Abstract
Sphingosine 1-phosphate (S1P) is a lipid mediator formed by the metabolism of sphingomyelin which is involved in the endothelial permeability and inflammation. Although the plasma S1P concentration is reportedly decreased in patients with cerebral malaria, the role of S1P in malaria is still unclear. The purpose of this study was to examine the impact of malaria on circulating S1P concentration and its relationship with clinical data in malaria patients. Serum S1P levels were measured in 29 patients with P. vivax, 30 patients with uncomplicated P. falciparum, and 13 patients with complicated P. falciparum malaria on admission and on day 7, compared with healthy subjects (n = 18) as control group. The lowest level of serum S1P concentration was found in the complicated P. falciparum malaria group, compared with P. vivax, uncomplicated P. falciparum patients and healthy controls (all p < 0.001). In addition, serum S1P level was positively correlated with platelet count, hemoglobin and hematocrit levels in malaria patients. In conclusions, low levels of S1P are associated with the severity of malaria, and are correlated with thrombocytopenia and anemia. These findings highlight a role of S1P in the severity of malaria and support the use of S1P and its analogue as a novel adjuvant therapy for malaria complications.
Highlights
It was estimated that 3.2 billion people still remain at risk of malaria in 2015
Duration of illness was generally longer in complicated P. falciparum malaria patients
The mean malaria parasite count was significantly higher in the group of complicated P. falciparum malaria patients (699,780 parasites/μl) compared to uncomplicated P. falciparum (19,540 parasites/μl) and P. vivax malaria patients (9,840 parasites/μl)
Summary
It was estimated that 3.2 billion people still remain at risk of malaria in 2015. According to the latest reports, 214 million cases of malaria occurred globally with estimated mortality of 438,000 deaths [1]. Malaria in humans is caused by 5 plasmodium species, namely Plasmodium falciparum, P. vivax, P. malariae, P. ovale and P. knowlesi. Most of the fatal cases, which predominantly occur in P. falciparum infection, are due to cerebral malaria or severe anemia, but different clinical complications such as acute kidney injury, pulmonary edema, metabolic acidosis and thrombocytopenia exist and vary in severity and outcome, depending on the parasite species, the organ involved and the access to care [2, 3]. The pathogenicity of severe malaria infection is complex and it is regulated by both parasite and host factors.
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