Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 18 years old female was admitted to hospital due to pancytopenia on May 25, 1987 and found to have petechiae, mild hepatomegaly and severe splenomegaly. The bone marrow was found to contain 12% of blast cells. Splenectomy was performed followed by CHOP therapy. In September, 1987 the peripheral blood was found to contain tumor cells, which turned out to be resistant to various combination chemotherapies. The patient died on August 21, 1988. The phenotype of tumor cells in this case was CD2+ CD7+ CD3+ CD4- CD8- WT31-. Genetic analysis detected rearrangement of the beta and gamma chain of TcR but not transcription or translation of the beta chain of TcR, while the antibodies of delta TCS 1 and TcR delta 1 to the delta chain of TcR were positive. From this fact, the present case was considered to be the malignant counterpart of normal CD3+ WT31- double negative T cells. The reactivity of this tumor cells to IL-2 and IL-1 beta suggested the association of the IL-2R beta chain.
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PMID:[T gamma lymphoma with CD3+ CD4- CD8- WT31- and TcR gamma delta]. 213 75

Administration of the thienopyridine P2Y12 receptor antagonist, clopidogrel, increased the erosive arthritis induced by peptidoglycan polysaccharide (PG-PS) in rats or by injection of the arthritogenic K/BxN serum in mice. To determine if the detrimental effects are caused exclusively by clopidogrel, we evaluated prasugrel, a third-generation thienopyridine pro-drug, that contrary to clopidogrel is mostly metabolized into its active metabolite in the intestine. Prasugrel effects were examined on the PG-PS-induced arthritis rat model. Erosive arthritis was induced in Lewis rats followed by treatment with prasugrel for 21 days. Prasugrel treated arthritic animals showed a significant increase in the inflammatory response, compared with untreated arthritic rats, in terms of augmented macroscopic joint diameter associated with significant signs of inflammation, histomorphometric measurements of the hind joints and elevated platelet number. Moreover, fibrosis at the pannus, assessed by immunofluorescence of connective tissue growth factor, was increased in arthritic rats treated with prasugrel. In addition to the arthritic manifestations, hepatomegaly, liver granulomas and giant cell formation were observed after PG-PS induction and even more after prasugrel exposure. Cytokine plasma levels of IL-1 beta, IL-6, MIP1 alpha, MCP1, IL-17 and RANTES were increased in arthritis-induced animals. IL-10 plasma levels were significantly decreased in animals treated with prasugrel. Overall, prasugrel enhances inflammation in joints and liver of this animal model. Since prasugrel metabolites inhibit neutrophil function ex-vivo and the effects of both clopidogrel and prasugrel metabolites on platelets are identical, we conclude that the thienopyridines metabolites might exert non-platelet effects on other immune cells to aggravate inflammation.
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PMID:Erosive arthritis and hepatic granuloma formation induced by peptidoglycan polysaccharide in rats is aggravated by prasugrel treatment. 2386 57