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L F Flores-Suárez

Publications and source records attributed to L F Flores-Suárez.

6 recordsLinked to original sources
PubMed2003

Effects of anti-neutrophil cytoplasm autoantibodies on tissue factor activity by HL-60 cells in vitro.

The effects of cytoplasmic anti-neutrophil cytoplasm autoantibodies (C-ANCA) and perinuclear ANCA (P-ANCA) immunoglobulin G (IgG) on tissue factor (TF) activity using HL-60 cells in vitro were compared with those of medium, lipopolysaccharide (LPS) and control IgG. Cells were also incubated with both ANCA IgG and control IgG in the presence of a submaximal concentration of LPS capable of upregulating TF procoagulant activity (TF-PCA) measured in arbitrary units of TF equivalent (AU-TFEq). The purpose was to search for an additive effect between LPS and ANCA IgG. All IgG preparations increased HL-60 cell TF-PCA in comparison with the medium. When cells were incubated with P-ANCA IgG and LPS (1 micro g/ml), a larger increase was seen (151.23 +/- 31.6 SEM (standard error of the mean) AU-TFEq) than when incubated with control IgG plus LPS (91.01 +/- 18.4 SEM AU-TFEq; P < 0.005), P-ANCA IgG alone (73.68 +/- 12.7 SEM AU-TFEq; P < 0.005) or LPS (1 micro g/ml) (58.11 +/- 7.9 SEM AU-TFEq; P < 0.005). There was concordance between PCA and TF total antigen content by enzyme-linked immunosorbent assay (ELISA). The fact that P-ANCA IgGs upregulate the function of TF in HL-60 cells in combination with LPS adds to information regarding the possible role of ANCAs in the enhancement of TF by different cells, although it does not support the fact that ANCAs alone play a role in mononuclear cell TF upregulation. The additive effects of LPS underline the possible role of pro-inflammatory stimuli in the pathogenesis of ANCA-associated diseases.

Adult↗
PubMed2003

Prevalence of antineutrophil cytoplasmic autoantibodies in patients with tuberculosis.

OBJECTIVE: To determine the prevalence of antineutrophil cytoplasmic autoantibodies (ANCA) in sera of patients with tuberculosis compared with healthy control subjects and a group of patients with atopic asthma. METHODS: The presence of ANCA was examined in patients with tuberculosis, and in asthmatic patients and healthy subjects as control groups, by means of indirect immunofluorescence (IIF) and enzyme-linked immunosorbent assay (ELISA) to detect anti-proteinase 3 (PR3-ANCA) and antimyeloperoxidase (MPO-ANCA) antibodies. RESULTS: ANCA were present in 20 (44.4%) of 45 tuberculosis patients by IIF (16 c-ANCA, four p-ANCA) and in 18 (40%) patients by ELISA (15 PR3-ANCA, three MPO-ANCA). High odds ratios for ANCA positivity were observed for tuberculosis patients when compared with both control groups. ANCA results were not related to the category of tuberculosis, stage of disease, presence of concomitant diseases or pharmacotherapy. CONCLUSIONS: As many clinical similarities between tuberculosis and Wegener's granulomatosis exist, we propose that a positive ANCA test in patients living in countries with a high prevalence of tuberculosis must be carefully interpreted as indicative of systemic vasculitis, especially when no signs of extrapulmonary involvement occur.

Adult↗
PubMed1999

Familial occurrence of systemic vasculitis and rapidly progressive glomerulonephritis.

Two familial clusters of systemic vasculitis are described. In one family, microscopic polyangiitis and rapidly progressive glomerulonephritis occurred in HLA-identical siblings; in the second family, 3 second- and fourth-degree related members were affected by Wegener's granulomatosis. Published clusters of systemic vasculitides and Goodpasture's syndrome are reviewed, and, together with the observed families, the evidence for genetic susceptibility and a causative role of environmental factors for these diseases with special emphasis on the HLA system is discussed.

Adult↗
PubMed1998

New developments in pathogenesis of systemic vasculitis.

Aspects of pathogenesis of primary systemic vasculitis are highlighted in this review. The cause of these entities is still obscure, although new information on the possible role of infections has emerged. Success of antimicrobial treatment to ameliorate systemic vasculitis, for which proof was recently provided, adds to the new information. Apart from new data that point to a precipitating role for environmental toxins the background for development of these diseases is most likely genetic predisposition. Reports on hereditary alpha 1-antitrypsin deficiency, the link between systemic vasculitis and human leukocyte antigen molecules, and an animal model of spontaneous granulomatous arteritis in mice with a hereditary deficit in Fas-mediated apoptosis, are some of the new data that strongly favor genetic predisposition. Progress has been made in the process of identification of the agonists and antagonists in the front line of vasculitic inflammation. The interaction of blood cells (e.g., neutrophils and monocytes) with vascular endothelium has become more evident as have the signals for the release of harmful proteolytic enzymes. Antineutrophil cytoplasmic antibodies, which are important markers of disease, may be actively involved in these processes.

Animals↗