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

Early in 1973 residents of 20 randomly selected rural villages in southern Ghana were studied to determine the prevalence of anaemia. Laboratory tests were conducted to learn what haemoglobin phenotypes were present and the distribution of white blood cell counts. Moderate anaemia (below 10 g%) was fairly common, particularly in children and 15--29 year old women, but severe anaemia (below 7 g%) was rare. Malaria infection and diets with low iron content were major factors affecting haemoglobin level, while hookworm infestation and high parity had little effect. Neutropenia (about two-thirds of Caucasian values) and the distribution of haemoglobin types (AS 16.3%; AC 11.1%) were similar to findings in earlier studies. To improve haemoglobin levels in children and young women, low-cost intervention programmes based on volunteer village workers are recommended.
 ...
PMID:Haematological values in a rural Ghanaian population. 59 29

A case of profound neutropenia and severe infection after the administration of amodiaquine is presented. The recommended dose for malaria prophylaxis was administered.
 ...
PMID:Amodiaquine agranulocytosis. 85 90

Levels of platelets and other hematological values were monitored in 21 Saimiri and 12 Aotus monkeys over a period of three weeks post-infection with monkey-adapted Indochina CDC-1 strain of Plasmodium falciparum. In both Saimiri sciureus boliviensis and Aotus nancymai karyotype-1 monkeys the severest thrombocytopenia was observed at 14 days post-infection coinciding with peak parasitemia, neutropenia, lymphocytosis, and anemia associated with severe hemoglobinemia and elevated fibrinogen degeneration products(FDP's). MCH and MCV profiles in Aotus monkeys decreased with ascending parasitemia. In contrast, these parameters in Saimiri were characterized by a significant compensatory increase correlating with parasitemia. In general, thrombocytopenia was one of the earliest clinical manifestations of the infection with the platelets returning to normal levels shortly after peak parasitemia at 14 days. Platelet kinetics had a strong correlation with hematologic and parasitologic values in the Aotus model. No consistent associations were observed between platelet kinetics and other parameters in the Saimiri model. These data indicate that the Aotus model for malaria is more predictable than the Saimiri. Further, platelet turnover rates and recovery provide a useful prognostic parameter during malaria infection. The results are discussed in relation to the value of the two species of monkeys as models for the pathogenesis of human malaria.
 ...
PMID:Platelet kinetics and other hematological profiles in experimental Plasmodium falciparum infection: a comparative study between Saimiri and Aotus monkeys. 142 30

Levels of mature lymphocytes, granulocytes, macrophages, platelets, their progenitor cells, and cytokines were monitored in the blood, marrow, and spleen during fatal or nonfatal murine malarial infections. In all four malaria models, before anemia developed, there was a lymphopenia, a rapid lymphocyte depletion in the marrow with a compensating rise in spleen lymphocytes, thrombocytopenia with increased megakaryocytic progenitor cell numbers, and monocyte increases in the bone marrow and later the spleen. The development of anemia was associated with a monocytosis and neutropenia, an increase in granulomonocytic progenitor cells in the spleen, and a reduction of spleen lymphocytes. Spleen granulocytes, monocytes, and their progenitor cells increased two- to threefold more in nonfatal than in fatal malaria and the spleen lymphocyte pool became severely depleted in fatal malaria. The data suggest that a defective effector cell response was of importance for the fatal outcome of the disease. Other than an early rise in serum macrophage colony stimulating factor levels in fatal infections, changes in levels of the regulators of these effector cells did not correlate well with the outcome of the infection.
 ...
PMID:Changes in hemopoietic and regulator levels in mice during fatal or nonfatal malarial infections. II. Nonerythroid populations. 214 42

Ninety-nine consecutive patients who received cytotoxic therapy for acute leukemia were retrospectively studied to determine the pattern of infection at the Tata Memorial Hospital, Bombay, India. In all, 224 infective episodes occurred in these patients. Bacterial infection was the commonest type, accounting for 152 (67.9%) of 224 infective episodes, followed by fungal and viral infections (15.6% and 14.3%, respectively). Gram-negative organisms (Pseudomonas and Klebsiella) were the commonest bacterial organisms isolated, constituting 38 (76%) of 50 positive cultures; infection with Staphylococcus was rare (10%). Infective hepatitis, malaria, and systemic tuberculosis were responsible for fever with neutropenia in 20, 4, and 2 patients, respectively. Three hundred fifty-two patients with lymphoproliferative malignancies were also retrospectively studied to determine the pattern of infection. Only 53 infective episodes were recorded. In these patients, in contrast to those with acute leukemia, viral infection (33 [62.3%] of 53) and pulmonary tuberculosis (18 [34%] of 53) were frequently seen. It is interesting that 50% of our patients with hairy cell leukemia also had tuberculosis. Bacterial infection was conspicuous by its absence. Knowledge of the prevailing pattern of infection permits the development of investigative and therapeutic approaches of optimal efficacy.
 ...
PMID:Pattern of infection in hematologic malignancies: an Indian experience. 260 80

6 out of 7 patients with severe neutropenia associated with the use of amodiaquine for malaria prophylaxis amodiaquine (400 mg weekly) plus proguanil (200 mg daily); 1 of these patients had also taken cotrimoxazole and another had taken sulphaguanidine. The 7th patient had taken amodiaquine alone, but at a higher dose. A retrospective analysis suggests that the frequency of severe neutropenia complicating amodiaquine taken prophylactically may be as high as 1 in 2000.
 ...
PMID:Frequency of severe neutropenia associated with amodiaquine prophylaxis against malaria. 286 40

Seven cases of agranulocytosis and two of liver damage that were probably due to amodiaquine treatment were studied. In five cases agranulocytosis was combined with liver damage, and in one case of primary liver damage moderate neutropenia was present. Three patients died. High total doses or prolonged duration of treatment, or both, appear to favour the occurrence of these reactions. The clustering of five of the seven cases of agranulocytosis within six months in one medical centre indicates that the risk to benefit ratio of amodiaquine for malaria prophylaxis should be re-evaluated.
 ...
PMID:Amodiaquine induced agranulocytosis and liver damage. 308 10

We applied the microlymphocytotoxicity method to the detection of lymphocytotoxic antibodies in case of 37 patients with acute malaria or 61 patients who sojourned in endemic malaria area and presented antibodies against plasmodial antigens (indirect immunofluorescence test greater than or equal to 1/20). Lymphocytotoxic antibodies were found in 16 patients of the first group and their occurrence may explain the lymphopenia and to a lesser extent the neutropenia and thrombopenia observed in some cases. In the second group lymphocytotoxic antibodies were present in 9 cases. In all samples no anti-HLA specificity was evidenced. Four patients were submitted to auto-cross-match test and 3 were found positive suggesting that among these antibodies some are auto-antibodies with anti-lymphocyte specificity.
 ...
PMID:[Lymphocytotoxic antibodies in malaria]. 636 21

The clinicohaematological findings of acute state (Group A, 30 patients) and chronic state (Group B, 34 patients) of falciparum malaria in paediatric patients are compared. The children with chronic falciparum malaria were apyrexic and presented with features of moderate to severe anaemia with hepato-splenomegaly. Greater severity of anaemia and haemolysis, higher incidence and severity of neutropenia, atypical lymphocytosis, monocytosis and thrombocytopenia were observed in patients with chronic falciparum malaria as compared to patients with acute falciparum malaria despite lesser degree of parasitaemia in the former as compared to the latter. While mechanical destruction of parasitised RBC's, ineffective and dysplastic erythropoiesis either due to unmasking of border line dierty folic acid deficiency or otherwise, transient hypoplasia of bone marrow, impaired utilization of iron and immune destruction of RBCs with hypersplenism may be the mechanisms for anaemia, transient hypoplasia of bone marrow and hypersplenism may be the factors responsible for thrombocytopenia and neutropenia.
 ...
PMID:Clinico-haematological profile in acute and chronic Plasmodium falciparum malaria in children. 796 80

Infection of CBA mice with Plasmodium berghei ANKA results in severe malaria, which is characterized by mortality 6 to 10 days after infection and is associated with alterations of the brain microcirculation. These alterations consist of (i) intravascular sequestration of monocytes, (ii) an increase in vascular permeability as documented by Evans blue diffusion, and (iii) microhemorrhages. This syndrome may be due to an increase of production of tumor necrosis factor alpha which upregulates the endothelial expression of ICAM-1 and thus leads to adhesion of CD11a/CD18 (LFA-1)-bearing cells. During severe malaria, we found an important sequestration of the CD11a-bearing polymorphonuclear neutrophil leukocytes (PMN) in the lung but not in the brain. Treatment with a monoclonal antibody (MAb) against PMN, which induces profound neutropenia, prevented mortality and Evans blue diffusion in the brain and the lung, while it unexpectedly increased the occurrence of microhemorrhages. The anti-PMN MAb abolished PMN sequestration in the lung and also partially decreased monocyte sequestration in the brain and the lung. Treatment with an anti-CD11a MAb also prevented mortality, Evans blue diffusion, and PMN and monocyte sequestration. This study shows that PMN contribute to the mortality and the microvascular lesions resulting from severe malaria. This may be due to their CD11a-dependent sequestration in the lung and also to their indirect influence on vascular permeability and the sequestration of monocytes.
 ...
PMID:Role of polymorphonuclear neutrophil leukocytes and their integrin CD11a (LFA-1) in the pathogenesis of severe murine malaria. 813 19


1 2 3 Next >>