OBJECTIVE: To explore the relationship between activity of plasma heparin cofactor II (HC II) and the incidence of in-stent restenosis aft er the intervention of arteriosclerosis obliterans in lower extremity. METHODS: A total of 62 patients with arteriosclerosis obliterans in lower extremity underwent femoropopliteal stent implantation. They were divided into 2 groups: A high HC II activity group (≥100%, n=40) and a low HC II activity group (<100%, n=22). All patients filled in follow up tables and conducted body examination. Possible risk factors resulting in restenosis were collected. Patients were followed up for 6 months after femoropopliteal stent implantation. RESULTS: Baseline clinical characteristics were not significantly different between the 2 groups. The degree and incidence of angiographic restenosis at the end of the 6th month after the implantation in the high HC II activity group were all significantly lower than those in the low HC II activity group (P<0.05). Multivariate analysis demonstrated that high plasma HC II activity was an independent factor in reducing the incidence of angiographic restenosis (OR=0.982, P=0.048, 95%CI, 0.966, 0.998). CONCLUSION High plasma HC II activity is an independent factor in reducing the degree of in-stent restenosis. The lower the plasma HC II activity, the severer the degree of in-stent restenosis.
Arteriosclerosis Obliterans ; surgery ; Constriction, Pathologic ; Heparin Cofactor II ; metabolism ; Humans ; Incidence ; Lower Extremity ; Risk Factors ; Stents

OBJECTIVETo study the plasma HCII activity and antigen level variations and their relationship with arterial and deep venous thrombotic diseases.

METHODSSeventy-five patients with brain infarction (BI), 50 myocardial infarction (MI), 36 deep venous thromboembolic disease (DVT) and 50 healthy controls were entered in this study. Plasma HCII activity was measured with chromogenic substrate method and the HCII antigen level by Western blotting assay. Plasma antithrombin (AT) activity was detected for the HCII deficiency individuals with DVT using chromogenic substrate method.

RESULTSThere was no significant difference in the mean plasma HCII activity and antigen levels between BI group [(99.97 +/- 21.14)% and 0.96 +/- 0.24], MI group [(98.18 +/- 29.35)% and 0.95 +/- 0.20] and healthy controls [(96.80 +/- 20.11)% and 0.93 +/- 0.19]. The plasma HCII activity and antigen concentrations in patients with DVT [(89.57 +/- 17.12)% and 0.87 +/- 10.18] tended to be decreased as compared with healthy controls, but they were not significant. No significant difference was found for the prevalence of HCII deficiency between patient groups and control group. The HCII deficiency individuals with DVT had normal AT activity and fibrinogen concentration.

CONCLUSIONSPlasma HCII deficiency may not be the risk factor for arterial thrombosis in the Han population of Hunan Chinese. It is needed to further confirm if decreased plasma HCII is correlated with venous thrombosis.

Adult ; Aged ; Blotting, Western ; Cerebral Infarction ; blood ; etiology ; Female ; Heparin Cofactor II ; analysis ; deficiency ; immunology ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; blood ; etiology ; Venous Thrombosis ; blood ; etiology

The etiology of ischemic stroke remains undetermined in nearly 40% of patients despite extensive evaluations. Coagulopathies associated with cerebrovascular ischemia may be familial or acquired and account for 4% of all strokes. The four important naturally occurring circulation proteins that inhibit coagulation are protein C, protein S, antithrombin III, and heparin cofactor II. A carefully balanced interaction between these proteins and normal vascular endothelial cells comprise a major barrier inhibiting thrombosis. The true deficiencies of these proteins are usually inherited although many conditions such as DIC, malignancy, malnutrition, infection, and neutropenia can be associated with acquired deficiencies. Although some data suggest an association between arterial strokes and the deficiency of these proteins in young adults, cerebral venous thrombosis and venous infarcts gave been reported far more commonly with deficiencies of any of these proteins. The understanding of the molecular events underlying coagulation has improved in recent years. This has led to development of specific assays that can identify genetic abnormalities which can cause coagulopathies. Although the technology has improved the fundamental approach to the patient has not changed. A primary care physician requires a basic knowledge of the principles of blood coagulation so as to treat patients with simple problems and refer patients with more unusual or complex disorders on to the specialist. The recognition that hypercoagulable states are sometimes found in ischemic stroke patients has led to testing for these rare conditions. Coagulopathies related to protein C, protein S, or antithrombin III deficiencies, activated protein C resistance, prothrombin gene mutation, anticardiolipin antibodies, or lupus anticoagulant can be evaluated with various coagulation testing strategies.
Activated Protein C Resistance ; Antibodies, Anticardiolipin ; Antithrombin III ; Antithrombin III Deficiency ; Blood Coagulation ; Dacarbazine ; Endothelial Cells ; Heparin Cofactor II ; Humans ; Ischemia ; Lupus Coagulation Inhibitor ; Malnutrition ; Neutropenia ; Physicians, Primary Care ; Protein C ; Protein S ; Prothrombin ; Specialization ; Stroke* ; Thrombosis ; Venous Thrombosis ; Young Adult

Respiratory syncytial virus (RSV) is a leading cause of acute lower respiratory tract infections. Qingfei oral liquid (QFOL), a traditional Chinese medicine, is widely used in clinical treatment for RSV-induced pneumonia. The present study was designed to reveal the potential targets and mechanism of action for QFOL by exploring its influence on the host cellular network following RSV infection. We investigated the serum proteomic changes and potential biomarkers in an RSV-infected mouse pneumonia model treated with QFOL. Eighteen BALB/c mice were randomly divided into three groups: RSV pneumonia model group (M), QFOL-treated group (Q) and the control group (C). Serum proteomes were analyzed and compared using a label-free quantitative LC-MS/MS approach. A total of 172 protein groups, 1009 proteins, and 1073 unique peptides were successfully identified. 51 differentially expressed proteins (DEPs) were identified (15 DEPs when M/C and 43 DEPs when Q/M; 7 DEPs in common). Classification and interaction network showed that these proteins participated in various biological processes including immune response, blood coagulation, complement activation, and so forth. Particularly, fibrinopeptide B (FpB) and heparin cofactor II (HCII) were evaluated as important nodes in the interaction network, which was closely involved in coagulation and inflammation. Further, the FpB level was increased in Group M but decreased in Group Q, while the HCII level exhibited the opposite trend. These findings not only indicated FpB and HCII as potential biomarkers and targets of QFOL in the treatment of RSV pneumonia, but also suggested a regulatory role of QFOL in the RSV-induced disturbance of coagulation and inflammation-coagulation interactions.
Animals ; Biomarkers ; blood ; Chromatography, Liquid ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Fibrinopeptide B ; analysis ; genetics ; Gene Expression Regulation ; drug effects ; Heparin Cofactor II ; analysis ; genetics ; Lung ; pathology ; Mice, Inbred BALB C ; Proteome ; drug effects ; Proteomics ; Respiratory Syncytial Virus Infections ; blood ; drug therapy ; Respiratory Syncytial Viruses ; drug effects ; Tandem Mass Spectrometry