Hepatosplenomegaly among Kenyan schoolchildren has been shown to be exacerbated
where there is transmission of both Schistosoma mansoni and Plasmodium
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 with S. 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 with S. mansoni or P. falciparum. In comparison,
SEA-specific Th2 cytokine responses were low, and the levels were negatively
correlated with S. mansoni infection intensities and were lower among children
who were coinfected with P. 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 beta(1) 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.