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

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

Procoagulant alterations and thrombocytopenia in falciparum malaria correlate with parasitemia, serum levels of tumor necrosis factor alpha (TNF alpha), and clinical severity. Thus, heparin or acetylsalicylic acid (ASA), which are used frequently to prevent thrombosis and (in the case of ASA) to control fever, could be potentially beneficial. We randomized 97 patients with falciparum malaria into three groups: 33 patients received low-dose heparin subcutaneously, 31 received ASA intravenously, and 33 did not receive either drug. All patients received appropriate antiparasitic treatment. Eighteen of 97 patients (seven receiving heparin, five receiving ASA, and 6 in the control group) had complications upon admission. During therapy, elevated TNF alpha and lactate dehydrogenase levels and decreased platelet counts returned to normal values. Except for a minimal partial thromboplastin time prolongation with heparin, heparin or ASA did not affect any laboratory parameter, duration of parasitemia, fever clearance, or the length of hospitalization. Thus, it appears that ASA and heparin do not influence the course of falciparum malaria. Hence, in view of possible side effects, these substances should not be recommended for routine use in the treatment of human malaria.
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PMID:Neither heparin nor acetylsalicylic acid influence the clinical course in human Plasmodium falciparum malaria: a prospective randomized study. 195 71

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

Swiss albino mice were infected by the intraperitoneal route with P. berghei berghei malaria parasite, and platelets, white cell counts and some coagulation parameters were monitored in order to find out whether changes reported in man also occurred in the mice. Parasitaemia developed form the 2nd post-infection day and reached significant levels by the 4th-6th day. Reduced circulating platelets which reached severe thrombocytopenic levels were observed. parallel with the increasing degree of parasitaemia. Anaemia which progressed to severe degree was also observed as was a slight leucocytosis attributed to the presence of normal mouse erythrocytes in the peritoneal space. All untreated animals died by the 6th day of infection. Intramuscular chloroquine sulphate (20 micrograms/g body wt.) given for 7 days completely cured the malaria, and white cell and platelet counts were restored to preinfection levels in each animal about 2 weeks after treatment had ceased. Platelet hypersensitivity to exogenous ADP was observed within 48 hours of infection and persisted with the parasitaemia. Prothrombin time (PT) and activated partial thromboplastin time (APTT) were prolonged while clottable fibrinogen concentration was reduced.
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PMID:Platelet reactions in acute Plasmodium berghei infection in Swiss albino mice. 330 58

Preclinical studies have shown that curdlan sulphate (CRDS), a sulphated 1-->3-beta-D glucan, inhibits Plasmodium falciparum in vitro and down-modulates the immune response. A direct, non-specific effect on cytoadherence and rosetting may be predicted, as has been described with other sulphated polysaccharides, e.g. heparin. The anticoagulant effect of CRDS is 10-fold lower than heparin. Curdlan sulphate has, therefore, emerged as a candidate for adjunct medication in the treatment of severe/cerebral malaria. Two clinical studies were conducted using CRDS as adjunct medication to conventional therapy (artesunate) in patients with severe and severe/cerebral malaria. Both studies were double-blind and placebo-controlled to evaluate the efficacy and safety of the combination. Curdlan sulphate appeared to reduce the severity of the disease process, e.g. fever clearance time was shortened. Due to the small number of patients, there was no difference in mortality. The two treatment arms in both studies showed similar results for all laboratory parameters. The only adverse event recorded during CRDS treatment was an increase in activated partial thromboplastin time. This can be monitored easily. It seems that the patients who may benefit most are severe/cerebral cases with no organ damage on admission.
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PMID:Curdlan sulphate in human severe/cerebral Plasmodium falciparum malaria. 1578 Mar 39

This study was undertaken to observe the changes in coagulation and platelet profile, and findings were correlated with their outcome. Forty consecutive children with severe falciparum malaria were studied for their coagulation status, i.e. prothrombin time (PT), activated thromboplastin time (APTT), thrombin time (TT) and anti-thrombin-III (AT-III), platelet profile (platelet count, platelet aggregation with adenine diphosphate (ADP) and ADR and PF3 availability). Derangements in the coagulation profile in the form of increased PT, APTT and/or TT were seen in 47.5, 35 and 62.5% cases, respectively, but bleeding was seen in only six cases. Thrombocytopenia was found in 34 patients. Platelet aggregation with ADP and ADR revealed hypoaggregation in 95.3 and 97.5% cases, respectively, and were statistically significant. Platelet factor-3 availability was also significantly prolonged. Patients with prolonged PT, PF-3 and hypoaggregation with adrenaline had 1.4, 1.7 and 1.45 times higher risk of mortality.
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PMID:Coagulation status and platelet functions in children with severe falciparum malaria and their correlation of outcome. 1940 6

Thrombocytopenia develops early in malaria, but the underlying mechanisms remain incompletely understood. We studied the aetiology of malaria-associated thrombocytopenia in volunteers experimentally infected with Plasmodium falciparum malaria, in Indonesian malaria patients and in ex vivo studies. In experimental human malaria, the decrease in platelet counts was associated with a concurrent rise in young platelets (immature platelet fraction) and thrombopoietin. D-dimer concentrations were moderately elevated without a prolongation in the activated partial thromboplastin time or decrease in fibrinogen. There was no increase in expression of the platelet surface markers CD62P, PAC-1 and CD63 and in plasma concentrations of the platelet factors P-selectin, CXCR4, CXCL7, RANTES and CD40L. In contrast, concentrations of soluble glycoprotein-1b (sGP1b), the external domain of the platelet receptor for von Willebrand factor (VWF), increased early. Indonesian malaria patients also had elevated concentrations of sGP1b, which correlated with VWF concentrations. Finally, incubation of platelets with parasitized erythrocytes in vitro failed to induce platelet aggregation or activation. We concluded that neither compromised platelet production nor platelet activation or consumptive coagulopathy were responsible for the early thrombocytopenia in malaria. We hypothesize that the increase in sGP1b concentrations results from VWF-mediated GP1b shedding; a process that may prevent excessive adhesion of platelets and parasitized erythrocytes.
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PMID:Thrombocytopenia in early malaria is associated with GP1b shedding in absence of systemic platelet activation and consumptive coagulopathy. 2095 4

Though both malaria and leptospirosis are frequent in the tropics, co-infections are under-recognized due to overlapping of clinical features. Here, we reviewed clinical manifestations of published co-infection along with our three cases. Out of a total of 18 patients, nine patients (50%) required ICU admission. Almost all patients had prodromal symptoms in the form of fever, headache and myalgia. Seven patients (37%) had altered sensorium, three patients (17%) had hypotension at admission, and 11 patients (61%) had acute kidney injury (AKI). Pulmonary manifestations in the form of pulmonary bleeding were present in four cases (22%). Three (17%) patients had acute lung injury/ acute respiratory distress syndrome. Almost 55% patients had DIC in the form of altered prothrombin time, activated partial thromboplastin time and low fibrinogen level. Four patients (22%) had subconjuctival suffusion, two of them had haematuria, while one presented with nasal bleeding. All patients had altered liver function tests. Of all the 18 patients, 17 (94%) survived, while one died.
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PMID:Clinical manifestations of co-infection with malaria and leptospirosis. 2172 89

A 5-year-old immunocompetent girl presented with fever, jaundice, hepatosplenomegaly and pancytopenia. The peripheral blood smear demonstrated mixed malaria infection (Plasmodium vivax and Plasmodium falciparum). Fever was persistent despite antimalarials in the absence of any coexisting bacterial or viral infection. Laboratory findings included cytopaenia, hyperbilirubinaemia, hyperferritinaemia, hypertriglyceridaemia, hyponatraemia, deranged partial thromboplastin time, decreasing ESR and megaloblastic changes on bone marrow aspiration. A final diagnosis of haemophagocytic lymphohistiocytosis (HLH) with megaloblastic anaemia associated with severe mixed malaria was made. There was a dramatic response to corticosteroid treatment with improvement in her clinical condition. This report endorses the use of corticosteroids in malaria-associated HLH whenever there is no clinical improvement with antimalarials alone.
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PMID:Haemophagocytic lymphohistiocytosis: a cause of unresponsive malaria in a 5-year-old girl. 2541 Jun 87

A 5-year-old immunocompetent girl presented with fever, jaundice, hepatosplenomegaly and pancytopenia. The peripheral blood smear demonstrated mixed malaria infection (Plasmodium vivax and Plasmodium falciparum). Fever was persistent despite antimalarials in the absence of any coexisting bacterial or viral infection. Laboratory findings included cytopaenia, hyperbilirubinaemia, hyperferritinaemia, hypertriglyceridaemia, hyponatraemia, deranged partial thromboplastin time, decreasing ESR and megaloblastic changes on bone marrow aspiration. A final diagnosis of haemophagocytic lymphohistiocytosis (HLH) with megaloblastic anaemia associated with severe mixed malaria was made. There was a dramatic response to corticosteroid treatment with improvement in her clinical condition. This report endorses the use of corticosteroids in malaria-associated HLH whenever there is no clinical improvement with antimalarials alone.
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PMID:Haemophagocytic lymphohistiocytosis: a cause of unresponsive malaria in a 5-year-old girl. 2674 59


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