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

Glucose-6-phosphate dehydrogenase (G6PD) is expressed in all tissues, where it catalyses the first step in the pentose phosphate pathway. G6PD deficiency is prevalent throughout tropical and subtropical regions of the world because of the protection it affords during malaria infection. Although most affected individuals are asymptomatic, there is a risk of neonatal jaundice and acute haemolytic anaemia, triggered by infection and the ingestion of certain drugs and broad beans (favism). A rare but more severe form of G6PD deficiency is found throughout the world and is associated with chronic non-spherocytic haemolytic anaemia. Many deficient variants of G6PD have been described. DNA sequence analysis has shown that the vast majority of these are caused by single amino acid substitutions. The three-dimensional structure of G6PD shows a classical dinucleotide binding domain and a novel beta + alpha domain involved in dimerization.
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PMID:Glucose-6-phosphate dehydrogenase deficiency. 1091 76

A prospective study, aimed to investigate the aetiology of an unusual clustering of cases of severe acute haemolytic anaemia affecting a high percentage of the adult population, was carried out in two isolated Yanomamo communities of the Upper Orinoco basin in Venezuela. Twenty-six patients with active or recent episodes of severe haemolysis were evaluated. All of them exhibited massive liver and spleen enlargement and fulfilled the diagnostic criteria of the hyperreactive malarious splenomegaly (HMS) syndrome. In four cases with advanced non-alcohol-related chronic liver disease, hypersplenism, severe haemolytic anaemia and acanthocytosis, the characteristic clinical and laboratory findings of spur cell anaemia were documented. Chronic infection by the HBV and HCV was present in three of them. However, in most of the 22 additional HMS cases, the acute haemolytic condition appeared associated with the occurrence of a cold agglutinin-mediated autoimmune response. The clustering of a significant number of cases of severe acute haemolysis in HMS patients from this small isolated aboriginal community is most unusual, and represents a serious complicating factor for a population already beleaguered by a high prevalence of malaria due to multiresistant strains of Plasmodium falciparum. Moreover, the coexistence of HMS and severe chronic HBV or HCV infection may further aggravate the course of the haemolytic disorder, because of the occurrence of spur cell anaemia.
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PMID:Spur cell anaemia and acute haemolysis in patients with hyperreactive malarious splenomegaly. Experience in an isolated Yanomamo population of Venezuela. 1111 87

Development of complications is very common among the patients suffering from Plasmodium falciparum infection. A total of 64 patients of Plasmodium falciprum infections were admitted to the District Hospital, Ukhrul, during the period of 1st May 1996 to 15th June 1999; 9.37% patients do not develop complication while the rest 90.63% developed one or more complications. The most common complication is anaemia accounting for 76.56% followed by cerebral malaria (59.38%). Other lesser complications were leucopenia (15.63%), thrombocytopenia (26.56%), adult respiratory distress syndrome (6.25%). There is no single record of blackwater fever, 12.5% died due to development of multiple complications like severe haemolytic anaemia, haemolytic jaundice, cerebral malaria and acute renal failure. This study confirms presence of severe and complicated falciparum malaria in this part of the country.
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PMID:Severe falciparum malarial complications in Ukhrul, Manipur. 1125 90

Imported malaria remains a difficult problem in nonendemic areas of the world. We describe the clinical presentation of 101 cases of malaria diagnosed at the Leuven University Hospital between 1 January 1990 and 31 December 1999. Ninety-three patients (92%) presented initially at the emergency department. Diagnosis was initially not suspected by the referring physician in 48 patients (47%). Plasmodium falciparum was the commonest species, accounting for 67% of the cases. All but three patients had fever as the presenting symptom, but only 10 had a typical tertian fever pattern. Haemolytic anaemia, thrombocytopenia and hyponatraemia represented a typical triad in 20% of the cases. Only 13% of the malaria patients had taken correct chemoprophylaxis according to WHO recommendations. Eighty-three per cent of the patients were admitted to the hospital with a median duration of hospitalization of 4 days. All complications occurred in cases with P. falciparum. All patients were cured.
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PMID:Imported malaria in the 1990s: a review of 101 patients. 1178 95

Heme, a ubiquitous iron-containing compound, is present in large amounts in many cells and is inherently dangerous, particularly when it escapes from intracellular sites. The release of heme from damaged cells and tissues is supposed to be higher in diseases such as malaria and hemolytic anemia or in trauma and hemorrhage. We investigated here the role of free ferriprotoporphyrin IX (hemin) as a proinflammatory molecule, with particular attention to its ability to activate neutrophil responses. Injecting hemin into the rat pleural cavity resulted in a dose-dependent migration of neutrophils, indicating that hemin is able to promote the recruitment of these cells in vivo. In vitro, hemin induced human neutrophil chemotaxis and cytoskeleton reorganization, as revealed by the increase of neutrophil actin polymerization. Exposure of human neutrophils to 3 microM hemin activated the expression of the chemokine interleukin-8, as demonstrated by quantitative reverse-transcription polymerase chain reaction, indicating a putative molecular mechanism by which hemin induces chemotaxis in vivo. Brief incubation of human neutrophils with micromolar concentrations of hemin (1-20 microM) triggered the oxidative burst, and the production of reactive oxygen species was directly proportional to the concentration of hemin added to the cells. Finally, we observed that human neutrophil protein kinase C was activated by hemin in vitro, with a K(1/2) of 5 microM. Taken together, these results suggest a role for hemin as a proinflammatory agent able to induce polymorphonuclear neutrophil activation in situations of clinical relevance, such as hemolysis or hemoglobinemia.
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PMID:Neutrophil activation by heme: implications for inflammatory processes. 1201 Aug 21

Malaria is a complex infectious disease in which the host/parasite interaction is strongly influenced by host genetic factors. The consequences of plasmodial infections range from asymptomatic to severe complications like the neurological syndrome cerebral malaria induced by Plasmodium falciparum in humans and Plasmodium berghei ANKA in rodents. Mice infected with P. berghei ANKA show marked differences in disease manifestation and either die from experimental cerebral malaria (ECM) or from hemolytic anemia caused by hyperparasitemia (HP). A majority of laboratory mouse strains so far investigated are susceptible to ECM; however, a number of wild-derived inbred strains show resistance. To evaluate the genetic basis of this difference, we crossed a uniquely ECM-resistant, wild-derived inbred strain (WLA) with an ECM susceptible laboratory strain (C57BL/6J). All of the (WLA x C57BL/6J) F(1) and 97% of the F(2) progeny displayed ECM resistance similar to the WLA strain. To screen for loci contributing to ECM resistance, we analyzed a cohort of mice backcrossed to the C57BL/6J parental strain. A genome wide screening of this cohort provided significant linkage of ECM resistance to marker loci in two genetic regions on chromosome 1 (chi(2) = 18.98, P = 1.3 x 10(-5)) and on chromosome 11 (chi(2) = 16.51, P = 4.8 x 10(-5)), being designated Berr1 and Berr2, respectively. These data provide the first evidence of loci associated with resistance to murine cerebral malaria, which may have important implications for the search for genetic factors controlling cerebral malaria in humans.
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PMID:Identification of two cerebral malaria resistance loci using an inbred wild-derived mouse strain. 1211 35

We report a 68-year-old woman with severe falciparum malaria contracted in Tanzania. She presented high parasitemia and was treated successfully with intravenous artesunate, a qinghaosu derivative, and aggressive supportive therapy. She developed hemolytic anemia and jaundice on day 11 and blood transfusion was required. This case illustrates that intravenous artesunate has excellent antimalarial activity with rapid efficacy and that no severe adverse effect but conventional aggressive supportive therapy is still important in the treatment of severe falciparum malaria.
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PMID:[Severe falciparum malaria with prolonged hemolytic anemia after successful treatment with intravenous artesunate]. 1232 18

Malaria in pregnancy is one of the most important preventable causes of low birthweight deliveries worldwide. It is also a major cause of severe maternal anaemia contributing to maternal mortality. It is estimated that 40% of the world's pregnant women are exposed to malaria infection during pregnancy. The clinical features of Plasmodium falciparum malaria in pregnancy depend to a large extent on the immune status of the woman, which in turn is determined by her previous exposure to malaria. In pregnant women with little or no pre-existing immunity, such as women from non-endemic areas or travellers to malarious areas, infection is associated with high risks of severe disease with maternal and perinatal mortality. Women are at particular risk of cerebral malaria, hypoglycaemia, pulmonary oedema and severe haemolytic anaemia. Fetal and perinatal loss has been documented to be as high as 60-70% in non-immune women with malaria. Adults who are long-term residents of areas of moderate or high malaria transmission, including large parts of sub-Saharan Africa, usually have a high level of immunity to malaria. Infection is frequently asymptomatic and severe disease is uncommon. During pregnancy this immunity to malaria is altered. Infection is still frequently asymptomatic, so may go unsuspected and undetected, but is associated with placental parasitization. Malaria in pregnancy is a common cause of severe maternal anaemia and low birthweight babies, these complications being more common in primigravidae than multigravidae. Preventative strategies include regular chemoprophylaxis, intermittent preventative treatment with antimalarials and insecticide-treated bednets.
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PMID:Importance and prevention of malaria in pregnancy. 1288 1

A case of congenital malaria infection has been studied in a 46-day old female Korean infant. Her mother suffered from malaria infection during pregnancy in Uppervolta, Africa, and returned to Korea at the 9th month of gestation for delivery. At 39 days of age, the clinical features characterized by fever, irritability, pallor, jaundice and hepatosplenomegaly were developed. The laboratory data revealed a hemolytic anemia with thrombocytopenia, hyperbilirubinemia and increased hepatic enzyme values. A peripheral blood smear demonstrated intraerythrocytic malarial parasites snd gametocytes of Plasmodium falcifarum. She was successfully treated with quinine sulfate (25 mg/kg/day in three doses for 5 days) and trimethoprim/sulfamethoxazole (8 mg/kg/day in two doses for 5 days) orally, and repeated blood smear had been negative for malaria. This report also signifies the frst description of congenital malaria in Korea imported from Uppervolta in Africa. A brief review of related literature was made.
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PMID:[A case of congenital malaria] 1289 Oct 34

The recombinant congenic mouse strains AcB55 and AcB61 are extremely resistant to malaria (Plasmodium chabaudi AS) despite the presence of susceptibility alleles at the known Char1/Char2 resistance loci. Resistance in AcB55 and AcB61 is controlled by a locus on chromosome 3 (Char4) shown to be allelic with or tightly linked to a loss-of-function mutation in pyruvate kinase (Pklr). AcB55 and AcB61 show important splenomegaly prior to infection caused by the expansion of the red pulp, and display histological signs of extramedullary erythropoiesis in the liver. Examination of splenic cell populations by flow cytometry demonstrates elevated numbers of TER119-positive erythroid precursor cells (>30% of total spleen cells), while RNA expression studies show elevated expression of erythrocyte-specific transcripts such as globin, transferrin receptor, and Nramp2/Slc11a2 in the spleen of both strains. Hematological profiling in both strains is consistent with the presence of anemia as evidenced by low total erythrocyte counts, decreased hemoglobin, as well as abnormally high numbers of circulating reticulocytes (15-20%). These results strongly suggest that the mutant Pklr allele (Pklr(269A)) of AcB55/61 strains causes hemolytic anemia compensated by constitutive erythropoiesis, which in turn protects the mice against P. chabaudi infection. The possible molecular basis of the Pklr protective effect is discussed and is under current investigation in these two strains.
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PMID:Phenotypic expression of pyruvate kinase deficiency and protection against malaria in a mouse model. 1502 38


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