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Ulrich Gembruch - One of the best experts on this subject based on the ideXlab platform.
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fetal hydrops and Hepatosplenomegaly in the second half of pregnancy a sign of myeloproliferative disorder in fetuses with trisomy 21
Ultrasound in Obstetrics & Gynecology, 2001Co-Authors: Juraj Smrček, A. A. Baschat, K Gloecknerhofmann, U Germer, Ulrich GembruchAbstract:Objective To demonstrate the relationship between fetal hydrops and/or Hepatosplenomegaly in the second half of pregnancy with a myeloproliferative disorder in fetuses with trisomy 21 or mosaic trisomy 21. Design A retrospective case series. Subjects Cases were selected from 79 cases of trisomy 21 diagnosed in our prenatal unit between 1993 and 1999. Methods All fetuses had a detailed sonographic anatomic survey and biometry. Doppler of the umbilical and middle cerebral arteries, ductus venosus, inferior vena cava and umbilical vein was performed whenever possible. Two-dimensional echocardiography supplemented by color Doppler flow mapping and spectral pulsed wave Doppler was performed in all cases of fetal hydrops. Fetal karyotyping was obtained by amniocentesis, chorionic villus sampling or fetal blood sampling. In the presence of fetal hydrops a cordocentesis was performed for fetal hematology, biochemistry and TORCH serology. In cases with diagnosis of myeloproliferative disorder, peripheral blast cells were characterized by microscopy, cytochemistry and determination of surface markers. All cases with myeloproliferative disorder were stillborn and subsequently had a postmortem examination performed. Results During the study period 79 cases of trisomy 21 were diagnosed. Eleven of these had fetal hydrops. Three of these fetuses presented with Hepatosplenomegaly and myeloproliferative disorder in the second and third trimesters. In addition, one fetus with sonographic markers of trisomy 21, where karyotyping was unfortunately unsuccessful, presented with Hepatosplenomegaly, hydrops and myeloproliferative disorder. In the four fetuses with Hepatosplenomegaly and hydrops, serology was negative for congenital infection. The characteristics of blast cells in the peripheral blood smear revealed a myeloproliferative disorder. Conclusion Fetal hydrops and/or Hepatosplenomegaly in the second half of pregnancy, although suggestive of infectious etiology, may be a sign of myeloproliferative disorder in fetuses with trisomy 21 or mosaic trisomy 21. There is a possibility that a transient myeloproliferative disorder is a more common cause of mid or late-trimester hydrops in cases of trisomy 21 than previously thought. In these hydropic fetuses the prognosis seems to be poor. On the other hand we can speculate that a myeloproliferative disorder and the associated Hepatosplenomegaly and/or hydrops may show spontaneous remission or that the transient myeloproliferative disorder may be without any detectable ultrasonographic signs and therefore may be more frequent in utero than realized. Copyright © 2001 International Society of Ultrasound in Obstetrics and Gynecology
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fetal hydrops and Hepatosplenomegaly in the second half of pregnancy a sign of myeloproliferative disorder in fetuses with trisomy 21
Ultrasound in Obstetrics & Gynecology, 2001Co-Authors: Juraj Smrček, A. A. Baschat, K Gloecknerhofmann, U Germer, Ulrich GembruchAbstract:Objective To demonstrate the relationship between fetal hydrops and/or Hepatosplenomegaly in the second half of pregnancy with a myeloproliferative disorder in fetuses with trisomy 21 or mosaic trisomy 21. Design A retrospective case series. Subjects Cases were selected from 79 cases of trisomy 21 diagnosed in our prenatal unit between 1993 and 1999. Methods All fetuses had a detailed sonographic anatomic survey and biometry. Doppler of the umbilical and middle cerebral arteries, ductus venosus, inferior vena cava and umbilical vein was performed whenever possible. Two-dimensional echocardiography supplemented by color Doppler flow mapping and spectral pulsed wave Doppler was performed in all cases of fetal hydrops. Fetal karyotyping was obtained by amniocentesis, chorionic villus sampling or fetal blood sampling. In the presence of fetal hydrops a cordocentesis was performed for fetal hematology, biochemistry and TORCH serology. In cases with diagnosis of myeloproliferative disorder, peripheral blast cells were characterized by microscopy, cytochemistry and determination of surface markers. All cases with myeloproliferative disorder were stillborn and subsequently had a postmortem examination performed. Results During the study period 79 cases of trisomy 21 were diagnosed. Eleven of these had fetal hydrops. Three of these fetuses presented with Hepatosplenomegaly and myeloproliferative disorder in the second and third trimesters. In addition, one fetus with sonographic markers of trisomy 21, where karyotyping was unfortunately unsuccessful, presented with Hepatosplenomegaly, hydrops and myeloproliferative disorder. In the four fetuses with Hepatosplenomegaly and hydrops, serology was negative for congenital infection. The characteristics of blast cells in the peripheral blood smear revealed a myeloproliferative disorder. Conclusion Fetal hydrops and/or Hepatosplenomegaly in the second half of pregnancy, although suggestive of infectious etiology, may be a sign of myeloproliferative disorder in fetuses with trisomy 21 or mosaic trisomy 21. There is a possibility that a transient myeloproliferative disorder is a more common cause of mid or late-trimester hydrops in cases of trisomy 21 than previously thought. In these hydropic fetuses the prognosis seems to be poor. On the other hand we can speculate that a myeloproliferative disorder and the associated Hepatosplenomegaly and/or hydrops may show spontaneous remission or that the transient myeloproliferative disorder may be without any detectable ultrasonographic signs and therefore may be more frequent in utero than realized. Copyright © 2001 International Society of Ultrasound in Obstetrics and Gynecology
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P42Hydrops fetalis and Hepatosplenomegaly in the second half of pregnancy as a sign of myeloproliferative disorder in fetuses with trisomy 21
Ultrasound in Obstetrics and Gynecology, 2000Co-Authors: Juraj Smrček, A. A. Baschat, U Germer, Ulrich GembruchAbstract:Background Fetal hydrops and/or Hepatosplenomegaly in the second half of pregnancy may be a sign of myeloproliferative disorder in fetuses with trisomy 21. Methods In order to search for fetuses with myeloproliferative disorder a retrospective study was performed in fetuses with trisomy 21 and hydrops diagnosed in our prenatal unit. Three of these fetuses presented Hepatosplenomegaly and myeloproliferative disorder. In addition, one fetus with sonographic signs of trisomy 21, where karyotyping was unfortunately unsuccessful, presented with Hepatosplenomegaly, hydrops and myeloproliferative disorder. Results The four fetuses reported presented with fetal Hepatosplenomegaly and hydrops in the second and third trimester. Infectious serology was negative. The characteristics of blast cells in the peripheral blood smear revealed a myeloproliferative disorder. The diagnosis was confirmed by postmortem examination, since all four cases ended up in fetal demise. Conclusion Fetal hydrops and/or Hepatosplenomegaly in the second half of pregnancy, although suggestive of infectious aetiology, may be a sign of myeloproliferative disorder in fetuses with trisomy 21 or mosaic trisomy 21. It seems to be possible, that a myeloproliferative disorder is the most common cause of hydrops in cases of trisomy 21, at least during late second and third trimester. Furthermore, the incidence of myeloproliferative disorder in utero may be more frequent than realized.
Juraj Smrček - One of the best experts on this subject based on the ideXlab platform.
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fetal hydrops and Hepatosplenomegaly in the second half of pregnancy a sign of myeloproliferative disorder in fetuses with trisomy 21
Ultrasound in Obstetrics & Gynecology, 2001Co-Authors: Juraj Smrček, A. A. Baschat, K Gloecknerhofmann, U Germer, Ulrich GembruchAbstract:Objective To demonstrate the relationship between fetal hydrops and/or Hepatosplenomegaly in the second half of pregnancy with a myeloproliferative disorder in fetuses with trisomy 21 or mosaic trisomy 21. Design A retrospective case series. Subjects Cases were selected from 79 cases of trisomy 21 diagnosed in our prenatal unit between 1993 and 1999. Methods All fetuses had a detailed sonographic anatomic survey and biometry. Doppler of the umbilical and middle cerebral arteries, ductus venosus, inferior vena cava and umbilical vein was performed whenever possible. Two-dimensional echocardiography supplemented by color Doppler flow mapping and spectral pulsed wave Doppler was performed in all cases of fetal hydrops. Fetal karyotyping was obtained by amniocentesis, chorionic villus sampling or fetal blood sampling. In the presence of fetal hydrops a cordocentesis was performed for fetal hematology, biochemistry and TORCH serology. In cases with diagnosis of myeloproliferative disorder, peripheral blast cells were characterized by microscopy, cytochemistry and determination of surface markers. All cases with myeloproliferative disorder were stillborn and subsequently had a postmortem examination performed. Results During the study period 79 cases of trisomy 21 were diagnosed. Eleven of these had fetal hydrops. Three of these fetuses presented with Hepatosplenomegaly and myeloproliferative disorder in the second and third trimesters. In addition, one fetus with sonographic markers of trisomy 21, where karyotyping was unfortunately unsuccessful, presented with Hepatosplenomegaly, hydrops and myeloproliferative disorder. In the four fetuses with Hepatosplenomegaly and hydrops, serology was negative for congenital infection. The characteristics of blast cells in the peripheral blood smear revealed a myeloproliferative disorder. Conclusion Fetal hydrops and/or Hepatosplenomegaly in the second half of pregnancy, although suggestive of infectious etiology, may be a sign of myeloproliferative disorder in fetuses with trisomy 21 or mosaic trisomy 21. There is a possibility that a transient myeloproliferative disorder is a more common cause of mid or late-trimester hydrops in cases of trisomy 21 than previously thought. In these hydropic fetuses the prognosis seems to be poor. On the other hand we can speculate that a myeloproliferative disorder and the associated Hepatosplenomegaly and/or hydrops may show spontaneous remission or that the transient myeloproliferative disorder may be without any detectable ultrasonographic signs and therefore may be more frequent in utero than realized. Copyright © 2001 International Society of Ultrasound in Obstetrics and Gynecology
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fetal hydrops and Hepatosplenomegaly in the second half of pregnancy a sign of myeloproliferative disorder in fetuses with trisomy 21
Ultrasound in Obstetrics & Gynecology, 2001Co-Authors: Juraj Smrček, A. A. Baschat, K Gloecknerhofmann, U Germer, Ulrich GembruchAbstract:Objective To demonstrate the relationship between fetal hydrops and/or Hepatosplenomegaly in the second half of pregnancy with a myeloproliferative disorder in fetuses with trisomy 21 or mosaic trisomy 21. Design A retrospective case series. Subjects Cases were selected from 79 cases of trisomy 21 diagnosed in our prenatal unit between 1993 and 1999. Methods All fetuses had a detailed sonographic anatomic survey and biometry. Doppler of the umbilical and middle cerebral arteries, ductus venosus, inferior vena cava and umbilical vein was performed whenever possible. Two-dimensional echocardiography supplemented by color Doppler flow mapping and spectral pulsed wave Doppler was performed in all cases of fetal hydrops. Fetal karyotyping was obtained by amniocentesis, chorionic villus sampling or fetal blood sampling. In the presence of fetal hydrops a cordocentesis was performed for fetal hematology, biochemistry and TORCH serology. In cases with diagnosis of myeloproliferative disorder, peripheral blast cells were characterized by microscopy, cytochemistry and determination of surface markers. All cases with myeloproliferative disorder were stillborn and subsequently had a postmortem examination performed. Results During the study period 79 cases of trisomy 21 were diagnosed. Eleven of these had fetal hydrops. Three of these fetuses presented with Hepatosplenomegaly and myeloproliferative disorder in the second and third trimesters. In addition, one fetus with sonographic markers of trisomy 21, where karyotyping was unfortunately unsuccessful, presented with Hepatosplenomegaly, hydrops and myeloproliferative disorder. In the four fetuses with Hepatosplenomegaly and hydrops, serology was negative for congenital infection. The characteristics of blast cells in the peripheral blood smear revealed a myeloproliferative disorder. Conclusion Fetal hydrops and/or Hepatosplenomegaly in the second half of pregnancy, although suggestive of infectious etiology, may be a sign of myeloproliferative disorder in fetuses with trisomy 21 or mosaic trisomy 21. There is a possibility that a transient myeloproliferative disorder is a more common cause of mid or late-trimester hydrops in cases of trisomy 21 than previously thought. In these hydropic fetuses the prognosis seems to be poor. On the other hand we can speculate that a myeloproliferative disorder and the associated Hepatosplenomegaly and/or hydrops may show spontaneous remission or that the transient myeloproliferative disorder may be without any detectable ultrasonographic signs and therefore may be more frequent in utero than realized. Copyright © 2001 International Society of Ultrasound in Obstetrics and Gynecology
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P42Hydrops fetalis and Hepatosplenomegaly in the second half of pregnancy as a sign of myeloproliferative disorder in fetuses with trisomy 21
Ultrasound in Obstetrics and Gynecology, 2000Co-Authors: Juraj Smrček, A. A. Baschat, U Germer, Ulrich GembruchAbstract:Background Fetal hydrops and/or Hepatosplenomegaly in the second half of pregnancy may be a sign of myeloproliferative disorder in fetuses with trisomy 21. Methods In order to search for fetuses with myeloproliferative disorder a retrospective study was performed in fetuses with trisomy 21 and hydrops diagnosed in our prenatal unit. Three of these fetuses presented Hepatosplenomegaly and myeloproliferative disorder. In addition, one fetus with sonographic signs of trisomy 21, where karyotyping was unfortunately unsuccessful, presented with Hepatosplenomegaly, hydrops and myeloproliferative disorder. Results The four fetuses reported presented with fetal Hepatosplenomegaly and hydrops in the second and third trimester. Infectious serology was negative. The characteristics of blast cells in the peripheral blood smear revealed a myeloproliferative disorder. The diagnosis was confirmed by postmortem examination, since all four cases ended up in fetal demise. Conclusion Fetal hydrops and/or Hepatosplenomegaly in the second half of pregnancy, although suggestive of infectious aetiology, may be a sign of myeloproliferative disorder in fetuses with trisomy 21 or mosaic trisomy 21. It seems to be possible, that a myeloproliferative disorder is the most common cause of hydrops in cases of trisomy 21, at least during late second and third trimester. Furthermore, the incidence of myeloproliferative disorder in utero may be more frequent than realized.
Joseph K. Mwatha - One of the best experts on this subject based on the ideXlab platform.
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Health implications of chronic Hepatosplenomegaly in Kenyan school-aged children chronically exposed to malarial infections and Schistosoma mansoni.
Transactions of the Royal Society of Tropical Medicine and Hygiene, 2009Co-Authors: Shona Wilson, Birgitte J. Vennervald, Hilda Kadzo, Edmund Ireri, Clifford Amaganga, Mark Booth, H. Curtis Kariuki, Joseph K. Mwatha, Gachuhi Kimani, John H. OumaAbstract:Hepatosplenomegaly among school-aged children in sub-Saharan Africa is highly prevalent. Two of the more common aetiological agents of Hepatosplenomegaly, namely chronic exposure to malaria and Schistosoma mansoni infection, can result in similar clinical presentation, with the liver and spleen being chronically enlarged and of a firm consistency. Where co-endemic, the two parasites are thought to synergistically exacerbate Hepatosplenomegaly. Here, two potential health consequences, i.e. dilation of the portal vein (indicative of increased portal pressure) and stunting of growth, were investigated in a study area where children were chronically exposed to malaria throughout while S. mansoni transmission was geographically restricted. Hepatosplenomegaly was associated with increased portal vein diameters, with enlargement of the spleen rather than the liver being more closely associated with dilation. Dilation of the portal vein was exacerbated by S. mansoni infection in an intensity-dependent manner. The prevalence of growth stunting was not associated with either relative exposure rates to malarial infection or with S. mansoni infection status but was significantly associated with Hepatosplenomegaly. Children who presented with Hepatosplenomegaly had the lowest height-for-age Z-scores. This study shows that Hepatosplenomegaly associated with chronic exposure to malaria and schistosomiasis is not a benign symptom amongst school-aged children but has potential long-term health consequences.
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Hepatosplenomegaly in Kenyan schoolchildren: exacerbation by concurrent chronic exposure to malaria and Schistosoma mansoni infection
Tropical medicine & international health : TM & IH, 2007Co-Authors: Shona Wilson, Birgitte J. Vennervald, Hilda Kadzo, Edmund Ireri, Clifford Amaganga, Mark Booth, H. Curtis Kariuki, Joseph K. Mwatha, Gachuhi Kimani, John H. OumaAbstract:OBJECTIVES Chronic exposure to malaria exacerbates Schistosoma mansoni-associated Hepatosplenomegaly in school-aged children. However, residual Hepatosplenomegaly after treatment of S. mansoni with concurrent mollusciciding suggests malaria could be an underlying cause of Hepatosplenomegaly. We investigated the role of chronic malaria in childhood Hepatosplenomegaly in the presence and absence of concurrent S. mansoni infection. METHODS Cross-sectional study of children in an study area where transmission of S. mansoni, but not malaria, is restricted to the eastern end. Clinical and ultrasound examinations were conducted, and parasitological and serological tests used to determine S. mansoni infection intensities and comparative exposure levels to malaria. RESULTS Chronic exposure to malaria, as determined by Pfs-IgG3 levels, was associated with Hepatosplenomegaly even in the absence of S. mansoni infection. Children infected with S. mansoni mostly had light to moderate infection intensities but greater enlargement of the liver and spleen than children who did not have schistosomiasis, and for the left liver lobe this was S. mansoni infection intensity dependent. CONCLUSIONS Children chronically exposed to malaria but without S. mansoni infection can have Hepatosplenomegaly, which even light S. mansoni infections can exacerbate in an intensity-dependent manner. Thus, concurrent chronic exposure to S. mansoni and Plasmodium falciparum can have an additive or synergistic effect on childhood morbidity.
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Regression of Hepatosplenomegaly in Kenyan school-aged children after praziquantel treatment and three years of greatly reduced exposure to Schistosoma mansoni.
Transactions of the Royal Society of Tropical Medicine and Hygiene, 2005Co-Authors: Birgitte J. Vennervald, Hilda Kadzo, Edmund Ireri, Clifford Amaganga, Mark Booth, H. Curtis Kariuki, Gachuhi Kimani, Anthony E. Butterworth, Leecarol Kenty, Joseph K. MwathaAbstract:Evaluating regression of morbidity associated with parasitic infections is an important component of community-based control programmes. We performed an intervention against Schistosoma mansoni infection, focusing on Hepatosplenomegaly in the absence of periportal fibrosis, in a cohort of 67 Kenyan children aged 7-18 years from Makueni District, selected on the basis of Hepatosplenomegaly detected by ultrasonography. Clinical and ultrasound examinations were conducted annually for three years after treatment, and the source of infection (a river) was regularly treated with molluscicide, thereby severely reducing exposure to schistosomiasis. Malaria transmission was uninterrupted. The prevalence of hard spleens, and the magnitude of clinically assessed splenomegaly along the mid-axillary and mid-clavicular lines decreased monotonically over time, independently of age, whereas clinically measured hepatomegaly along the mid-sternal line and the prevalence of firm livers decreased in an age-specific manner, being more pronounced amongst children aged 14 years or older at enrolment. Ultrasound data were less informative, and did not concur with clinical observations. These results demonstrate that praziquantel treatment reduces Hepatosplenomegaly in the absence of exposure to S. mansoni, even with continuing exposure to malaria. The lack of complete resolution of Hepatosplenomegaly in most children suggests, among other things, a residual organomegaly attributable to malaria.
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Exposure to malaria affects the regression of Hepatosplenomegaly after treatment for Schistosoma mansoni infection in Kenyan children
BMC medicine, 2004Co-Authors: Mark Booth, Birgitte J. Vennervald, Clifford Amaganga, Joseph K. Mwatha, Gachuhi Kimani, John H. Ouma, Anthony E. Butterworth, H. C. Kariuki, Amos Otedo, David W. DunneAbstract: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.
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Associations between Anti-Schistosoma mansoni and Anti-Plasmodium falciparum Antibody Responses and Hepatosplenomegaly, in Kenyan Schoolchildren
The Journal of infectious diseases, 2003Co-Authors: Joseph K. Mwatha, Gachuhi Kimani, John H. Ouma, Frances M. Jones, Gamal Mohamed, Cynthia W. A. Naus, Eleanor M. Riley, Anthony E. Butterworth, Curtis H. Kariuki, Davy K. KoechAbstract:Schoolchildren from 2 areas of Kenya, Kangundo and Kambu, have contrasting prevalences of Hepatosplenomegaly, despite having similar prevalences and intensities of Schistosoma mansoni infection. However, in individual children, S. mansoni infection intensity is positively correlated with organomegaly. In a previous study, Hepatosplenomegaly was associated with Th1-type anti-schistosome cytokine responses. Although the high-morbidity Kambu area had higher malaria transmission than did low-morbidity Kangundo, Hepatosplenomegaly was not associated with clinical malaria or with patent malarial parasitemia. However, chronic exposure to malaria might be involved. Here, retrospectively, we assayed plasma from this original study, for anti-Plasmodium falciparum and anti-S. mansoni antibodies, to test whether greater exposure to Plasmodium was a cofactor for Hepatosplenomegaly. We found that hepatosplenic children had significantly higher levels of anti- P. falciparum antibodies, compared with nonhepatosplenic children, a finding that strongly suggests that some experience of P. falciparum influenced the development of Hepatosplenomegaly in these S. mansoni-infected children.
John H. Ouma - One of the best experts on this subject based on the ideXlab platform.
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Health implications of chronic Hepatosplenomegaly in Kenyan school-aged children chronically exposed to malarial infections and Schistosoma mansoni.
Transactions of the Royal Society of Tropical Medicine and Hygiene, 2009Co-Authors: Shona Wilson, Birgitte J. Vennervald, Hilda Kadzo, Edmund Ireri, Clifford Amaganga, Mark Booth, H. Curtis Kariuki, Joseph K. Mwatha, Gachuhi Kimani, John H. OumaAbstract:Hepatosplenomegaly among school-aged children in sub-Saharan Africa is highly prevalent. Two of the more common aetiological agents of Hepatosplenomegaly, namely chronic exposure to malaria and Schistosoma mansoni infection, can result in similar clinical presentation, with the liver and spleen being chronically enlarged and of a firm consistency. Where co-endemic, the two parasites are thought to synergistically exacerbate Hepatosplenomegaly. Here, two potential health consequences, i.e. dilation of the portal vein (indicative of increased portal pressure) and stunting of growth, were investigated in a study area where children were chronically exposed to malaria throughout while S. mansoni transmission was geographically restricted. Hepatosplenomegaly was associated with increased portal vein diameters, with enlargement of the spleen rather than the liver being more closely associated with dilation. Dilation of the portal vein was exacerbated by S. mansoni infection in an intensity-dependent manner. The prevalence of growth stunting was not associated with either relative exposure rates to malarial infection or with S. mansoni infection status but was significantly associated with Hepatosplenomegaly. Children who presented with Hepatosplenomegaly had the lowest height-for-age Z-scores. This study shows that Hepatosplenomegaly associated with chronic exposure to malaria and schistosomiasis is not a benign symptom amongst school-aged children but has potential long-term health consequences.
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Hepatosplenomegaly in Kenyan schoolchildren: exacerbation by concurrent chronic exposure to malaria and Schistosoma mansoni infection
Tropical medicine & international health : TM & IH, 2007Co-Authors: Shona Wilson, Birgitte J. Vennervald, Hilda Kadzo, Edmund Ireri, Clifford Amaganga, Mark Booth, H. Curtis Kariuki, Joseph K. Mwatha, Gachuhi Kimani, John H. OumaAbstract:OBJECTIVES Chronic exposure to malaria exacerbates Schistosoma mansoni-associated Hepatosplenomegaly in school-aged children. However, residual Hepatosplenomegaly after treatment of S. mansoni with concurrent mollusciciding suggests malaria could be an underlying cause of Hepatosplenomegaly. We investigated the role of chronic malaria in childhood Hepatosplenomegaly in the presence and absence of concurrent S. mansoni infection. METHODS Cross-sectional study of children in an study area where transmission of S. mansoni, but not malaria, is restricted to the eastern end. Clinical and ultrasound examinations were conducted, and parasitological and serological tests used to determine S. mansoni infection intensities and comparative exposure levels to malaria. RESULTS Chronic exposure to malaria, as determined by Pfs-IgG3 levels, was associated with Hepatosplenomegaly even in the absence of S. mansoni infection. Children infected with S. mansoni mostly had light to moderate infection intensities but greater enlargement of the liver and spleen than children who did not have schistosomiasis, and for the left liver lobe this was S. mansoni infection intensity dependent. CONCLUSIONS Children chronically exposed to malaria but without S. mansoni infection can have Hepatosplenomegaly, which even light S. mansoni infections can exacerbate in an intensity-dependent manner. Thus, concurrent chronic exposure to S. mansoni and Plasmodium falciparum can have an additive or synergistic effect on childhood morbidity.
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Exposure to malaria affects the regression of Hepatosplenomegaly after treatment for Schistosoma mansoni infection in Kenyan children
BMC medicine, 2004Co-Authors: Mark Booth, Birgitte J. Vennervald, Clifford Amaganga, Joseph K. Mwatha, Gachuhi Kimani, John H. Ouma, Anthony E. Butterworth, H. C. Kariuki, Amos Otedo, David W. DunneAbstract: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.
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Associations between Anti-Schistosoma mansoni and Anti-Plasmodium falciparum Antibody Responses and Hepatosplenomegaly, in Kenyan Schoolchildren
The Journal of infectious diseases, 2003Co-Authors: Joseph K. Mwatha, Gachuhi Kimani, John H. Ouma, Frances M. Jones, Gamal Mohamed, Cynthia W. A. Naus, Eleanor M. Riley, Anthony E. Butterworth, Curtis H. Kariuki, Davy K. KoechAbstract:Schoolchildren from 2 areas of Kenya, Kangundo and Kambu, have contrasting prevalences of Hepatosplenomegaly, despite having similar prevalences and intensities of Schistosoma mansoni infection. However, in individual children, S. mansoni infection intensity is positively correlated with organomegaly. In a previous study, Hepatosplenomegaly was associated with Th1-type anti-schistosome cytokine responses. Although the high-morbidity Kambu area had higher malaria transmission than did low-morbidity Kangundo, Hepatosplenomegaly was not associated with clinical malaria or with patent malarial parasitemia. However, chronic exposure to malaria might be involved. Here, retrospectively, we assayed plasma from this original study, for anti-Plasmodium falciparum and anti-S. mansoni antibodies, to test whether greater exposure to Plasmodium was a cofactor for Hepatosplenomegaly. We found that hepatosplenic children had significantly higher levels of anti- P. falciparum antibodies, compared with nonhepatosplenic children, a finding that strongly suggests that some experience of P. falciparum influenced the development of Hepatosplenomegaly in these S. mansoni-infected children.
David W. Dunne - One of the best experts on this subject based on the ideXlab platform.
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Chronic Hepatosplenomegaly in African school children: a common but neglected morbidity associated with schistosomiasis and malaria.
PLoS neglected tropical diseases, 2011Co-Authors: Shona Wilson, Birgitte J. Vennervald, David W. DunneAbstract:Chronic Hepatosplenomegaly, which is known to have a complex aetiology, is common amongst children who reside in rural areas of sub-Saharan Africa. Two of the more common infectious agents of Hepatosplenomegaly amongst these children are malarial infections and schistosomiasis. The historical view of Hepatosplenomegaly associated with schistosomiasis is that it is caused by gross periportal fibrosis and resulting portal hypertension. The introduction of ultrasound examinations into epidemiology studies, used in tandem with clinical examination, showed a dissociation within endemic communities between presentation with Hepatosplenomegaly and ultrasound periportal fibrosis, while immuno-epidemiological studies indicate that rather than the pro-fibrotic Th2 response that is associated with periportal fibrosis, childhood Hepatosplenomegaly without ultrasound-detectable fibrosis is associated with a pro-inflammatory response. Correlative analysis has shown that the pro-inflammatory response is also associated with chronic exposure to malarial infections and there is evidence of exacerbation of Hepatosplenomegaly when co-exposure to malaria and schistosomiasis occurs. The common presentation with childhood Hepatosplenomegaly in rural communities means that it is an important example of a multi-factorial disease and its association with severe and subtle morbidities underlies the need for well-designed public health strategies for tackling common infectious diseases in tandem rather than in isolation.
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Exposure to malaria affects the regression of Hepatosplenomegaly after treatment for Schistosoma mansoni infection in Kenyan children
BMC medicine, 2004Co-Authors: Mark Booth, Birgitte J. Vennervald, Clifford Amaganga, Joseph K. Mwatha, Gachuhi Kimani, John H. Ouma, Anthony E. Butterworth, H. C. Kariuki, Amos Otedo, David W. DunneAbstract: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.