencies of iron, folate and (locally) vitamin B12, to infestations by hookworm and schistosomes, to malaria, and to the natural selection for the genes for sickle-cell diseases, beta-thalassaemias, alpha-thalassaemias, glucose-6-phosphate dehydrogenase deficiency, ovalocytosis and possibly (locally) elliptocytosis. The present explosion of population is driving an expansion of agriculture, especially the cultivation of rice, and this has led often to disastrous increases of transmission of malaria, schistosomiasis and other diseases, to widespread chemical pollution, and to degradation of the environment. Anaemia, as the commonest manifestation of human disease, is a frequent consequence. The urgent need for increased food production is matched by the urgent need for assessment and control of the health impact of agricultural development.
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PMID:Agriculture-related anaemias. 775 42


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