Plasmodium falciparum Infection Modulates Platelet Count than Leucocyte Parameters in Carriage of Different Haemoglobin Beta Subunit (HBB) Genotypes

Abstract

Background: Sickle cell disease is a prime genetic disorder due to a single nucleotide mutation resulting in haemoglobin gene (HbS) occurring in the regions where malaria is endemic. Though it primarily a disease of erythrocytes, non-erythrocytic cells are equally affected just like in malaria infection. Furthermore, leucocytes and thrombocytes have equally been hypothesized to be the driving force for sickle cell crisis. However, the modulatory trends and magnitude of Plasmodium falciparum infection on platelet and leucocyte parameters in sickle cell disease is not entirely explored.

Objectives: The current study therefore determined the modulatory effects of P. falciparum infection on platelet and leucocyte parameters in carriage of different haemoglobin beta subunit (HBB) genotypes.

Methodology: This cross-sectional study evaluated leucocytes and thrombocytes parameters in P. falciparum-infected and non-infected children (n=217, aged 1-192 months) with different HBB genotypes.  Children with acute febrile conditions were randomly selected and enrolled at Jaramogi Oginga Odinga Teaching and Referral Hospital for a period of ten months at outpatient clinic.  Haematological parameters were determined using Beckman Coulter counter ACTdiff2^TM while HBB genotyping was done using TaqMan^® SNP genotyping assay.  Chi-square (χ²) analysis was used to determine differences between proportions.  Mann-Whitney U test and Kruskal Wallis test were used for comparisons of demographic and laboratory characteristics wherever applicable.  Partial correlation test was used to determine relationship between leucocytes and thrombocyte parameters in carriage of different HBB genotypes while adjusting for age and sex as covariates.

Results: Generally, there were no differences in WBC (p=0.746), lymphocytes (p=0.103), monocyte (p=0.084) and granulocytes (p=0.354) between the infected and non-infected children. Platelet count [median (IQR); 236 (129.5), p=0.001] and PCT, [median (IQR); 0.13 (0.1), p=0.001] were markedly reduced in infected children. Specifically, monocytes had a positive correlation with platelet count (r= 0.742, p=0.002) in non-infected children with HbSS genotype. WBC revealed a positive correlation with platelet count in both infected and non-infected children (r =0.358, r² =0.128, p =0.047 and r = -0.638, r² =0.407, p= 0.047) in carriage of HbSS respectively WBC and RDW in children infected with falciparum in carriage of HbSS genotypes (r =0.818, r² =0.669, p =0.004). Monocyte count revealed a positive correlation with platelet count in non-infected children and no correlation in children infected with malaria (r= -0.742, P=0.022 and r= -0.245, P=0.525, respectively).

Conclusion: P. falciparum infection is responsible for a decrease the platelet count as WBC count increases in children with HbSS. Therefore, a decrease in platelet count against leukocytosis in carriage of HbSS should warrant a test for P. falciparum infection.

Keywords: Correlation, Haemoglobin, Haemoglobin beta sub-unit, genotype, Leucocyte, Thrombocyte.

DOI: 10.7176/JNSR/14-10-05

Publication date:August 31^st 2023