Functional and ultrastructural changes of platelets in malarial infection

Mohanty, Dipika; Marwaha, Neelam; Ghosh, Kanjaksha; Sharma, Sanjeev; Garewal, G.; Shah, Seema; Devi, Surekha A.; Das, K. C.

doi:10.1016/0035-9203(88)90122-8

Cited by 55 publications

(61 citation statements)

References 18 publications

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“…The negative association between age and platelet counts could support the involvement of immune mechanisms in the pathogenesis of thrombocytopenia. 7,[9][10][11] Another important issue could be the negative association between parasitemia and platelet counts, another finding previously reported in small series of patients. 2,26 Little attention has been paid to circulating platelets in severe malaria.…”

Section: Discussionmentioning

confidence: 85%

“…2,17 It could be explained by platelet activation 2,6 and an enhanced aggregability. 11,28 Although the purpose of this study was not to determine the mechanisms of malaria-related thrombocytopenia, the results can be interpreted in light of several issues involving platelets in patients with severe malaria. The negative association between age and platelet counts could support the involvement of immune mechanisms in the pathogenesis of thrombocytopenia.…”

Section: Discussionmentioning

confidence: 99%

“…1,13 Disseminated intravascular coagulopathy is now considered quite rare. 2,3,11,14 Although platelet invasion by malarial parasites 15 and platelet phagocytosis 16 have been reported, it appears to have little clinical relevance. 17 These mechanisms, which were studied mostly in adults, may coexist in a patient and interfere with each other.…”

Section: Introductionmentioning

confidence: 99%

“…A central mechanism is unlikely since increased numbers of megakaryocytes are found in patients with acute malaria. 7,8 There are converging arguments in favor of immunemediated destruction, 7,9-11 platelet activation, 2,6,11 removal by the reticuloendothelial system 2,7,12 or consumption in different steps of coagulation. 1,13 Disseminated intravascular coagulopathy is now considered quite rare.…”

Section: Introductionmentioning

confidence: 99%

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Prognostic value of thrombocytopenia in African children with falciparum malaria.

Gérardin¹,

Rogier²,

Ka³

et al. 2002

The American Journal of Tropical Medicine and Hygiene

152

122

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Abstract. Thrombocytopenia is a common finding in malaria, but its prognostic value has not been addressed in children. The relationship between thrombocytopenia (platelet count < 100,000/mm 3 on admission) and severity and outcome was investigated prospectively in children hospitalized with falciparum malaria in Dakar, Senegal, an area that is hypoendemic for malaria. Of 288 falciparum cases, 215 matched the 2000 World Health Organization definition of severe malaria. Median platelet counts were lower (98,000/mm 3 versus 139,000/mm 3 ; P < 0.02) among severe cases than in mild cases, and in children who died than among those who recovered (68,500/mm 3 versus 109,000/mm 3 ; P < 0.002). In severe cases, children presenting with a platelet count < 100,000/mm 3 were more likely to die (odds ratio [OR] ‫ס‬ 6.31, 95% confidence interval [CI] ‫ס‬ 2.0-26.0). Moreover, multivariate analysis identified thrombocytopenia as an independent predictor of death (OR ‫ס‬ 13.3, 95% CI ‫ס‬ 3.2-55.1). Our data show an association between thrombocytopenia and either severity or prognosis in childhood falciparum malaria.

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Prognostic value of thrombocytopenia in African children with falciparum malaria.

Gérardin¹,

Rogier²,

Ka³

et al. 2002

The American Journal of Tropical Medicine and Hygiene

152

122

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“…Actually, the incubation of platelets with P. falciparum-parasitised RBCs also increases platelet aggregation per se in vitro, especially after ADP and thromboxane A 2 addition (Inyang et al 1987). Even electron microscopic examination of non-stimulated, fresh platelets from malarial patients show centralisation of dense granules, glycogen depletion and microaggregates and phylopoids as a sign of in vivo activation, which could be responsible for a pseudothrombocytopenia due to sequestration of these activated particles in the interior of the vessels (Mohanty et al 1988). Contradictory data were presented showing aggregation impairment in severe falciparum patients after ADP addition in vitro (Srichaikul et al 1988).…”

mentioning

confidence: 99%

Thrombocytopenia in malaria: who cares?

Lacerda

Mourão

Coelho

et al. 2011

Mem. Inst. Oswaldo Cruz

186

173

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Key words: Plasmodium falciparum -Plasmodium vivax -malaria -thrombocytopenia -plateletsMalaria and thrombocytopenia • Marcus Vinícius Guimarães Lacerda et al. 53Data on the real burden of thrombocytopenia associated with malaria is contradictory in the literature and it is not usually considered when conducting patient selection. Table I shows the major publications estimating the frequency of thrombocytopenia. Most of these data were published in the late 1990s, probably in time with the surge in the availability of affordable automated machines capable of performing full blood counts (FBC). Manual platelet counting is time-consuming and usually needs to be requested by the physician with the routine blood count in most of the endemic areas for malaria. In only three publications is there an adequate randomised enrollment of patients with appropriate sample size calculation to estimate the frequency of bleeding and its association with the respective platelet count (Lacerda 2007, Silva 2009, Kochar et al. 2010. Only one study has ruled out other common causes of thrombocytopenia that are also endemic in the studied area (Lacerda 2007). There is a wide range of thrombocytopenia occurrence in these reports, which may be explained by distinct selection criteria of the enrolled patients. There are also differences in the selection of outpatients or inpatients from tertiary care centres that tend to present with severe thrombocytopenia. Furthermore, clinical manifestations of thrombocytopenia are usually described as case reports and most of these are due to P. vivax (Table II).In 2005, 138 of 684 (20.1%) malarial cases hospitalised in a tertiary care centre in Manaus had thrombocytopenia as the cause of admission, which corresponded to 6.8% of hospitalisations due to all causes in this reference institution (unpublished observations). Hospitalisation, however, does not add any benefit to the patient and because there is no evidence for any intervention, this simply increases public health costs in underdeveloped and under-resourced areas.Pathogenesis of malarial thrombocytopenia -Coagulation disturbances -A study based on 31 American soldiers in Vietnam with chloroquine-resistant falciparum malaria noted the following changes in the acute phase of the disease using the same patients as their own controls during convalescence: decrease in the platelet count and prothrombim activation time, increase in the activated thromboplastin time, and reduction in factors V, VII and VIII with normal fibrinogen (Dennis et al. 1967). This report suggested that thrombocytopenia was simply a consequence of the coagulation disorders presented by these patients, an idea that persisted for many decades in the literature. In another series of 21 patients with falciparum malaria, six had developed disseminated intravascular coagulation (DIC). The authors noted that the patients with more severe thrombocytopenia also had DIC and that there was correlation between platelet count and C3 protein levels. However, the reduction in C3 was pr...

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Fibrinolysis, inhibitors of blood coagulation, and monocyte derived coagulant activity in acute malaria

et al. 1997

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Different parameters of fibrinolytic systems like t-PA, PAI, D-dimer, and inhibitors of blood coagulation, i.e., protein C (PC), protein S(PS), and antithrombin III (AT-III), have been studied in cases of acute malaria due to Plasmodium falciparum and plasmodium vivax infection, and these patients were followed up. It was observed that the plasma PAI-1 was very high in cases of P. falciparum malaria infection as compared to normal controls and P. vivax infection. The changes in complicated cases of P. falciparum were remarkable as compared to uncomplicated ones. The PC, PS, and AT-III levels were also low in P. falciparum, particularly so in complicated cases, and were normal in P. vivax infection. The factor VIII R:Ag levels were invariably high in acute malaria. On follow-up of some of these cases the values came back to normal after the antiparasite treatment. The monocyte procoagulant activity was found to be significantly higher in P. falciparum infection as compared to that of P. vivax infection. All these findings therefore contribute towards the production of a hypercoagulable state in P. falciparum infection and partly explain the complications of P. falciparum infection like cerebral malaria.

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Functional and ultrastructural changes of platelets in malarial infection

Cited by 55 publications

References 18 publications

Prognostic value of thrombocytopenia in African children with falciparum malaria.

Prognostic value of thrombocytopenia in African children with falciparum malaria.

Thrombocytopenia in malaria: who cares?

Fibrinolysis, inhibitors of blood coagulation, and monocyte derived coagulant activity in acute malaria

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