article · The Journal of Infectious Diseases
Severe and potentially fatal outcomes in Schistosoma mansoni infections stem largely from portal hypertension caused by hepatic periportal fibrosis. An ultrasound study of liver and spleen conditions in a Sudanese community with endemic infection identified early fibrosis in 58 per cent, moderate fibrosis in 9 per cent, and advanced fibrosis in 3 per cent of residents. While early stages were common among children and adolescents, moderate fibrosis rose dramatically among men aged 21 to 30 and correlated with heavy infection burdens. Severe disease involving portal hypertension and splenomegaly affected 6 per cent of the community, appearing predominantly in adult men and clustering within specific family pedigrees. These findings indicate that the duration and intensity of infection, gender-linked influences, and genetic susceptibility drive the progression to severe hepatic fibrosis.
Schistosoma mansoni causes debilitating and potentially fatal liver complications in endemic regions. By identifying that severe fibrosis concentrates among adult men and specific family lineages, this research helps healthcare providers recognise who is at the greatest risk of lethal complications. This insight can support targeted clinical monitoring and timely medical intervention in vulnerable communities.
This work represents early-stage epidemiological research rather than a direct commercial product. The identification of genetic clustering and demographic risk markers could inform future diagnostic screening tools, prognostic risk-scoring systems, or public health surveillance programmes managed by health authorities. However, the abstract does not indicate an immediate application pathway or commercially available technology.
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Lethal disease in Schistosoma mansoni infections is mostly due to portal hypertension caused by hepatic periportal fibrosis. To evaluate the factors that may determine severe disease, livers and spleens were examined by ultrasound in a Sudanese population living in a village where S. mansoni is endemic. Early (FI), moderate (FII), or advanced (FIII) fibrosis was observed in 58%, 9%, and 3% of the population, respectively. Although FI affected 50%-70% of the children and adolescents, FII prevalence was low in subjects </=20 years old but increased sharply (45%-58%) in men 21-30 years old and was associated with the highest infections. Portal and splenic vein diameters were increased in one-third of persons with FII and in almost all with FIII disease. Severe disease, FII or FIII with portal hypertension, affected 6% of the population, was associated with splenomegaly, occurred mostly in adult men, and was clustered in a few pedigrees. These observations suggest that infection intensity and duration, gender-related factors, and inherited factors are important in fibrosis development.
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DOI: 10.1086/314999
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