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  1. Home
  2. Browse by Author

Browsing by Author "Alarcon, M"

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    Anti phospholipid antibodies in Chilean patients with systemic lupus erythematosus
    (2002) Palomo, I; Pereira, J; Alarcon, M; Larrain, AM; Pinochet, C; Vasquez, M; Velez, MT; Leon, M; Espinola, R; Pierangeli, S
    Antiphospholipid antibodies (aPLs) are a heterogeneous family of antibodies found in autoimmune disorders, infectious diseases, and other situations. The presence of different aPLs has been associated with various clinical manifestations of the antiphospholipid syndrome (APS). The objective of this study was to investigate the prevalence of aPLs in a group of 90 Chilean patients with systemic lupus erytematosus (SLE) and 90 healthy controls. We measured anticardiolipin antibodies (aCLs), antiphosphatidylserine antibodies (aPSs), anti-beta(2) glycoprotein I antibodies (anti-beta(2)GPIs), and antiprothrombin antibodies (aPTs) with an enzyme-linked immunosorbent technique using "in-house" assays. Fifty-four of 90 SLE patients (60.0%) had some type of aPL. Forty of 90 (44.4%) were positive for aCLs, 9 of 61 (14.8%) had aPSs, 21 of 90 (23.3%) had anti-beta(2)GPIs, and 18 of 90 (20.0%) had aPTs. In the control group, prevalences were as follows: aCLs, 3.3%; aPSs, 1.1%; anti-beta2GPIs, 1.1%; aPTs, 2.2%. In most cases, values were in the low-positive range. Of all aPL detected, 29.5% was of the IgG isotype, 37.5% IgM, and 33.0% IgA. We observed a correlation between aCLs and aPSs and of these antibodies with anti-beta(2)GPIs and aPTs but not between anti-beta2GPIs and aPTs. Our results show a high prevalence of aPLs in SLE patients. An association between different specificities and isotypes of aPLs was also observed.
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    Prevalence of antiphospholipid and antiplatelet antibodies in human immunodeficiency virus (HIV)-infected Chilean patients
    (WILEY, 2003) Palomo, I; Alarcon, M; Sepulveda, C; Pereira, J; Espinola, R; Pierangeli, S
    Antiphospholipid (aPL) and antiplatelet (aPlt) antibodies, found in patients with autoimmune diseases, are also detected in infectious diseases. The purpose of this study was to examine the prevalence of these antibodies in HIV patients and to evaluate an association of these antibodies with thrombocytopenia and/or thrombosis. Sixty-three HIV-seropositive patients and 52 normal controls were studied. Anticardiolipin (aCL), anti-beta(2) glycoprotein I (anti-beta(2)GPI), and antiprothrombin (aPT) antibodies were determined and the lupus anticoagulant (LA) test was performed. Antiplatelet antibodies (aPlt) were also determined. Seven out of 63 (12.7%) HIV patients were positive for aCL, four of 63 (6.3%) for anti-beta(2)GPI, and five of 63 (7.9%) for aPT. No patients studied were LA positive. Six out of 63 (9.5%) patients were positive for aPlt. One of them showed weak reactivity for GPIb-IX. The platelet count of patients (202 +/- 63 x 10(3) platelets/muL) was significantly lower than in the controls (343+/-6 x 10(3) platelets/muL) (P<0.001). There was no correlation between the presence of aPL and/or aPlt and thrombocytopenia. Of the HIV-infected patients, 22.2% presented aPL and 9.4% aPlt antibodies. In this study, the presence of aPL and aPlt antibodies was not associated with the development of thrombosis and/or thrombocytopenia. (C) 2003 Wiley-Liss, Inc.
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    Prevalence of heparin-induced antibodies in patients with chronic renal failure undergoing hemodialysis
    (WILEY, 2005) Palomo, I; Pereira, J; Alarcon, M; Diaz, G; Hidalgo, P; Pizarro, I; Jara, E; Rojas, P; Quiroga, G; Moore Carrasco, R
    Heparin-induced thrombocytopenia (HIT) type II is a serious complication of heparin therapy. It presents initially as thrombocytopenia, and is associated with thrombosis in 20-50% of the cases. HIT is related to the presence of heparin-induced antibodies (HIA), which show specificity for the PF4-heparin (PF4-H) complex. The Fc gamma RIIa receptor has been suggested to participate in the pathogenic mechanism of HIA. Since patients undergoing chronic hemodialysis (HD) are exposed repeatedly to heparin, we studied the prevalence of HIA and their eventual relationship with thrombocytopenia and/or thrombosis, and the possible participation of the Fc gamma RIIa polymorphism. We studied 207 patients with chronic renal failure (CRF) undergoing HID. As a control we included 130 blood donors and 28 patients with CRF without HID. The HIA patients were studied with the use of a PF4-H ELISA. Additionally, in some positive cases for the previous test, a C-14- serotonin release assay (C-14-SRA) was performed. The polymorphism Fc gamma RIIa H/R131 was studied by polymerase chain reaction (PCR) with allele-specific primers. Thirty-seven patients (17.9%) undergoing HD presented with HIA. The majority of these antibodies were IgG, IgM, and IgA. The HIA investigated presented specificity against the PF4-H complex, but not against PF4 alone (P < 0.001). Twelve out of 22 (54.5%) PF4-H antibodies were positive when tested with the C-14-SRA. The distribution of the Fc gamma RIIa polymorphism in patients and healthy controls was 42.6% and 41.6% for H/H131, 41% and 48.9% for the H/R131 isoform, and 16.4% and 9.5% for the R/R131 isoform, respectively. No statistically significant difference in the Fc gamma RIIa isoform distribution was found. Twenty-nine out of 156 patients (18.5%) presented thrombocytopenia, and 21/207 (12.4%) had thrombosis of the native vein arterio-venous fistula (AVF). We did not find any statistically significant between HIA and thrombocytopenia or thrombosis. An important proportion of patients with CRF undergoing HD developed HIA, but these cases were not associated with thrombocytopenia or thrombosis of AVF. The frequency of the Fc gamma RIIa polymorphism did not statistically differ between HIT type II and normal controls.

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