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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess immune responses to malaria-induced thrombocytopenia, an haematologic and immunologic study was performed on 25 patients with imported malaria upon admission and 8 days after treatment. Thrombocytopenia (150 x 10(9)/litre) was detected in 19 cases (P. falciparum: 11 cases, P. ovale: 6 cases, P. vivax: 2 cases). No laboratory evidence of disseminated intravascular coagulation impairment was found in any of the patients. Bone marrow examination performed in 9 cases showed no abnormality in the megakaryocyte series. Platelet count was independent of circulating parasite levels (r = 0.27) and inversely related to the number of antibody binding sites (ABS) on platelets (r = -0.6, p. less than 0.01). The indirect Coombs test (r = -0.54; p less than 0.01) and IgG and IgE levels (p less than 0.02) gave similar findings. A statistical correlation was observed between the level of circulating immune complex and the number of ABS (r = 0.525, p less than 0.01). Thus malaria-induced thrombocytopenia seems to mainly involve IgG type antiplatelet antibody activity. Although they may be implicated in the binding of antibodies to platelets, circulating immune complexes do not appear to mediate thrombocytopenia.
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PMID:[Platelet antibody activity in malaria thrombocytopenia]. 223 82

Malaria associated with complications or a fatal outcome is almost always caused by Plasmodium falciparum. The mortality due to this disease parallels the degree of parasitemia. Successful use of exchange blood transfusion as a therapeutic adjunct for this infection was first reported in 1974, although the efficacy of this procedure has not been established by randomized, controlled trials. The rationale for this form of therapy is based on: (1) rapid reduction in the parasite load by direct removal; (2) decreased risk of severe intravascular hemolysis and its consequences (disseminated intravascular coagulation and renal dysfunction); (3) improved rheology with transfused blood and reduced microcirculatory sludging; and (4) improved oxygen-carrying capacity with transfused erythrocytes. We describe a case of severe falciparum malaria and review the literature describing the use of exchange transfusion for treatment of this infection.
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PMID:Exchange transfusion as an adjunct to the treatment of severe falciparum malaria: case report and review. 192 97

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

This paper describes changes in the circulating platelets of 25 patients with acute malaria within 2 to 6 days of onset of illness. Thrombocytopenia was observed in 10 out of 15 patients with Plasmodium falciparum infection, and in 4 out of 9 patients with P. vivax infection. One patient with a mixed infection of both species had a disseminated intravascular coagulation. Platelet antibody was detected in the sera of 8 out of 11 cases by the complement lysis inhibition technique and indirect immunofluorescence. The mean platelet antibody concentrations in the sera of 11 patients and 53 control subjects were 122.70 +/- 80.25 ng/10(7) platelets and 36.69 +/- 18.72 ng/10(7) platelets, respectively. An inverse relationship between the platelet count and platelet antibody levels in serum supported the view that thrombocytopenia in malaria may be partly immune-mediated. Platelet aggregation responses to agonists such as ADP, adrenaline, collagen and ristocetin revealed hyperactivity. Ultrastructural study of unstimulated platelets from patients revealed several changes such as centralization of dense granules, glycogen depletion, and formation of pseudopods and microaggregates, indicating in vivo activation of the platelets, which may also lead to thrombocytopenia.
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PMID:Functional and ultrastructural changes of platelets in malarial infection. 306 47

Five imported falciparum malaria cases with severe evolution are reported. Treatment associated a blood exchange transfusion and an antimalaria chemotherapy (mefloquine in three patients and quinine in two patients). All patients were successfully cured despite of serious visceral complications occurring in two patients (pulmonary and cerebral oedema). Technical management of treatment is detailed. Exchange transfusion should be considered in falciparum malaria when parasitaemia overcomes 20% and when serious visceral impairment, hemolysis or consumption coagulopathy are occurring.
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PMID:[Value of exchange transfusion in the treatment of severe malaria (apropos of 5 cases)]. 331 64

Eleven of 43 nonimmune patients with falciparum malaria had one or several organ complications: cerebral malaria, acute respiratory failure, acute renal failure, secondary infection, autoimmune haemolysis, spontaneous spleen rupture, and acute pancreatitis. Parasitaemia was 0.1 to 60%. Initial antiparasitic therapy with quinine given parenterally resulted in rapid regression of parasitaemia. An additional schizonticide agent was given depending on parasitic resistance. Supportive therapy comprised intensive-care monitoring including fluid and electrolyte balance and, if necessary, early haemodialysis and (or) endotracheal intubation with PEEP breathing. In one patient with excessive parasitaemia exchange transfusion was performed. Heparin was given only in proven disseminated intravascular coagulation, corticosteroids only in persistent autoimmune haemolysis. All patients survived without suffering permanent defects. Retrospective analysis shows that, apart from rapid specific therapy, supportive treatment of the individual organ complications determines course and prognosis of complicated falciparum malaria.
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PMID:[Complicated malaria tropica: specific and supportive therapy in the imported diseases]. 351 46

We describe a case of fatal falciparum malaria, with severe pulmonary insufficiency in the absence of fluid overload or cardiac failure. At autopsy the most striking change was a marked pulmonary interstitial edema. The endothelial cell was the most altered structure, showing marked cytoplasmic swelling which narrowed the capillary lumen. Monocytes were also found occupying the capillary lumen. The edematous interstitium also showed macrophages with endocytes and malarial pigment. There was no disseminated intravascular coagulation or other terminal complications. The patient's respiratory insufficiency seems not to have derived from the complications usually associated with the fatal malaria but from malaria-induced alveolar septal changes.
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PMID:Ultrastructure of the lung in falciparum malaria. 388 10

Three cases of severe falciparum malaria with high parasitaemia, one of them complicated by disseminated intravascular coagulation, were treated with exchange transfusion in addition to conventional chemotherapy. All three made a good recovery. There are few previous reports of this treatment which deserves wider attention and further assessment.
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PMID:Exchange transfusion in severe falciparum malaria. 391 21

Fibrin(ogen) degradation products, platelet counts, antithrombin III, and the components of the Factor VIII complex were studied in a total of 80 patients with Plasmodium falciparum, Plasmodium vivax or Plasmodium ovale infections. The haemostatic findings were correlated to the numbers of parasitized erythrocytes and to each other. The results indicate that haemostatic changes in malaria correlate with the degree of parasitaemia. Evidence for moderate hyperfibrinolysis was found in patients with high P. falciparum parasitaemias only. Thrombocytopenia closely corresponded to parasitaemia and to von Willebrand factor levels, but appeared not to be linked to a consumption of coagulation factors. It was concluded that thrombocytopenia in malaria is not indicative of disseminated intravascular coagulation (DIC) but may relate to endothelial damage.
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PMID:Haemostatic alterations in malaria correlate to parasitaemia. 393 96

Research since the World War II has confirmed that, apart from the production of haemozoin from haemoglobin, most of the pathological processes in the evolution of malaria are nonspecific. A few of these nonspecific host reactions are discussed, including the production of inflammatory stasis in certain areas (including the brain) where the vascular endothelium is normally highly impermeable to heavy molecules. This production of stasis is regarded as the basic phenomenon in local obstruction to blood flow. So-called "plugging" of small vessels with "sticky" infected erythrocytes is discussed in relation to stasis and to deep intravascular schizogony. Nonspecific vasomotor effects including shock and renal and hepatic failure are also discussed. Intravascular coagulation is not regarded as a potentially important host response despite demonstrable consumption coagulopathy. The disease malaria is regarded as an example of a chain reaction of physiological-pathological responses in the host, which in the early stages are reversible.
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PMID:Other pathological processes in malaria. 421 9


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