Sudan is the most afflicted country with malaria in the Eastern Mediterranean, accounting for approximately 46% of cases in the region with a predominance of P. falciparum [1]. This study revealed that the majority of patients infected with P. falciparum in Kosti city had low-level parasitemia. Although hematological indices in P. falciparum-infected patients can provide clues to the associated hematological abnormalities, no published study was found among patients from Kosti. In the present study, P. falciparum-infected patients showed significantly lower median values of Hb, RBC count, MCH, MCHC, neutrophils, lymphocytes and platelets compared to malaria-negative counterparts. In line with the present study, a significantly lower median platelet count was found among Sudanese children with falciparum malaria compared to malaria-negative ones [13]. In contrast, a significantly higher median WBC count and non-significant differences between the median values of Hb and RBC count were observed in infected children [13]. The significantly lower values of hematological indices among P. falciparum-infected patients in Kosti city are consistent with those reported in malaria-endemic areas elsewhere [9, 27–31].
Substantial proportions of patients with falciparum malaria and malaria-negative subjects in Kosti city were anemic. However, the majority of P. falciparum-infected patients (60.4%) were anemic compared to less than a third of malaria-negative subjects, with a significant association between falciparum malaria and anemia. In contrast, anemia was reported among approximately 21.0% of patients and was not significantly associated with falciparum malaria in West Kordufan state [22]. In agreement with the present findings, a slightly higher anemia prevalence of 67.0% with a significant association with malaria was reported among Ethiopian patients [9]. Malaria-associated anemia is multi-factorial and could be attributed, among other factors, to mechanical or autoimmune hemolysis, splenic sequestration of infected and non-infected RBCs and suppressed erythropoiesis following cytokine release [18, 32–34].
Thrombocytopenia has been assumed to occur in P. falciparum-infected patients irrespective of exposure frequency or disease severity [35]. In line with this assumption, more than two-thirds of P. falciparum-infected patients in Kosti were thrombocytopenic. Thrombocytopenia was a significant predictor of falciparum malaria, which is consistent with that recently reported for patients with falciparum malaria in West Kordufan, even though a lower thrombocytopenia prevalence of 21.3% (75/353) was found [22]. In another context, malaria-positive blood donors were found to have significantly higher platelet counts than malaria-negative ones in Khartoum [36]. The significantly lower platelet count among patients in the present study is consistent with the findings reported among patients in other malaria-endemic countries [8, 9, 28–31]. The inclusion of thrombocytopenia as a criterion for the re-definition of severe malaria has been proposed [37]. Likewise, a recent study among Sudanese children in Gezira state recommended thrombocytopenia as a prognostic tool for assessing falciparum malaria severity [38]. In Khartoum state, the prevalence of thrombocytopenia was significantly higher among children with severe malaria compared to those with uncomplicated malaria [39]. Several factors contribute to malaria-related thrombocytopenia, including platelet agglutination at early stages of the disease, splenic sequestration and pooling of platelets and immune-mediated destruction [17, 40, 41].
The present study revealed normal total WBC counts among P. falciparum-infected and malaria-negative subjects, with comparable and non-significantly different proportions of leucopenia. Nevertheless, the prevalence of leucopenia among patients in the present study is higher than that (6.3%) reported from West Kordufan [22]. The lack of association between falciparum malaria and thrombocytopenia among patients from Kosti city disagrees with the significant association reported for patients from West Kordufan [22]. Despite the significant differences in the median percentages of differential WBC counts between the infected and non-infected populations, these were within normal ranges. This makes the total and differential WBC counts not useful in predicting falciparum malaria in the study area and could be partially attributed to the low parasitemia and uncomplicated nature of falciparum malaria among the study participants. Low-to-normal WBC counts in malaria patients is a frequent observation that could also be explained by their localization outside the peripheral blood [42]. Therefore, the mobilization of WBCs could not be ruled out in case of severe falciparum malaria.
This study is limited by the fact that it was hospital-based, and the hematological findings might not reflect the situation at the population level. However, it provides information that can guide clinical predictions about malaria of low-level parasitemia among patients with abnormal hematological indices in the study area. With the lack of previous studies, this could be a pilot one that warrants further community-based assessment of the profile of hematological indices and abnormalities in falciparum-infected patients in relation to malaria exposure frequency and severity.