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

Nine non-immune patients with imported falciparum malaria were examined for signs of diffuse intravascular coagulation (DIC). Although all had thrombocytopenia initially and some later had a decline in plasma fibrinogen concentrations, DIC was never detected, even in severely affected patients with coma and kidney damage. None of the patients were given heparin and all recovered without residual symptoms. Heparin administration should probably be considered only when clear-cut DIC, which possibly never occurs in falciparum malaria, has been demonstrated.
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PMID:Haemostatic defect in non-immune patients with falciparum malaria: no evidence of diffuse intravascular coagulation. 35 86

A serial study of coagulation activation and whole-blood viscosity was performed on 37 patients with local or systemic bacterial infection, malaria, or a viral infection. Thrombocytopenia, without consumption of coagulation factors, was the main feature of benign tertian malaria and viral infection, whereas in septicaemia and malignant tertian malaria it was associated with activation of coagulation and fibrinolysis. Patients with evidence of intravascular coagulation showed the highest levels of factor VIII related antigen which did not correlate with fibrinogen and probably reflected vascular endothelial cell damage rather than an acute-phase protein reaction. Hyperviscosity, which has been implicated in the pathogenesis of endotoxic shock and cerebral malaria, occurred in parallel with the acute-phase rise in plasma fibrinogen. There was, however, no evidence to implicate hyperviscosity as a major causative factor in the pathogenesis of septic shock or severe infective illness.
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PMID:Coagulation activation and hyperviscosity in infection. 47

Uniformly fatal simian malaria was induced in ten rhesus monkeys by injection of Plasmodium knowlesi. The results of serial studies of platelet and blood coagulation factor levels suggested the occurrence of intravascular coagulation during the last 48 hours of the disease, concurrent with a marked fall in hematocrit levels. Fibrinogen survival was slightly decreased (two animals), but quantitative fibrinogen levels were elevated. Pathologic studies revealed only minimal evidence of fibrin deposition without indication of resultant tissue damage. The results are consistent with terminal intravascular coagulation possibly triggered by massive destruction of parasitized red blood cells.
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PMID:Simian Plasmodium knowlesi malaria: studies of coagulation and pathology. 81 Nov 25

A pathophysiologic study was made in 15 patients with acute renal failure due to falciparum malaria. Marked increase in plasma fibrinogen and elevation of serum fibrin degradation products were observed in all cases. The other coagulation parameters including prothrombin time, partial thromboplastin time, factor V and factor VIII were within the normal limits. Plasma hemoglobin was minimal. The blood viscosity was significantly increased. Blood volume study in 5 patients showed initial hypovolemia followed by hypervolemia and normovolemia. Decreased cortical renal blood flow was noted in renal hemodynamic study using 133Xe. Plasma renin activity was increased. Intravenous pyelography during the oliguric phase of renal failure revealed a poor nephrogram which increased in density at 24 and 48 h after the injection of the contrast material. The findings suggest the significance of reduction of renal blood flow in the pathogenesis of renal failure in human malaria. The roles of blood hyperviscosity and hypovolemia are emphasized.
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PMID:Renal failure in malaria: a pathophysiologic study. 86 56

A global review of the porblem of malaria accidentally transmitted by blood transfusion is reported in France during these ten last years. Biological and epidemiological studies of malariae are recorded. Among the factors involved in the transmission of malariae by blood transfuction, the persistence of the parasites in the donors is very important. It is often longer than usual in the subjects who have lived in endemic malarious areas for many years or are always travelling in these countries, because they are partly protected by their acquired immunity and may be carriers of asymptomatic infection. The viability of parasites in stored blood, red cells and preparations with platelets, leucocytes or plasma containing a few red cells with parasites is discussed. The prevention depended on the elimination of any blood donor who has ever had malaria appears to be the simplest method but it is also the most failible. The screening of donors by direct microscopy is obviously impracticable because of low density and often submicroscopic level of their parasitoemia. Screening donors by IFA test is the best method. If IFA test is negative four months after coming back from endemic areas and two months after ending suppressive therapeutic, whole blood, red cells, leucocytes, platelets and fresh plasma can be used on condition that the stay of donors in endemic areas had been not too long. If the stay in these countries was very long, blood will be only used for preparing lyophilized plasma, fibrinogen immunoglobulins or albumin.
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PMID:[Post-tranfusional malaria in France]. 98 71

Monocytes are active elements of the host response against Plasmodium falciparum. They are able to express tissue factor and trigger the extrinsic pathway of blood coagulation the activation of which remained unclear in malaria. Our aim was to assess the tissue factor expression of purified blood monocytes stimulated by cultured Plasmodium falciparum-infected erythrocytes. Malaria parasite induced an early generation of tissue factor with a peak between 8 and 12 h of stimulation. Maximum expression was observed for parasitemia ranging from 1 to 2%. Plasmodium falciparum culture supernatants had the same effect showing the existence of a soluble factor able to induce the tissue factor expression. These data, demonstrating an activation of the tissue factor pathway by the malaria parasite, emphasize thrombin generation. Therefore, thrombin could participate in malaria pathology either in the microcirculatory blockade via platelet and fibrinogen activation or as a mitotic.
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PMID:Monocyte tissue factor expression induced by Plasmodium falciparum-infected erythrocytes. 141 53

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.
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PMID:Platelet kinetics and other hematological profiles in experimental Plasmodium falciparum infection: a comparative study between Saimiri and Aotus monkeys. 142 30

There are four hypotheses which have been advanced to explain the pathophysiology of severe and complicated malaria such as cerebral malaria. However, none of them adequately explains all the features of cerebral malaria in man. One such hypotheses is Disseminated Intravascular Coagulation (DIC). To determine whether this condition occurs in patients with uncomplicated malaria, the authors conducted a study on fibrinogen and its degradation products, euglobulin lysis time and parasite counts in 30 cases of uncomplicated malaria. By spectrophotometric method, plasma fibrinogen in patients with uncomplicated malaria was found to be normal as compared to normal healthy adults. There were no fibrinogen degradation production (FDP) detected in either patients or healthy controls, using latex agglutination tests at a dilution of 1:5. This method for FDP estimation is significant in that a serum agglutination with 1:5 dilution indicates a concentration of FDP in the original serum in excess of 10g/ml, designated as positive results of experiment. High values of euglobulin lysis time (ELT) were noted in patients with low parasitaemia. Analysis of these results showed that disseminated intravascular coagulation did not occur in uncomplicated cases of malaria. In this study on cases of uncomplicated malaria and low parasitaemia the biochemical parameters relating to to DIC have been essentially normal, although DIC is thought to be a primary stage in the development of cerebral malaria. According to Reid, DIC is an important intermediate mechanism in the pathophysiology of severe and complicated malaria such as cerebral malaria.
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PMID:Estimation of plasma fibrinogen and its degradation products in uncomplicated cases of malaria with low parasitemia. 147 15

Fourty eight patients with falciparum malaria (14) and vivax malaria (34) were evaluated retrospectively as to whether DIC (disseminated intravascular coagulation) had been complicated or not. Serum concentration of fibrin-degradation products (FDP) was elevated in 8 cases (57%) of falciparum malaria and 3 cases (9%) of vivax malaria. Thrombocytopenia was found in 12 cases (88%) of falciparum malaria and in 30 cases (86%) of vivax malaria. Prothrombin time elongated in 4 cases (8%) and plasma concentration of fibrinogen decreased in 3 cases (17%). Only 4 patients, all of them were infected with falciparum malaria and all of three cases of cerebral malaria were included, met the criteria for the diagnosis of DIC complication and one case in vivax malaria suspected of the DIC. Abnormality grades in FDP concentration has closest association with DIC among the coagulation tests, therefore FDP test is indispensable for checking complication of DIC in malaria cases. The clinical profiles of 3 cases of cerebral malaria complicated with DIC are presented in this report.
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PMID:[Incidences of DIC complication in Japanese patients with malaria]. 221 61

The incidence and progression of coagulation abnormalities were studied in 52 patients with acute falciparum malaria. The patients were prospectively divided into 3 groups; severe (parasitaemia greater than or equal to 5% or vital organ dysfunction), 12 patients; moderate (parasitaemia 1%- less than 5% without complications), 16 patients; and mild (parasitaemia less than 1%), 24 patients. No case died or developed clinical evidence of disseminated intravascular coagulation. Conventional indices of coagulation (prothrombin time, partial thromboplastin time, fibrinogen, fibrin degradation products) were usually within the normal range but reduced plasma concentrations of antithrombin III (AT-III) levels were noted in all groups, and the incidence was significantly higher in patients with severe and moderate malaria (83% and 81%) compared with the mild group (37%; P less than 0.005). Depletion of AT-III was associated with thrombocytopenia, decreased AT-III activity and elevated plasma concentrations of thrombin-antithrombin III complexes (P less than 0.01), confirming activation of the coagulation cascade and increased clotting factor consumption. AT-III levels returned to normal coincident with clinical improvement. Activation of coagulation is a common and sensitive measure of disease activity in acute falciparum malaria. It is not a specific feature, nor is there evidence to suggest it has a primary pathological role in severe infections.
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PMID:Activation of the coagulation cascade in falciparum malaria. 248 60


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