Assessment of platelet indices and platelet activation markers in children with Plasmodium falciparum malaria

Asare, Renate; Opoku-Okrah, Clement; Danquah, Kwabena Owusu; Opare-Sem, Ohene; Addai‐Mensah, Otchere; Gyamfi, Daniel; Amponsah, Francis Agyei; Afriyie, Edward Y.; Duneeh, Richard Vikpebah; Ofosu, David Ntiamoah; Frimpong, Michael

doi:10.1186/s12936-020-03218-4

Cited by 9 publications

(5 citation statements)

References 16 publications

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“…Overall, our findings confirm previous observations by our group that platelets are not or only mildly activated during early asexual parasitemia in CHMI and that platelet activation is unlikely to explain the early drop in platelet count [27]. Our findings also do not provide evidence that activation of coagulation, and more specific thrombin, underlies the decrease in platelet count [28][29][30]. We assessed activation of the coagulation by measuring plasma concentrations of different plasma pro-and anticoagulation markers, as well as assays of TG and thrombin dynamics [31,32].…”

Section: Plos Onesupporting

confidence: 90%

Functional changes in hemostasis during asexual and sexual parasitemia in a controlled human malaria infection

Huang

Heijden²,

Reuling

et al. 2022

PLoS ONE

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Decreased platelet count is an early phenomenon in asexual Plasmodium falciparum parasitemia, but its association with acute or long-term functional changes in platelets and coagulation is unknown. Moreover, the impact of gametocytemia on platelets and coagulation remains unclear. We investigated the changes in platelet number and function during early asexual parasitemia, gametocytemia and convalescence in 16 individuals participating in a controlled human malaria infection study, and studied its relationship with changes in total and active von Willebrand factor levels (VWF) and the coagulation system. Platelet activation and reactivity were determined by flow cytometry, and the coagulation system was assessed using different representative assays including antigen assays, activity assays and global functional assays. Platelet count was decreased during asexual blood stage infection but normalized during gametocytemia. Platelet P-selectin expression was slightly increased during asexual parasitemia, gametocytemia and at day 64. In contrast, platelet reactivity to different agonists remained unchanged, except a marked decrease in reactivity to low dose collagen-related peptide-XL. Thrombin generation and antigen assays did not show a clear activation of the coagulation during asexual parasitemia, whereas total and active VWF levels were markedly increased. During gametocytemia and on day 64, the endogenous thrombin potential, thrombin peak and velocity index were increased and prothrombin conversion and plasma prothrombin levels were decreased. We conclude that the decreased platelet count during asexual parasitemia is associated with increased active VWF levels (i.e. endothelial activation), but not platelet hyperreactivity or hypercoagulability, and that the increased platelet clearance in asexual parasitemia could cause spontaneous VWF-platelet complexes formation.

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Section: Plos Onesupporting

confidence: 90%

Functional changes in hemostasis during asexual and sexual parasitemia in a controlled human malaria infection

Huang

Heijden²,

Reuling

et al. 2022

PLoS ONE

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“…Blood platelets have been found to be activated by substances secreted by Plasmodium falciparum . Circulating resting platelets taken from patients suffering for malaria show decreased expression of activation markers than resting platelets obtained from control subjects; however, following agonist stimulation, the platelets from malaria patients demonstrate greater expression of the markers of activation than non-malaria volunteers, thus indicating a hypersensitive state [ 90 , 91 , 92 ]. Therefore, in malaria patients, blood platelets may more readily adhere to endothelial cells [ 93 ], which also demonstrate a procoagulant phenotype characterised by increased endothelial production of reactive oxygen species, enhanced expression of P-selectin, tissue factor and plasminogen activator inhibitor 1 (PAI-1), and decreased expression of thrombomodulin [ 94 , 95 ].…”

Section: Platelet Tgfβ In Cerebral Malariamentioning

confidence: 99%

Blood Platelets as an Important but Underrated Circulating Source of TGFβ

Karolczak¹,

Watała²

2021

IJMS

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When treating diseases related primarily to tissue remodeling and fibrosis, it is desirable to regulate TGFβ concentration and modulate its biological effects. The highest cellular concentrations of TGFβ are found in platelets, with about 40% of all TGFβ found in peripheral blood plasma being secreted by them. Therefore, an understanding of the mechanisms of TGFβ secretion from platelets may be of key importance for medicine. Unfortunately, despite the finding that platelets are an important regulator of TGFβ levels, little research has been carried out into the development of platelet-directed therapies that might modulate the TGFβ-dependent processes. Nevertheless, there are some very encouraging reports suggesting that platelet TGFβ may be specifically involved in cardiovascular diseases, liver fibrosis, tumour metastasis, cerebral malaria and in the regulation of inflammatory cell functions. The purpose of this review is to briefly summarize these few, extremely encouraging reports to indicate the state of current knowledge in this topic. It also attempts to better characterize the influence of TGFβ on platelet activation and reactivity, and its shaping of the roles of blood platelets in haemostasis and thrombosis.

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“…Thrombocytopenia was observed in the current study, as in previously published reports. 15 Plasmodium falciparum infection affects platelets and directly contributes to thrombocytopenia, 48 which is a feature of malaria infection regardless of its severity. 49 Platelets play various roles in hemostasis, thrombosis, inflammation, immunity, and angiogenesis due to their wide array of stored chemokines and chemoattractants; 50 they play a similar role in malaria infection.…”

Section: Discussionmentioning

confidence: 99%

Elevated Levels of Procoagulant Microvesicles and Tissue-Factor Bearing Microvesicles in Malaria Patients

Madkhali¹,

Mobarki²,

Ghzwani³

et al. 2023

IJGM

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Background: Procoagulant microvesicles (MVs) are submicron membrane fragments released from activated cells and cells undergoing apoptosis. The procoagulant activity of MVs is enhanced in the presence of tissue factor (TF). MVs and TF are active mediators that induce pro-inflammatory response and prothrombotic tendency and have been linked to the severity of several disorders, including malaria infection. The current study aimed to measure the levels of circulating procoagulant MVs and TF-bearing MVs in malaria patients and correlate these levels with other hematological parameters and parasitemia. Materials and Methods: Levels of MVs and TF-bearing MVs in the plasma of children and adult patients infected with Plasmodium falciparum were measured alongside matched healthy controls. Results: Patients with Plasmodium falciparum infection had ~3.8 times MVs (p < 0.0001) and ~13.0 times TF-bearing MVs compared to the matched healthy controls. MVs showed inverse significant correlation with platelet count (p = 0.0055), hemoglobin (p = 0.0004) and parasitemia. Conclusion: Elevated levels of MVs and TF-bearing MVs could be useful biomarkers to evaluate the procoagulant activity, inflammatory response and parasitemia levels in malaria infection, aiding in better management of the disease.

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Assessment of platelet indices and platelet activation markers in children with Plasmodium falciparum malaria

Cited by 9 publications

References 16 publications

Functional changes in hemostasis during asexual and sexual parasitemia in a controlled human malaria infection

Functional changes in hemostasis during asexual and sexual parasitemia in a controlled human malaria infection

Blood Platelets as an Important but Underrated Circulating Source of TGFβ

Elevated Levels of Procoagulant Microvesicles and Tissue-Factor Bearing Microvesicles in Malaria Patients

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