Prevalence of heparin-induced antibodies in patients with chronic renal failure undergoing hemodialysis

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‐hep...

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Published inJournal of clinical laboratory analysis Vol. 19; no. 5; pp. 189 - 195
Main Authors Palomo, Iván, Pereira, Jaime, Alarcón, Marcelo, Díaz, Gonzalo, Hidalgo, Patricia, Pizarro, Isabel, Jara, Eric, Rojas, Patricio, Quiroga, Guillermo, Moore-Carrasco, Rodrigo
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 2005
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Summary: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 FcγRIIa 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 FcγRIIa polymorphism. We studied 207 patients with chronic renal failure (CRF) undergoing HD. As a control we included 130 blood donors and 28 patients with CRF without HD. The HIA patients were studied with the use of a PF4‐H ELISA. Additionally, in some positive cases for the previous test, a 14C‐ serotonin release assay (14C‐SRA) was performed. The polymorphism FcγRIIa 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 14C‐SRA. The distribution of the FcγRIIa 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 FcγRIIa 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 FcγRIIa polymorphism did not statistically differ between HIT type II and normal controls. J. Clin. Lab. Anal. 19:189–195, 2005. © 2005 Wiley‐Liss, Inc.
Bibliography:ArticleID:JCLA20076
istex:D23C13F9AEE033FD1408E74CA7E416EDAF5F645C
Research Department, Universidad de Talca - No. 454-65
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ISSN:0887-8013
1098-2825
DOI:10.1002/jcla.20076