Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026986 (myelodysplastic syndrome)
 14,926 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The FcRIII on human granulocytes is a glycosyl-phosphatidylinositol-anchored membrane protein. In PNH, proteins with this type of membrane linkage are known to be deficient on blood cells. The purpose of this study was to assess the diagnostic value of flow cytometric FcRIII quantification on granulocytes in PNH. Immunofluorescence measurements were performed in 105 patients, including 7 patients with PNH, 16 patients with aplastic anemia, and 12 with myelodysplastic syndrome, by a whole blood immunofluorescent staining procedure using monoclonal antibodies to FcRIII. In all 7 PNH patients and in 3 patients with aplastic anaemia, a distinct FcRIII-deficient granulocyte population of variable size was found. None of the remaining patients showed a similar population of FcRIII-deficient granulocytes. Quantification of FcRIII-deficient neutrophils is shown to be a highly specific and sensitive diagnostic test for PNH. It is easy, fast and highly reproducible and, therefore, suitable for routine diagnostic and follow-up studies in PNH patients and patients with aplastic anemia.
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PMID:Fc III receptors (FcRIII) on granulocytes: a specific and sensitive diagnostic test for paroxysmal nocturnal hemoglobinuria (PNH). 183 36

The surface expression of effector cell molecules on neutrophils was examined in 18 patients with myelodysplastic syndromes (MDS) and 20 healthy control subjects. The MDS patients were further classified as low clinical risk (L-MDS, n=7) and high clinical risk (H-MDS, n=11). The expression of Fc receptors for IgG (FcR), complement receptors (CR) and cellular adhesion molecules on neutrophils was determined by flow cytometry and monoclonal antibodies. The effect of granulocyte colony-stimulating factor (G-CSF) and tumour necrosis factor-alpha (TNF) on L-selectin shedding and CR up-regulation on neutrophils was also examined. The percentage of FcRI-positive neutrophils and CD11b/CR3 expression on neutrophils were significantly increased in the H-MDS patients when compared to the controls. In contrast, the expression of FcRII, FcRIII, L-selectin, LFA-1 and CD18 on neutrophils was significantly reduced in the H-MDS patients compared with the controls. The L-MDS neutrophils exhibited lower expressions of CR1, L-selectin, LFA-1 and CD18 than those of the controls. Neutrophils from some H-MDS patients showed impaired L-selectin shedding and CR up-regulation after stimulation with G-CSF or TNF, although these were not significantly different when assessed in the whole H-MDS group. These findings suggest that an altered surface expression of effector cell molecules and an impaired modulation of cellular adhesion molecules on neutrophils may contribute to the increased susceptibility to bacterial infections in MDS patients.
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PMID:Altered surface expression of effector cell molecules on neutrophils in myelodysplastic syndromes. 923 72