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Hepatosplenomegaly among Kenyan schoolchildren has been shown to be exacerbated where there is transmission of bothSchistosoma mansoni andPlasmodium falciparum . This highly prevalent and chronic morbidity often occurs in the absence of ultrasound-detectable periportal fibrosis and may be due to immunological inflammation. For a cohort of school-age children, whole-blood cultures were stimulated withS. mansoni soluble egg antigen (SEA) or soluble worm antigen (SWA). Responses to SWA were found to be predominantly Th2 cytokines; however, they were not significantly associated with either hepatosplenomegaly or infection withS. mansoni orP. falciparum . In comparison, SEA-specific Th2 cytokine responses were low, and the levels were negatively correlated withS. mansoni infection intensities and were lower among children who were coinfected withP. falciparum . Tumor necrosis factor alpha levels in response to stimulation with SEA were high, and a negative association between presentation with hepatomegaly and the levels of the regulatory cytokines interleukin-6 and transforming growth factor β1 suggests that a possible mechanism for childhood hepatomegaly in areas where both malaria and schistosomiasis are endemic is poor regulation of an inflammatory response to schistosome eggs.

Hepatosplenomegaly Is Associated with Low Regulatory and Th2 Responses to Schistosome Antigens in Childhood Schistosomiasis and Malaria Coinfection