Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Pf4”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed2005

Preoperative anti-PF4/heparin antibody level predicts adverse outcome after cardiac surgery.

OBJECTIVE: Preexisting serum antibodies to heparin/platelet factor 4 complexes may predispose adult cardiac surgical patients to increased perioperative morbidity and mortality. We sought to determine the association between preoperative serum antibodies directed against platelet factor 4/heparin complexes and major complications (in-hospital death or length of stay >10 days) in adult cardiac surgical patients. METHODS: In a prospective observational study of 466 patients undergoing elective coronary artery bypass grafting, valvular heart surgery, or both, preoperative serum was assayed for anti-platelet factor 4/heparin antibody by using a commercially available enzyme-linked immunosorbent assay (Asserachrom HPIA). Known preoperative risk factors were assessed, and patients were assigned a risk score by using the validated method of Parsonnet and colleagues. RESULTS: Major complications (death or postoperative hospitalization >10 days) occurred in 108 patients (23%). Overall, 59 (13%) patients had a positive preoperative anti-platelet factor 4/heparin antibody screen (upper limit of normal is 0.5 optical density units). A positive assay result independently predicted an increased risk of major complications (P = .0284; odds ratio, 1.98; 95% confidence interval, 1.06-3.62) over and above the effect of the Parsonnet risk score (P < .001; odds ratio, 1.07; 95% confidence interval, 1.05-1.10). The level of preoperative anti-platelet factor 4/heparin antibody was also significantly associated with major complications (P = .036; odds ratio, 1.31; 95% confidence interval, 1.02-1.68) independently of the Parsonnet risk score. No association (P > .75) existed between the Parsonnet risk score and preoperative anti-platelet factor 4/heparin antibody level. CONCLUSIONS: Serum antibodies directed against platelet factor 4/heparin complexes are prevalent in the adult patient population undergoing cardiac surgery. The presence of these antibodies before surgery is an independent predictor for death or prolonged hospitalization after adult cardiac surgery.

Aged↗
PubMed2004

Differential prevalence of anti-heparin-PF4 immunoglobulin subtypes in patients treated with clivarin and heparin: implications in the HIT pathogenesis.

Heparin-induced thrombocytopenia (HIT) syndrome is a catastrophic complication of heparin therapy that may result in arterial/venous thromboembolic events. The pathophysiology of HIT is mediated by the generation of a functionally and molecularly heterogeneous group of anti-heparin-platelet factor 4 (AHPF4) antibodies that cause platelet/endothelial cell activation/destruction. These AHPF4 antibodies may be of various subtypes and cause differential pathogenic responses during HIT. This study evaluated the differential prevalence and functionality of AHPF4 Ig subtypes (IgA, IgG, and IgM) in plasma samples obtained from clinically suspected HIT patients (n = 111) and two clinical trials. In these trials, a low-molecular-weight heparin, clivarin and unfractionated heparin (UFH) were used to treat deep-vein thrombosis (CORTES) and for prophylaxis of the orthopedic surgery (ECHOS). In the CORTES study, three randomized groups of patients (n = 312-328) received prophylactic treatment with either UFH or clivarin (o.d. or b.i.d.). In the ECHOS study, there were approximately 600 patients per group. Citrated plasma samples were analyzed for cumulative IgA/IgG/IgM and individual Ig subtypes of AHPF4 utilizing ELISA. Functionality of the ELISA-positive samples was ascertained by 14C-serotonin release assay. In clinically confirmed HIT patients (and UFH-treated CORTES and ECHOS samples), the Ig subtyping revealed a predominance of IgG AHPF4 antibodies in contrast to the asymptomatic high AHPF4 antibody titers, which were found to be mostly IgM and/or IgA subtypes. In the clivarin-treated patients in both trials, the prevalence of AHPF4 antibodies was found to be lower (2-3 fold, p < 0.01) in comparison to UFH group. In addition, the clivarin-treated patients with positive AHPF4 antibodies were found to be predominantly of the non-functional type and were found in the order of IgM > IgA > IgG Together, these observations demonstrate that ELISA-detectable IgG subtype in UFH-treated patients may be more likely to cause functional/pathologic responses during HIT syndrome. Thus, determination of IgG subtype of AHPF4 antibodies during HIT syndrome may be crucial in the diagnosis; however, the relevance of the pathologically non-functional (IgA and/or IgM) antibodies and the overall mechanism(s) of these HIT-associatied antibodies need further investigation.

Anticoagulants↗
PubMed2003

Thrombopoietin-induced CXC chemokines, NAP-2 and PF4, suppress polyploidization and proplatelet formation during megakaryocyte maturation.

BACKGROUND: We previously reported that the expressions of two CXC chemokines, neutrophil activating peptide-2 (NAP-2) and platelet factor-4 (PF-4), were induced by megakaryocyte-specific cytokine thrombopoietin (TPO) in mouse bone marrow megakaryocytes. The roles of these chemokines on megakaryocyte maturation/differentiation processes, including polyploidization and proplatelet formation (PPF) remain unresolved. RESULTS: NAP-2 and PF-4 suppressed the PPF of mature megakaryocytes freshly prepared from mouse bone marrow as well as that of the megakaryocyte progenitors, c-Kit+CD41+ cells, isolated from mouse bone marrow and cultured with TPO. NAP-2 and PF-4 inhibited polyploidization of c-Kit+CD41+ cells in the presence of TPO, and also inhibited the proliferation of c-Kit+CD41+ cells. CONCLUSIONS: NAP-2 and PF-4 produced by TPO stimulation in megakaryocytes suppress megakaryocyte maturation and proliferation as a feedback control.

Animals↗
PubMed2004

Prevalence of anti-PF4/heparin antibodies and the HIT syndrome in cardiovascular medicine.

Heparin-induced thrombocytopenia (HIT) is a potentially life-threatening adverse effect of heparin treatment. HIT is mediated by antibodies directed at complexes that form between heparin and platelet factor 4 in plasma and are located on the platelet surface and on endothelium. HIT occurs in 1 to 2% of patients receiving unfractionated heparin (UFH) and with lower frequency in patients receiving low-molecular-weight heparins and heparinoids. Despite recent insights into the mechanisms of HIT, there remain important unresolved issues. For example, the reason for the wide difference in the frequency of HIT in patients treated with UFH in various clinical trials is not yet clear. There are patient population-dependent differences in the risk for HIT immunoglobulin G and the development of thrombotic episodes. The complex nature of this syndrome may relate to the composition of the responsible antigen. Patients with HIT need a more accurate evaluation of platelet counts and a better assessment of clinical evidence for thrombosis. Alternative anticoagulant therapy approaches are being studied, but there is at this time no firm clinical evidence for which treatment is best for patients with HIT and HIT-related thromboses.

Adult↗