Severe thrombocytopaenia in patients with vivax malaria compared to falciparum malaria: a systematic review and meta-analysis

Abstract

BackgroundPlasmodium vivax is the most geographically widespread species among human malaria parasites. Immunopathological studies have shown that platelets are an important component of the host innate immune response against malaria infections. The objectives of this study were to quantify thrombocytopaenia in P. vivax malaria patients and to determine the associated risks of severe thrombocytopaenia in patients with vivax malaria compared to patients with P. falciparum malaria.Main bodyA systematic review and meta-analysis of the available literature on thrombocytopaenia in P. vivax malaria patients was undertaken. Relevant studies in health-related electronic databases were identified and reviewed. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were followed. Fifty-eight observational studies (n = 29 664) were included in the current review. Severe thrombocytopaenia (< 50 000/mm3) to very severe thrombocytopaenia (< 20 000/mm3) was observed in 10.1% of patients with P. vivax infection. A meta-analysis of 11 observational studies showed an equal risk of developing severe/very severe thrombocytopaenia between the patients with P. vivax malaria and those with P. falciparum malaria (OR: 1.98, 95% CI: 0.92–4.25). This indicates that thrombocytopaenia is as equally a common manifestation in P. vivax and P. falciparum malaria patients. One study showed a higher risk of developing very severe thrombocytopaenia in children with severe P. vivax malaria than with severe P. falciparum malaria (OR: 2.80, 95% CI: 1.48–5.29). However, a pooled analysis of two studies showed an equal risk among adult severe cases (OR: 1.19, 95% CI: 0.51–2.77). This indicates that the risk of developing thrombocytopaenia in P. vivax malaria can vary with immune status in both children and adults. One study reported higher levels of urea and serum bilirubin in patients with P. vivax malaria and severe thrombocytopaenia compared with patients mild thrombocytopaenia or no thrombocytopaenia, (P < 0.001 in all comparisons). A pooled analysis of two other studies showed a similar proportion of bleeding episodes with thrombocytopaenia in severe P. vivax patients and severe P. falciparum patients (P = 0.09). This implied that both P. vivax and P. falciparum infections could present with bleeding episodes, if there had been a change in platelet counts in the infected patients. A pooled analysis of another two studies showed an equal risk of mortality with severe thrombocytopaenia in both P. vivax and P. falciparum malaria patients (OR: 1.16, 95% CI: 0.30–4.60). However, due to the low number of studies with small sample sizes within the subset of studies that provided clinically relevant information, our confidence in the estimates is limited.ConclusionThe current review has provided some evidence of the clinical relevance of severe thrombocytopaenia in P. vivax malaria. To substantiate these findings, there is a need for well designed, large-scale, prospective studies among patients infected with P. vivax. These sho...

Increased platelet distribution width and reduced IL-2 and IL-12 are associated with thrombocytopenia in Plasmodium vivax malaria

“…Thrombocytopenia is the most common haematological disorder in patients with malaria and one of the major concerns when accompanied by multiple organ failures. (5,6) In our study, thrombocytopenia was the main manifestation among patients with vivax malaria, though the reduction in platelet count was not associated with parasitaemia. Although some patients presented severe thrombocytopenia, none of them presented bleeding.…”

“…(4,5,6) The mortality rate in vivax malaria patients with severe thrombo-cytopenia alone can be comparable to that of falciparum malaria when associated with other danger signs of malaria (such as seizures, jaundice, bleeding, among others), and these can serve as red flags in order to promptly identify patients who may have severe malaria. (4,6,7,8) The pathogenesis of thrombocytopenia caused by malaria involves multifactorial phenomenon and leads to destruction and consumption of platelets. (9) In particular, in falciparum malaria, platelets also bind diffusely in systemic microvasculature, rather than pooling in the liver or spleen.…”

Late onset acute pancreatitis in P. falciparum malaria – An adverse reaction to intravenous artesunate?

“…A meta-analysis of 11 observational studies showed an equal risk of developing severe and/or very severe thrombocytopenia between the patients with P. vivax malaria and those with P. falciparum malaria. [ 3 ].…”

Empiric Treatment for Suspected Malaria in the United States: A Case Report

“…Thrombocytopenia commonly occurs in malaria as well. The exact mechanism is not completely understood but centers around immunologic mechanisms damaging thrombocytes and causing excess platelet removal [13]. Thrombocytopenia is reported to have high sensitivity (94%), high specificity (73%), and a high negative predictive value (97%) for malaria [14].…”