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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A Ghanaian family is described in which a sickle-cell haemoglobin C man married to a sickle-cell thalassaemia woman produced 12 children (eight alive). Four children have sickle-cell anaemia, two sickle-cell haemoglobin C disease, one has sickle-cell thalassaemia, and one is asymptomatic haemoglobin C thalassaemia.It is emphasized that the contribution that adult sickle-cell disease patients make, through procreation, to the persistence of the S gene may be greater than is normally supposed, and that this contribution may soon outstrip that made by balanced polymorphism through falciparum malaria. Widespread haemoglobin genotyping in schools leading to genetic counselling is advocated to decrease the incidence of sickle-cell disease.
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PMID:Sickle-cell anaemia, sickle-cell thalassaemia, sickle-cell haemoglobin C disease, and asymptomatic haemoglobin C thalassaemia in one Ghanaian family. 576 26

Haemoglobin Bart's was detected in cord blood samples from 81% of 217 infants born in Madang on the north coast of Papua New Guinea. Analysis of the alpha globin genes of 30 infants and adults from the same region showed that all but 3 were heterozygous or homozygous for the deletion form of alpha + thalassaemia. None of 18 cord blood samples from infants born in Goroka in the Eastern Highlands Province had haemoglobin Bart's, and in each case the alpha globin genes were normal. Preliminary geographical and linguistic analyses of both groups suggest that the prevalence of alpha thalassaemia may be related to altitude rather than to linguistic grouping and hence that resistance to malaria may be at least one reason why alpha thalassaemia is so common in some populations.
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PMID:Alpha thalassaemia in Papua New Guinea. 614 52

A great deal of work has been in the recent years concerning sickle cell anemia, both its theoretical aspects and its medico-social consequences being involved. From the pathophysiological point of view, investigations have resulted in a better knowledge of the mechanism of the hemoglobin S polymerization. Other factors such as the role of the membrane, the ionic environment, the rheologic conditions have also been emphasized. These known disorders may explain the high clinical polymorphism of the disease. They are also the basis of a research for a potential specific treatment. Two factors have been specially investigated as potentially responsible for a benign course of the disease, namely fetal hemoglobin and an associated alpha-thalassemia. As a new field of investigation, a DNA polymorphism close to the beta-gene and linked to the mutation itself has been demonstrated. It proves the pluricentric origin of this mutation. It is also a tool for antenatal diagnosis of the homozygous forms of the disease using amniotic fluid cells. Finally the possible direct culture of P. falciparum as allowed a better understanding of the equilibrium between malaria and sickle cell anemia.
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PMID:[Recent data in the biology of sickle cell disease (author's transl)]. 617 65

The mild course of the diseased state of haemoglobinopathies and the thalassaemias in Arabia and the interaction of the genetic abnormality and environmental factors are particularly interesting as the Peninsula exhibits a diverse climate and topography that encourages study of the interactions between various genetic and environmental factors. The present study is aimed at elucidating the incidence and frequency of these genetic abnormalities in various regions of Saudi Arabia. The relationship between haemoglobinopathies, thalassaemia and glucose-6-phosphate dehydrogenase deficiency on the one hand and malaria parasites on the other are elucidated. The results are presented in the light of the environmental factors prevailing in the area.
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PMID:Haemoglobin disorders: a pattern for thalassaemia and haemoglobinopathies in Arabia. 618 41

A double-blind, randomized, dose-finding, phase II mefloquine trial was carried out in 147 adult male patients suffering from acute, uncomplicated, falciparum malaria and admitted to the Hospital for Tropical Diseases, Bangkok, between January 1980 and April 1981. Mefloquine was administered as a single oral dose of 500, 750, or 1000 mg (base) in the form of the hydrochloride. The clinical and parasitological responses were satisfactory with all three dosage regimens. The cure rates for the 1000-, 750-, and 500-mg doses were 100%, 92.5%, and 95% respectively, over an observation period of 63 days.The side-effects, which were transient and generally mild, included nausea, vomiting, and diarrhoea. No significant changes were noted in haematological or biochemical parameters in any of the three groups. Sinus bradycardia, which started 4-7 days after drug administration and lasted for a few weeks, was seen in 10 patients. It was symptomless and needed no treatment.Acute brain syndrome was observed in one patient on day 21 after receiving a 1000-mg dose of mefloquine.Mefloquine was well tolerated in one case of acute renal failure, in 10 cases of moderately severe malaria with jaundice, in 13 cases with glucose-6-phosphate dehydrogenase deficiency, and in one case of thalassaemia.Mefloquine showed no effect on either gametocytes of Plasmodium falciparum or tissue forms of P. vivax.Mefloquine hydrochloride was found to be an effective drug for the treatment of falciparum malaria and tended to produce a more rapid clinical and parasitological response at the highest tested dose of 1000 mg (base).
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PMID:A phase II clinical trial of mefloquine in patients with chloroquine-resistant falciparum malaria in Thailand. 634 13

A case-control study was carried out on 558 patients with malaria attending a hospital in Yekepa, northern Liberia; 94 patients (16.8%) were aged at least ten years, probably because of a low level of protective immunity in town dwellers due to malaria control. The proportion of sickle cell traits (1.8%) among the patient group was lower than in the population (7.2%) served by the hospital (chi 2, 21.455, 1 df, P less than 0.001). A stratified analysis showed the relative risk for Plasmodium falciparum malaria in sickle cell trait over normal homozygotes, as 0.29 (upper 95%) confidence interval, 0.56). For beta-thalassaemia trait, the proportion among patients was 5.5% as against 9.0% in the general population (chi 2, 6.158, 1 df, 0.025 greater than P greater than 0.010). Stratified analysis gave a weighted relative risk for beta-thalassaemia heterozygotes of 0.49 (upper 95% confidence interval, 0.74). Although there were four beta-thalassaemia traits in the 10-14 year stratum with moderate to high parasitaemias, we consider that the overall results are consistent with relative resistance against P. falciparum malaria of both sickle cell and beta-thalassaemia heterozygotes in this population. No conclusions were possible from this investigation with regard to HbC and the malaria hypothesis. We found no evidence that P. falciparum malaria elevates HbA2 concentrations into the beta-thalassaemia range.
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PMID:A case-control study in northern Liberia of Plasmodium falciparum malaria in haemoglobin S and beta-thalassaemia traits. 635 14

In a study in northern Liberia of the malaria and beta-thalassaemia hypothesis, the frequencies of beta-thalassaemia and HbS traits were 9.1 and 3.4% in the Mano and 9.5 and 1.7% in the Gio tribal samples. HbC and HbN were present at low frequency. G6PD deficiency was found in 16% of males. An observed increase with age of beta-thalassaemia trait frequencies was consistent with the selection hypothesis. However, we could not entirely exclude that associated iron deficiency influenced the results in the six to 11 month age group. Malaria was holoendemic; Plasmodium falciparum predominated, P. malariae and P. ovale were also identified. Plasmodium falciparum prevalence rates were similar in normal and beta-thalassaemia trait children but parasite densities were consistently lower in the latter. Using the criterion of a falciparum parasite density of 1 x 10(9) 1(-1) or greater to indicate a potentially important infection, the relative risk in beta-thalassaemia traits one to four years old from the cross-sectional study was 0.45 (upper 95% confidence interval 0.79) and 0.41 (0.61) in two to nine year trait carriers from a longitudinal study. Plasmodium falciparum gametocyte rates were lower in beta-thalassaemia trait children (P less than 0.005). The geometric mean titre of P. falciparum antibodies was lower in beta-thalassaemia trait children from the one to four year group (P less than 0.05). Otherwise immunological studies showed little difference between the different Hb types. Parasitological findings were consistent with relative resistance of HbS trait carriers towards P. falciparum infection. We found no evidence for relative resistance of beta-thalassaemia traits towards P. malariae infection nor that G6PD deficient males were more resistant to P. falciparum than those with normal activity. We conclude that the results are consistent with relative resistance of beta-thalassaemia trait carriers to P. falciparum malaria.
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PMID:Falciparum malaria and beta-thalassaemia trait in northern Liberia. 635 19

The author was a biochemist who, because he had experience in plasma iron estimations, became involved in the investigation of a hypochromic anemia in India during World War II. This led to another such study in Uganda after the war. There, an investigation of the incidence of sickling led to the discovery of overall differences between Hamitic-speaking tribes and the Bantu and Nilotes. A few exceptions could later be explained on the basis of the effect of malaria on sickling incidence. A mapping of the world distribution of sickle-cell and other hemoglobins followed, as well as a search for factors which cause the severity of sickle-cell anemia to vary. A most important lowering influence on this severity seems to be that of alpha-thalassemia. It is suggested that the high incidence of alpha-thalassemia type 2 (alpha/alpha alpha) in malarial regions is not related to malaria itself but to the beta-chain abnormalities which protect against malaria and therefore are frequent in the same populations. Alpha thalassemia in turn has a selective value because it lowers the pathological effect of sickle-cell anemia, as well as the consequences of Hemoglobin E and beta-thalassemia.
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PMID:Sickle cell anemia 35 years ago: reminiscence of early African studies. 637 13

It is suggested here that a Hemoglobin S (HbS)-mediated membrane oxidant injury is responsible for both the protection from malaria infection in the heterozygous sickle cell state, and for a critical pathologic process in homozygous sickle cell disease. This suggestion is arrived at by applying to the HbS condition the oxidant stress model for malaria resistance. Such a model had been developed to explain the protection from malaria in thalassemia and in glucose-6-phosphate dehydrogenase (G6PD) deficiency (9).
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PMID:Hemoglobin S-mediated membrane oxidant injury: protection from malaria and pathology in sickle cell disease. 647 60

There are no definitive data on the frequency of beta-thalassaemia in the Province of Terni; a mass screening programme has not been carried out. Preliminary studies confirm that there is a strong incidence of beta-thalassaemia heterozygotes. A theory can be put forward for the presence of beta-thalassaemia trait, based on the notion of the multicentric genesis of the disorder: the malaria may have been the dominant selective factor.
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PMID:[Beta thalassemia: motivation for screening in Terni]. 651 14


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