Mechanisms of Thrombocytopenia in Malignant Tertian Malaria

Skudowitz, R. B.; Katz, J.; Lurie, A.; Levin, Joseph; Metz, J.

doi:10.1136/bmj.2.5865.515

Cited by 114 publications

(68 citation statements)

References 16 publications

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“…15,[19][20][21] As previously reported, thrombocytopenia was more profound in the severe than uncomplicated cases. 22 This may be due to excessive splenic pooling of platelets 23 and macrophage-mediated platelet destruction. 24 Blood urea nitrogen (BUN) level was more elevated in the severe than in the uncomplicated group.…”

Section: Patient Characteristicsmentioning

confidence: 99%

CR1 density polymorphism on erythrocytes of falciparum malaria patients in Thailand.

Nagayasu

Ito²,

Akaki³

et al. 2001

The American Journal of Tropical Medicine and Hygiene

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Abstract. Complement receptor type 1 (CR1) on erythrocytes shows an inherited numerical polymorphism which correlates with a HindIII-RFLP (restriction fragment length polymorphism) of the CR1 gene in various populations. To investigate the relationship between CR1 density polymorphism and disease severity, we typed 185 Thai patients with acute falciparum malaria (55 severe and 130 uncomplicated) for their genotypes of this polymorphism. The level of expression of erythrocyte CR1 from 42 randomly selected patients was measured by enzyme-linked immunosorbent assay (ELISA). We observed a significantly higher frequency of homozygotes of the CR1 low density allele (LL) among the severe group as compared to the uncomplicated group (P ϭ 0.005). CR1 expression on erythrocytes from patients with the LL genotype was significantly lower than homozygotes with the high density allele (HH) (P Ͻ 0.0001) and heterozygotes (HL) (P ϭ 0.013). The results suggest that a genetically-determined low CR1 density on erythrocytes may be a risk factor for developing a more severe form of malaria in Thai subjects.

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Section: Patient Characteristicsmentioning

confidence: 99%

CR1 density polymorphism on erythrocytes of falciparum malaria patients in Thailand.

Nagayasu

Ito²,

Akaki³

et al. 2001

The American Journal of Tropical Medicine and Hygiene

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“…Some data suggested that platelets were sequestered in the spleen during the acute infection (Skudowitz et al 1973). In the experimental model with Plasmodium chabaudi, thrombocytopenia was absent in splenectomised mice, showing that the spleen was essential for thrombocytopenia (Watier et al 1992).…”

mentioning

confidence: 99%

Thrombocytopenia in malaria: who cares?

Lacerda

Mourão

Coelho

et al. 2011

Mem. Inst. Oswaldo Cruz

174

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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“…Early studies demonstrated a shortened lifespan of platelets [4] and uninfected erythrocytes [5] in non-immune patients with falciparum malaria [6]. Ingestion of non-infected and ring-stage infected RBCs by splenic macrophages has been documented by electron microscopy [7], and evidence for hemophagocytosis by bone marrow macrophages is available [8,9].…”

Section: Introductionmentioning

confidence: 99%