Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An haematological, biological, parasitological and immunological study about anaemia of pregnancy was carried out in two rural village of Mali Republic, where P. flaciparum malaria is hyper-endemic. The 25 pregnant women found in the villages were compared with 23 controls. One could observe that anaemia more often normochromic and regenerative usually appears during the second trimestre of pregnancy. Only a few cases with haemaglobin levels below 8 g. % are hypochromic. Serum transferrin levels were slightly higher among pregnant. None among 31 bone marrows examined showed megaloblastic changes. Haptoglobin levels below 10 mg. % were observed in 3/4 of the pregnant women versus 1/4 in controls. Like some others, this study confirms the primary responsability of malaria haemolysis in the aetiology of anaemia of pregnancy and the interest of systematic chemoprophylaxis, at least from the third month of pregnancy. Vitamin and iron therapy is to consider therafter in hyper-endemic areas of P. falciparum malaria when nutritional problems are not predominant.
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PMID:Malaria and anemia of pregnancy in an African savanna zone. Epidemiological, hematological, biological and immunological study of 2 villages of the Bamako region, Republic of Mali. 58 Sep 10

Haptoglobin (Hp) polymorphism and its relationship to malaria infections was examined in Solomon Islanders under 25 years of age. The slide positive rate for malaria was 48% (53/111): Plasmodium vivax (Pv) 21 cases, Plasmodium falciparum (Pf) 16 cases and the remaining 16 were a mixture of Pv/Pf/P. malariae. Of 111 subjects examined, 17% (19 subjects) were ahaptoglobinemic (HpO). No association was observed between HpO and parasitemia, gender, anemia, serum insulin-like growth factor-1 (IGF-1) level, blood glucose level and enlargement of the spleen. These results suggest that malaria may not be the major cause of HpO in the people of the Solomon Islands.
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PMID:Relationship of haptoglobin polymorphism to malaria in the Solomon Islands. 764 99

Haptoglobin gene knockout mice and wild-type controls were infected with Plasmodium berghei ANKA or Plasmodium chabaudi. The peak parasitaemia and parasite burden were higher in Hp-/- mice than in Hp+/+ mice. The increase in spleen weight following malaria infection was smaller in Hp-/- mice than in Hp+/+ animals. The occurrence of cerebral malaria in P. berghei ANKA infection was not different in Hp gene knockout mice and their controls.
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PMID:Haptoglobin and malaria. 1186 83

Severe malarial anaemia (SA) is a major complication of malaria and an important cause of child mortality and morbidity. However, the pathogenesis behind SA is poorly understood. Nitric oxide (NO) is known to play a protective role against clinical malaria but is also suggested to have a pathogenic role in cerebral malaria (CM). Erythrophagocytosis by splenic macrophages has been implicated in the pathogenesis of SA. In this study, plasma levels of NO, neopterin, haptoglobin and C-reactive protein (CRP) were measured in paediatric patients with CM, n=77, SA (n=28) and uncomplicated malaria (UM n=53). Haptoglobin levels were significantly lower in SA (median (interquartile range) 25 (17-59) mg/l) than in both CM and UM (40 (24-80) mg/l and 110 (60-160) mg/l, respectively, P<0.001). In contrast, NO levels were higher in SA (38 (28-51) micromol/l) than in CM and UM (21 (15-32) micromol/l and 10.3 (5.6-17) micromol/l, respectively, P<0.001). A significant negative correlation between haptoglobin and NO was seen in the SA group. No such correlation was observed within the UM or CM groups. No significant differences in neopterin levels were observed between any of the three groups, neither was there any correlation between parasitaemias and neopterin levels. The low haptoglobin and high levels of NO in this SA group may contribute to haemolysis. Taken together our results support the hypothesis that immune-mediated erythrocyte destruction is involved in the pathogenesis of malarial anaemia.
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PMID:Elevated levels of nitric oxide and low levels of haptoglobin are associated with severe malarial anaemia in African children. 1208 54

Intravascular hemolysis is associated with several pathologic conditions that include hemoglobinopathies, trauma, malaria, and bacterial infections. Among plasma-protective proteins against oxidative damage caused by red blood cell rupture, haptoglobin and hemopexin are thought to play a crucial role. Haptoglobin and hemopexin, by binding with high-affinity hemoglobin and heme, respectively, exert an antioxidant action by preventing heme-catalyzed free radical production. Moreover, these proteins prevent iron loss by inhibiting glomerular filtration of hemoglobin and heme diffusion through plasma membranes. Analysis of single-null mice demonstrated the antioxidant action of haptoglobin and hemopexin in vivo and suggests that the 2 proteins cooperate in the resolution of hemolytic stress. To evaluate the physiological relevance of the haptoglobin-hemopexin system and the principal targets of its action, we generated haptoglobin-hemopexin double-knockout mice and analyzed them under basal conditions and after acute hemolysis. Whereas haptoglobin-hemopexin double-null mice displayed no obvious alteration in phenotype under basal conditions, nonlethal hemolytic stress in these animals led to pronounced splenomegaly as well as liver inflammation and fibrosis. These data demonstrate that haptoglobin and hemopexin together are essential for protection from splenomegaly and liver fibrosis resulting from intravascular hemolysis.
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PMID:Enhanced splenomegaly and severe liver inflammation in haptoglobin/hemopexin double-null mice after acute hemolysis. 1239 71

Haptoglobin (Hp) polymorphism analysed among P. vivax and P. falciparum patients and malaria negative subjects from areas with different epidemiological situations had shown high incidence of ahaptoglobinemia (HpO) among malaria patients. A definite association of HpO with P. vivax as well as P. falciparum malaria in Indian subjects had been observed. However, low sensitivity and reliability of HpO index indicates that it can not be a good indicator for determination of malaria endemicity. About 75 per cent of HpO subjects with P. vivax infection when treated with chloroquine showed typable Hp polymorphs by 8-9 days of post-treatment.
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PMID:Ahaptoglobinemia (HpO) and malaria in India. 1468 4

Haptoglobin (Hp) polymorphisms in sub-Saharan Africa have been associated with an increased risk of severe malaria. However, available data are inconclusive. We examined the role of Hp polymorphisms in susceptibility to Plasmodium falciparum infection and to severe malaria in northern Ghana. Three groups each of 290 age and sex-matched children with severe malaria, children with asymptomatic P. falciparum infection and aparasitaemic healthy controls were studied. Hp typing was based on PCR. In all children, Hp1-1, Hp2-1, and Hp2-2 occurred in 32.4%, 54.1%, and 13.5%, respectively. The prevalence of the Hp genotypes did not differ significantly between groups. However, Hp2 alleles were least common in healthy children (0.379), more frequent in parasitaemic controls (0.402), and most common in severe malaria patients (0.434; = 3.7; P = 0.06). In matched pair analysis, no Hp genotype increased the risk of severe malaria. However, using Hp1-1 as a reference, children with Hp2-2 exhibited a slightly increased risk of severe malaria (odds ratio, 1.6; P = 0.04). These results indicate that Hp polymorhisms may have a rather limited influence on the development of severe malaria.
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PMID:Limited influence of haptoglobin genotypes on severe malaria in Ghanaian children. 1596 Jul 5

Haptoglobin (Hp) levels were investigated in relation to host genotype in a malaria-endemic area in Gabon. A cross-sectional study of 1-12-year-old children was conducted in the rainy season, a period of high malaria transmission, to examine this relationship. Variables that influenced Hp levels were Hp genotype, location, and age interacting with parasite density. At low parasite densities, there was a negative correlation between Hp levels and age. At higher densities, there was a positive correlation with age. This suggests that in the presence of greater parasite-induced hemolysis, older children are capable of increased production of Hp. Sickle cell trait and ABO blood group was not associated with Hp levels in this population.
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PMID:Association of haptoglobin levels with age, parasite density, and haptoglobin genotype in a malaria-endemic area of Gabon. 1640 42

Haptoglobin (Hp) is an acute phase protein that removes free hemoglobin (Hb) released during hemolysis. Hp has also been shown to be toxic for malaria parasites. alpha(+)-Thalassemia is a hemoglobinopathy that results in subclinical hemolytic anemia. alpha(+)-Thassemia homozygosity confers protection against severe malarial disease by an as yet unidentified mechanism. Hp levels were measured in a serial cross-sectional survey of children in Madang Province, Papua New Guinea (PNG). Hp levels were related to age, Hp genotype, Hb levels, parasitemia, splenomegaly, and alpha(+)-thalassemia genotype. Surprisingly, children who were homozygous for alpha(+) -thalassemia had significantly higher levels of Hp than did heterozygotes, after controlling for relevant confounders. We suggest that this is the result of either reduced mean cell Hb associated with alpha(+) -thalassemia homozygosity or an elevated IL-6-dependent acute phase response.
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PMID:Haptoglobin levels are associated with haptoglobin genotype and alpha+ -Thalassemia in a malaria-endemic area. 1676 May 5

Haptoglobin is an acute phase protein that scavenges haemoglobin in the event of intravascular or extravascular haemolysis. The protein exists in humans as three main phenotypes, Hp1-1, Hp2-2 and Hp2-1. Accumulated data on the protein's function has established its strong association with diseases that have inflammatory causes. These include parasitic (malaria), infectious (HIV, tuberculosis) and non-infectious diseases (diabetes, cardiovascular disease and obesity) among others. Phenotype-dependent poor disease outcomes have been linked with the Hp2-2 phenotype. The present review brings this association into perspective by looking at the functions of the protein and how defects in these functions associated with the Hp2 allele affect disease outcome. A model is provided to explain the mechanism, which appears to be largely immunomodulatory.
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PMID:Haptoglobin, inflammation and disease. 1848 67


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