Exposure to malaria affects the regression of hepatosplenomegaly after treatment for Schistosoma mansoniinfection in Kenyan children
| Autor: | David W. Dunne, H. C. Kariuki, John H. Ouma, Clifford Amaganga, Anthony E. Butterworth, Amos Otedo, Birgitte J. Vennervald, Mark Booth, Gachuhi Kimani, Joseph K. Mwatha |
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| Přispěvatelé: | Dunne, David [0000-0002-8940-9886], Apollo - University of Cambridge Repository |
| Rok vydání: | 2004 |
| Předmět: |
Adolescent
030231 tropical medicine Population Hepatosplenomegaly lcsh:Medicine Spleen 03 medical and health sciences 0302 clinical medicine parasitic diseases Medicine Animals Humans 030212 general & internal medicine education Child Pathological Medicine(all) education.field_of_study biology business.industry lcsh:R General Medicine Schistosoma mansoni medicine.disease biology.organism_classification Kenya Schistosomiasis mansoni 3. Good health Malaria Praziquantel medicine.anatomical_structure Immunology Cohort Splenomegaly medicine.symptom business Research Article medicine.drug Hepatomegaly |
| Zdroj: | BMC medicine, 2004, Vol.2(1), pp.36 [Peer Reviewed Journal] BMC Medicine, Vol 2, Iss 1, p 36 (2004) BMC Medicine |
| Popis: | Background Schistosoma mansoni and malaria infections are often endemic in the same communities in sub-Saharan Africa, and both have pathological effects on the liver and the spleen. Hepatosplenomegaly associated with S. mansoni is exacerbated in children with relatively high exposure to malaria. Treatment with praziquantel reduces the degree of hepatosplenomegaly, but the condition does not completely resolve in some cases. The present analysis focused on the possibility that exposure to malaria infection may have limited the resolution of hepatosplenomegaly in a cohort of Kenyan schoolchildren. Methods Ninety-six children aged 6–16, from one community in Makueni district, Kenya, were treated with praziquantel. At baseline, all children had hepatomegaly and most had splenomegaly. The source of S. mansoni infection, a river, was molluscicided regularly over the following three years to limit S. mansoni re-infection, whereas malaria exposure was uninterrupted. Hepatic and splenic enlargement was assessed annually outside the malaria transmission season. Results Children living in an area of relatively high exposure to both infections presented with the largest spleens before treatment and at each follow-up. Spleens of firm consistency were associated with proximity to the river. The regression of hepatomegaly was also affected by location, being minimal in an area with relatively low S. mansoni exposure but high exposure to malaria, and maximal in an area with relatively low exposure to both infections. Conclusions The outcome of treating cases of hepatosplenomegaly with praziquantel in this cohort of Kenyan children depended strongly on their level of exposure to malaria infection. Furthermore, a residual burden of hepatosplenic morbidity was observed, which was possibly attributable to the level of exposure to malaria. The results suggest that exposure to malaria infection may be a significant factor affecting the outcome of praziquantel treatment to reduce the level of hepatosplenic morbidity. |
| Databáze: | OpenAIRE |
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