Low Molecular Weight Heparin Has An Impact On VWf And IL-32 In Copd Prethrombotic State

Background:Chronic obstructive pulmonary disease?COPD?is not a kind of fully reversible airflow limited lung disease.The Global Initiative for Chronic Obstructive Lung Disease?GOLD?predicts that COPD would lead to the third major categories cause of death and cause the fifth economic burden of disease and disability by 2020.Now COPD has still relatively high incidence,we only give symptomatic treatment,but the illness will also continue to progress.Exploring the pathogenesis might provide a train of thought for the diagnosis and treatment of COPD.COPD pathogenesis is inflammatory and blood coagulation dysfunction which leads to the destruction of the alveolar wall and blood vessels.Prethrombotic state?PTS?form is a cause of acute aggravating period of COPD,endothelial cells release specific protein von willebrand factor?vWF?at PTS form,which is the high expression in pulmonary artery and the main role of activated platelets and extended the?factor coagulation time.it maintains the balance of blood coagulation system in a physiological condition,but it facilitates the formation of microthrombus when activing PLT,white blood cells,macrophages,and dendritic cell which could release large amounts of inflammatory mediators,among them inflammatory mediators ILterleukin–32?IL-32?was found in 2005,which is different from any other family of cytokines,and has six kinds of homogeneous structure.IL-32 initially was thought to be derived from Natural Killer cells,but it was found in T cells and epithelial cells also.IL-32 induces proinflammatory cytokines and cell apoptosis via activating four main kinds of signaling pathways including?NF--B,p38mitogen-activated protein kinase?MAPKp38?,caspase-1,caspase-3?.IL–32 is also a high expression in the alveolar cells and lung macrophage,which can generate more cytokines when stimulated by IL–32 stimulus.Research shows that IL-32 could increase the secretion of TNF-?,IL–1,IL-18 leading to the inflammatory cascade reaction.Until now the correlation between IL-32 and vWF is rarely researched,and not unified with the relevant reports of PH,PaO₂,PaCO₂.Researching the correlation of the above indicators enriches the mechanism of blood coagulation and inflammation interaction and provides valuable indicators for the early diagnosis of PTS and a theoretical basis for anticoagulation therapy.Low molecular weight heparin?LMWH?has anti-inflammatory and anticoagulant dual function as a reinforcing agent of antithrombin?.Its main functions are to interfere the activation of clotting factors in intrinsic and extrinsic coagulation pathway,and to reduces 5-HT,IL-6,IL–8 releasing in the lung.LMWH adjuvant therapy could reduce the resistance of pulmonary circulation,and increases the gas exchange.we study CAT,vWF,IL-32,PH,PaO₂,PaCO₂ level changes after LWMH adjuvant therapy,which can provide more theoretical basis for the use of LWMH.Aim:This study is to evaluate the significance of vWF IL-32 in diagnosing COPD acute aggravating at early period of PTS and whether LWMH improve the effectiveness of the PTS or not.Methods:We choose AECOPD patients from September 22.2015 to August 2.2016 at the Huai He hospital and divided them into two groups at random,a group of low molecular heparin therapy plus conventional therapy,a group of conventional treatment group.The two groups received conventional treatment including giving low flow oxygen,alleviating phlegm and breathing or antibiotics.The LMWH group also received LMWH injection every 12 h for 6days.Stable COPD?STCOPD?group was a follow-up of patients after AECOPD discharged at least 2 months.Normal healthy group was screened from medical examination center,all of the participants were inspected including their routine blood,hepatic and renal function,blood lipid and glucose,pulmonary function,blood gas analysis and chest X-ray or CT examination.vWF and IL-32 were tested with ELISA kit.We used SPSS 17.0 to analyze all results.Results:We collected 100 cases of AECOPD,LMWH ancillary treatment AECOPD?n=50?;alone conventional treatment AECOPD?n=50?;STCOPD?n=50?;normal healthy?n=50?.These indicators vWF,IL-32,PH,PaO₂,PaCO₂,Lac,FEV1,FVC were meaningful at comparison of the four group?P<0.05?.We studied the correlation analysis among vWF and IL-32,PLT,PH,PaO₂,PaCO₂ in the AECOPD.the correlation between them respectively are?r=0.9,P=0.00?,?r=0.75,P=0.00?,?r=-0.29,P=0.04?,?r=0.62,P=0.00?,?r=0.38,P=0.01?,the correlation among IL-32 and PLT,PaO₂,PaCO₂ are?r=0.72,P=0.00?,?r=-0.54,P=0.00?,?r=0.32,P=0.02?in the AECOPD respectively.We show that CAT,vWF,IL-32,PH,PaO₂,PaCO₂,Lac are different?P<0.05?between two groups after treatment AECOPD.LMWH ancillary therapy more obviously reduce CAT,vWF,IL-32,Pa CO₂,Lac and more markedly improve PH,PaO₂ than conventional treatment group?P<0.05?.But the number of PLT has no obvious difference?P>0.05?after two groups treatment AECOPD and LMWH ancillary therapy also has no obvious adverse reactions.Conclusion:vWF and IL-32 can prompt the formation of thrombus state,which could become sensitive indicators to detect stable COPD exacerbations,and LMWH adjuvant therapy is safe and effective in PTS of COPD exacerbation.