RESUMO
BACKGROUND: Sickle cell disease (HbSS) is a major health problem in Nigeria and malaria has been implicated as a leading cause of morbidity/mortality in sickle cell disease patients. Few reasons were put forward to explain the observed morbidity/mortality of HbSS subjects due to Plasmodium falciparum (P. falciparum) malaria. OBJECTIVES: To determine the level of immunoglobulin classes (IgM, IgA, and IgG) and regulators of complement system (C1 inhibitor and C3 activator) in Nigerian HbSS patients with and without P. falciparum parasitemia. METHODS: A total of 64 subjects were considered, including 10 HbSS genotypic subjects with P. falciparum parasitemia (HbSS+PfM), 18 HbAA genotypic subjects with P. falciparum parasitemia (HbAA+PfM), 20 HbSS without P. falciparum parasitemia (HbSS-PfM), and 16 HbAA genotypic subjects without P. falciparum parasitemia (HbAA-PfM). IgM, IgA, IgG, C1 inhibitor, and C3 activator titers were quantified by single radial immunodiffusion method. RESULTS: The mean levels of IgG in HbSS+PfM (2373.90+/-1772.81mg/dl) and HbAA+PfM (1868.80+/-0.00mg/dl) were significantly higher compared with HbSS-PfM (644.55+/-171.15mg/dl) or HbAA-PfM (659.75+/-158.01mg/dl) patients. HbAA-PfM subjects had the lowest level of IgM (67.27+/-63.7mg/dl), though no significant difference was observed comparing mean levels of IgM between the four groups. IgA titer was significantly higher in HbSS-PfM patients (249.00+/-94.8mg/dl) compared with HbAA-PfM (p<0.05), HbAA+PfM (p<0.05), or HbSS+PfM (p<0.05). The mean values of C1 inhibitor were lower in HbSS+PfM and HbAA+PfM compared with HbSS-PfM or HbAA-PfM. However, HbAA+PfM had a significantly lower value of C1 inhibitor compared with HbAA-PfM (p<0.01). C3 activator was highest in HbSS-PfM (17.10+/-7.35mg/dl) and was significantly higher compared with HbSS+PfM (p<0.05). CONCLUSION: Increased C1 inhibitor and decreased C3 activator in HbSS+PfM compared with HbAA+PfM shows that deranged regulation of complement factors may be responsible for increased susceptibility of HbSS to P. falciparum malaria.
