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

The effect of iron therapy on malarial infection was investigated in Papua New Guinea, where malaria is endemic. Prepubescent schoolchildren with hemoglobin levels of 8-12 g/dl were randomly assigned to receive either 200 mg ferrous sulfate or a placebo twice daily for 16 weeks. Iron status and malarial infection were assessed at baseline, after 6 and 16 weeks of therapy, and 8 weeks after therapy was discontinued. Iron status was significantly improved by the treatment. The treatment did not significantly affect parasite rate, parasite density, or levels of anti-malarial IgG. No changes in spleen size were observed in either group. Furthermore, there was no significant difference between the groups in reported episodes of suspected malaria during the therapy. These results suggest that, in malaria endemic areas, oral treatment for iron deficiency can be carried out in semi-immune or immune schoolchildren without adverse consequences.
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PMID:The effect of iron therapy on malarial infection in Papua New Guinean schoolchildren. 264 55

Diferric transferrin reductase, assayed by formation of ferrous - bathophenanthroline, is detectable in the plasmamembrane of intact mature erythrocytes infected with Plasmodium falciparum. The absence of this transmembrane redox system in uninfected mature erythrocytes suggests its synthesis and incorporation by the intraerythrocytic parasite. The presence of diferric transferrin reductase, together with parasite-derived transferrin-receptor in the erythrocyte membrane, suggests a transferrin receptor-mediated uptake of iron by the malaria parasite.
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PMID:Diferric transferrin reductase in Plasmodium falciparum-infected erythrocytes. 264 31

Nine Thai adults with P. vivax malaria were investigated. Light and electron microscope studies of marrow aspirates revealed morphological evidence of dyserythropoiesis in six of them. Dyserythropoiesis was most marked in the four most anaemic patients. In these four patients the electron microscope also revealed the presence of erythroblasts at various stages of degradation within the cytoplasm of macrophages. Neither the dyserythropoiesis nor the ineffective erythropoiesis could be attributed to a deficiency of vitamin B12, folate or iron. The abnormalities of erythropoiesis seemed to result from the P. vivax infection itself. Other bone marrow reactions seen in this infection included macrophage hyperplasia, plasmacytosis and increased eosinophil granulocytopoiesis. Unlike in severe P. falciparum malaria, the microvasculature of the marrow was not obstructed by parasitized red cells.
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PMID:Dyserythropoiesis and ineffective erythropoiesis in Plasmodium vivax malaria. 266 Sep 3

The aetiology of severe anaemia (haemoglobin less than 7.0 g dl-1) has been studied in 37 pregnant Zambians. Aetiology was usually multiple; 31 (84%) had Plasmodium falciparum malaria, 23 (62%) were folate deficient, 13 (35%) were iron deficient, one had sickle-cell anaemia and one had the acquired immunodeficiency syndrome (AIDS). Folate deficiency was most often secondary to malarial haemolysis: iron deficiency was nutritional, but hookworm was contributory in about one-third of patients. The anaemia of malaria and folate deficiency was both more common and more severe than anaemia due to iron deficiency; it was seen in younger women although primigravidae were not over-represented, it occurred earlier in pregnancy, and was associated with low birthweight. AIDS must now be included in the differential diagnosis of anaemia in pregnancy. Vigorous antimalarial treatment and prophylaxis are essential in the management and prevention of anaemia in pregnancy. Total dose iron infusion is indicated only when severe iron deficiency anaemia has been proven, and must be accompanied by antimalarial therapy and folic acid supplements. Because of the risk of transmission of human immunodeficiency virus, it is more important than ever to prevent anaemia and malaria in pregnancy, and to give blood transfusion only as a life-saving treatment.
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PMID:The aetiology of severe anaemia in pregnancy in Ndola, Zambia. 268 77

Haemozoin (malaria pigment) was isolated from 2 strains of Plasmodium falciparum cultivated in vitro. The purest preparations contained 41 to 45% ferriprotoporphyrin IX and a glycine-rich polypeptide ('apohaemozoin') of approximately 14 kDa molecular weight which is synthesized by the parasite. In the two strains studied, NF54 and K1, it was calculated that about 15 and 18 iron porphyrin molecules, respectively, were associated with each molecule of apohaemozoin, which contained more hydrophobic amino acid residues in strain K1. One molecule of iron porphyrin was associated with every 9-10 amino acid residues in the haemozoin of both strains. Our observations support the idea that the intraerythrocytic malaria parasite, incapable of cleaving the haem ring, detoxifies the iron porphyrin residuum from haemoglobin digestion in a crystalline complex with a specially synthesized protein.
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PMID:The composition of haemozoin from Plasmodium falciparum. 269 24

Major causes of anaemia in pregnancy in tropical Africa are malaria, iron deficiency, folate deficiency and haemoglobinopathies: now there is added also the acquired immune deficiency syndrome (AIDS). Anaemia is often multifactorial, with the different causes interacting in a vicious cycle of depressed immunity, infection and malnutrition. Anaemia progresses through 3 stages: compensation, with breathlessness on exertion only; decompensation, with breathlessness at rest and haemoglobin (Hb) below about 70 g/litre; cardiac failure, with Hb below about 40 g/litre. Without treatment, over half of the women with haematocrit less than 0.13 and heart failure die. Maternal anaemia, malaria and deficiencies of iron and folate cause intrauterine growth retardation, premature delivery and, when severe, perinatal mortality. Surviving infants have low birthweights, immune deficiency and poor reserves of iron and folate. They have entered already the vicious cycle of infection, malnutrition and impaired immunity. Treatment with blood transfusions is even more hazardous since the advent of AIDS, and should be limited to saving the life of the mother. Treatment of malaria is complex as chloroquine-resistant strains are now common. Prevention remains relatively easy with proguanil and supplements of iron and folic acid and is highly cost-effective in the improvement of maternal and infant health; it is more important than ever as it avoids the unnecessary exposure of women and infants to HIV transmitted through blood transfusion.
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PMID:Tropical obstetrics and gynaecology. 1. Anaemia in pregnancy in tropical Africa. 269 76

Sera from non-malarial (control) and Plasmodium falciparum-infected (malaria) subjects were assayed for transferrin and iron. The mean serum transferrin concentration in the malaria sera was found to be elevated by 44% above the control value. The mean serum iron was also raised in the malaria sera, but the increase (19%) was found to be well below that of transferrin. The mean saturation of serum transferrin with iron fell from 42 +/- 17% in the control group to 37 +/- 9% in the malaria group. It is suggested that the increase in transferrin concentration in the sera of malaria subjects probably resulted from an increase in the rate of transferrin synthesis, perhaps in response to the raised serum iron and/or the hypoxia which is known to be associated with malaria infection.
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PMID:Changes in serum transferrin and iron concentrations in humans suffering from malaria with parasitaemia. 269 81

Secretion of TNF from mouse peritoneal macrophages exposed to LPS in vitro was enhanced in the presence of H2O2 or sodium periodate. Neither of these agents induced release of TNF in the absence of LPS. Both iron chelators and free radical scavengers inhibited this enhanced secretion of TNF, implying the involvement of free radicals via a Fenton-type reaction. Oxidant stress, in the form of alloxan or divicine, also enhanced serum levels of TNF in mice made sensitive to LPS by low-level infection with malaria, and then given i.v. LPS. Pretreatment with the iron chelator, desferal, or the free radical scavenger, BHA, inhibited TNF release in these animals. Less TNF was also detected in mice given desferal before LPS in the absence of exogenous radical generator. These results could have implications for understanding the details of the MLR, the adherence of neutrophils to the walls of pulmonary vessels in free radical-induced lung pathology, and the side effects of bleomycin.
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PMID:Reactive oxygen species facilitate the in vitro and in vivo lipopolysaccharide-induced release of tumor necrosis factor. 274 81

The effect of iron supplementation on attending behavior of 96 1-y-old infants was assessed in a double-blind, randomized, controlled trial of iron dextran in Papua New Guinea. The treatment group received an injection of iron dextran at 2 mo; the controls received a placebo injection. Because many children had malarial parasitemia at testing, presence of malaria was used in the analysis. A significant interaction was found between iron and malaria infection on total fixation time: iron-supplemented groups and placebo-treated parasitemic children showed significantly higher total fixation scores than did placebo-treated aparasitemic children. Blood analysis of iron status showed similar results, with lowest iron status evident in the placebo-treated aparasitemic group. There was no effect of treatment on rate of habituation or dishabituation. Supplemental iron treatment has a significant effect on attention but the direction of the effect depends on the presence of malaria infection.
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PMID:Behavioral effects of iron supplementation in infants in Madang, Papua New Guinea. 277 41

The association of pruritus and ingestion of chloroquine phosphate in Saradidi, Kenya, was determined by randomly giving 437 children (less than 18 years) and 182 adults either 10 mg base kg-1 of regular chloroquine, 10 mg base kg-1 of enteric-coated chloroquine, 10 mg base kg-1 of amodiaquine, or one 300 mg tablet of enteric-coated ferrous sulphate. Before treatment, a blood smear was taken. Paired urine samples were tested for 4-aminoquinolines to exclude prior drug ingestion, to document drug absorption, and to exclude chloroquine or amodiaquine intake in persons who received iron. The following day, the incidence of itching was ascertained. More adults (20.3%) reported itching than did children (12.8%) (P less than 0.05); no significant difference between males and females was noted. A history of itching 24 hours after treatment was not significantly more common in persons with malaria parasitaemia. Pruritus was more frequent in those receiving regular chloroquine (21.5% of 186) and enteric-coated chloroquine (17.8% of 118) than after amodiaquine (11.6% of 173) or iron (8.5% of 142) (P less than 0.005). Amodiaquine which is a 4-aminoquinoline like chloroquine did not appear to cause significant pruritus in this population. These results demonstrate that chloroquine-associated pruritus is experienced frequently in Saradidi. This side effect of malaria treatment could influence usage of chloroquine phosphate provided by village health workers.
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PMID:Epidemiology of chloroquine-associated pruritus in Saradidi, Kenya. 296 16


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