1966
DOI: 10.1016/s0140-6736(66)91982-9
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125i-Labelled Fibrinogen in Cerebral Malaria

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Cited by 62 publications
(16 citation statements)
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“…Different mechanisms are postulated including lysis, splenic sequestration, phagocytosis of platelets or decreased production from the marrow. [5] Disseminated intravascular coagulation was also suggested to be responsible for thrombocytopenia [14,15] but it was later shown that most patients with malaria do not have disseminated intravascular coagulation. [16] A direct interaction with platelets and plasmodium has been suggested as plasmodium vivax has been demonstrated by electron microscopy to exist inside the platelets with vivax malaria.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Different mechanisms are postulated including lysis, splenic sequestration, phagocytosis of platelets or decreased production from the marrow. [5] Disseminated intravascular coagulation was also suggested to be responsible for thrombocytopenia [14,15] but it was later shown that most patients with malaria do not have disseminated intravascular coagulation. [16] A direct interaction with platelets and plasmodium has been suggested as plasmodium vivax has been demonstrated by electron microscopy to exist inside the platelets with vivax malaria.…”
Section: Discussionmentioning
confidence: 99%
“…It was difficult to ascertain whether anaemia was due to malaria or some other disease like nutritional deficiency anaemia or worm infestation or gastrointestinal bleeding as previous reports of haemoglobin were not available in most of the patients. Many workers have reported high incidence of anaemia [25,26,27] in falciparum malaria. Normocytic and normochromic morphology of red blood cells was observed in 78% of cases which was similar to findings of White NJ et al [28] The pathophysiology of anaemia in malaria could be multifactorial envolving a complex series of interactions envolving destruction of parasitized red blood cells, ineffective erythropoiesis or immune mechanisms.…”
Section: Discussionmentioning
confidence: 99%
“…Several factors, including various chemical mediators, dehydration, toxic damage to tubules due to intravascular hemolysis and hemoglobinuria, direct toxic effect of severe hyperbilirubinemia, cytoadherence of parasitized erythrocytes, disseminated intravascular coagulation, sepsis, and hyperparasitemia leading to impaired microcirculation in peritubular capillary network, have been implicated in the pathogenesis of the renal failure in malaria. [10][11][12][13][14][15] Acute tubular necrosis is the principal pathologic mechanism in malaria-induced renal failure, whereas acute glomerulonephritis and acute interstitial nephritis are less commonly observed. This study was conducted including the patients suffering from malarial AKI, to describe the clinical characteristics, laboratory parameters and outcome of malarial AKI.…”
Section: Introductionmentioning
confidence: 99%
“…Active platelet extractions have been found to be phospholipids, a platelet factor 3 (PF-3) which becomes available to the coagulant enzymes and cofactor at various stages of haemostasis. Many investigators [2][3][4][5][6][7] have observed marked alteration in haemostatic functions in malaria including thrombocytopaenia and bleeding disorders as a result of coagulation factors. Anaemia is an almost inevitable consequence of malaria infection but its pathophysiology is complex and has relatively little in common with anaemia of other infections 4 .…”
Section: Introduction: According To Marcfaclenementioning
confidence: 99%