Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019214 (hepatosplenomegaly)
 4,408 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parasitic infections and malnutrition coexist in many tropical and subtropical areas. Studies of Leishmania donovani and of experimentally infected Syrian hamsters have provided important insights into the complex interrelationships between malnutrition and this parasitic disease. Malnutrition, which adversely affects cell-mediated immunity, is associated with the development of visceral leishmaniasis (kala-azar) in children living in endemic areas. In turn, L. donovani can cause wasting as well as hepatosplenomegaly, fever, and anemia. Syrian hamsters infected with L. donovani develop a disease that is comparable to that of humans with kala-azar. Weight loss in infected hamsters is associated with splenic macrophage secretion of potentially catabolic cytokines as measured by the D10.G4.1 assay for interleukin-1 and the L929 cytotoxicity assay for tumor necrosis factor/cachectin. Although decreased food intake contributes to wasting in infected hamsters, studies of skeletal muscle function indicate that it is not the sole factor. Leishmania donovani-infected hamsters have also been used to study drugs with the potential to prevent or reverse cachexia.
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PMID:Visceral leishmaniasis: a model for infection-induced cachexia. 163 76

Familial hemophagocytic lymphohistiocytosis (FHL) is a frequently missed and almost uniformly fatal childhood disorder. It is characterized by fever, hepatosplenomegaly, cytopenia, coagulopathy, and hypertriglyceridemia. The pathogenesis of FHL is not known but the above clinical and laboratory findings are compatible with reported in vitro and in vivo effects of several inflammatory cytokines. We measured circulating interferon-gamma (IFN-gamma), tumor necrosis factor/cachectin (TNF), and interleukin-6 (IL-6) in nine children with FHL. During active disease, elevated IFN-gamma was detected in seven of seven children, TNF in six of six, and IL-6 in two of six children studied. Thus, important inflammatory cytokines are augmented in active FHL and may contribute to the pathogenesis of the disease. Soluble CD8 was also increased in seven of seven children, which suggests a pathophysiologic importance of cytotoxic T lymphocytes. Because FHL appears to be associated with a systemic hypercytokinemia, our results also indicate that studies of FHL may contribute to the understanding of cytokine effects in vivo. Moreover, FHL is a hereditary disorder, suggesting that the hypercytokinemia is caused by a genetic defect in cytokine regulation.
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PMID:Hypercytokinemia in familial hemophagocytic lymphohistiocytosis. 195 80

Analysis of T-lymphocytes by flowcytometry, estimation of serum TNFa level by solid phase enzyme amplified sensitivity immunoassay (EASIA) and IHAT were done for chronic schistosomiasis mansoni patients without hepatic fibrosis, with hepatosplenomegaly and 20 healthy controls. The sensitivity and specificity of IHAT in schistosomiasis mansoni were 85% & 90% respectively. Chronic schistosomiasis mansoni patients showed increase in CD8% (27.3 +/- 5.3) and decrease in CD4% (44.2 +/- 4.68). Hepatosplenomegaly cases showed increase in CD4% (46.5 +/- 4.1) & decrease in CD8% (23.2 +/- 2.18). Serum level of TNF-a was significantly higher in cases with hepatosplenomegaly compared to either cases of chronic schistosomiasis mansoni or controls. No significant difference was between chronic schistosomiasis mansoni patients and controls. A correlation between hepatosplenonomegaly and increase of CD4 and/or decrease of CD8 and significant high level of TNF-a indicated TNF-alfa role in granuloma formation.
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PMID:Flowcytometric analysis of T-lymphocytes and serum tumour necrosis factor alpha (TNF-alpha) levels in schistosoma mansoni patients. 1838 6