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The impact of smoking on inflammatory biomarkers in patients with chronic obstructive pulmonary disease.
accepted April 2016 EgyptianJournalofChestDiseasesandTuberculosis

Research Authors
YasserA.Korani
¹,AlaaT.Hassan¹
,EffatA.E.Tony²,
MadleenAdelA.Abdou
Research Department
Research Journal
EgyptianJournalofChestDiseasesandTuberculosis
Research Member
Research Publisher
Egyptian Journal of Chest Diseases and Tuberculosis www.elsevier.com/locate/ejcdtwww.sciencedirect.com
Research Rank
1
Research Vol
NULL
Research Website
Egyptian Journal of Chest Diseases and Tuberculosis www.elsevier.com/locate/ejcdtwww.sciencedirect.com
Research Year
2016
Research_Pages
NULL
Research Abstract

ABSTRACT

Background:Chronicobstructivepulmonarydisease(COPD)isachronicprogressiveinflammatorydiseasecharacterizedbylimitationsairflowthatisnotfullyreversible(42).ThepathophysiologyofCOPDisnotcompletelyunderstood. Cigarettesmoking is amajorriskfactorforchronicobstructivepulmonarydisease(COPD).ElevatedCRPhasbeenincreasinglyusedasasurrogatemarkerofsystemicinflammationindiverseconditions.TNF-α,apowerfulpro-inflammatorycytokineprimarilyproducedbyactivatedmacrophages,isthoughttoacriticalroleinthepathogenesisofCOPD[13,14].
Theaimofthework:toevaluatetheimpactofsmokingoninflamatorybiomarkersandrelationsbetweenthesebiomarkersandthedeclineoflungfunctioninCOPDpatients.
Methods:Thiscase–controlobservationalprospectivestudywasconductedonfifty-eightclinicallystableCOPDpatients(26non-smokersand32current smokers;at differentstagesrangedfrommildtoverysevere),theirmeanage53.1±14.25and53.9±5.95yearsrespectively),recruitedfromChestDepartment,AssiutUniversityHospitals.AllpatientsmettheGlobalInitiativeforObstructiveLungDisease(GOLD)[4].Allparticipantsweresubjectedtothoroughhistorytaking,fullclinicalexamination,anthropometricmeasurementswithspirometryandchest X-ray.Peripheralhemogram,liverfunctiontests,kidneyfunctiontests,highsensitivityC-reactiveprotein(hsCRP)andserumlevelofTNF-αweremeasuredforbothpatientsandcontrols.
Results:Theconcentrationsofcirculatinghs-CRPandTNF-α,werehighlysignificantlyelevatedinpatientswithCOPDincomparisontothecontrolgroup(3.74±0.2vs.1.30±0.14forhs-CRP;33.88±5.97vs.8.79±0.57forTNF-αwithp<0.0001foreach)andthelevelsofmeasuredTNF-αweresignificantlyincreasedwiththeincreaseddegreeandseverityofCOPDandincreasedseverityofsmokingstatus.RegardingthesmokingstatusofCOPDpatients,therewasahighlysignificantlydifferencefor the measuredTNF-α(53.74±9.52versus12.73±1.20withp<0.0001)withnosignificantdifferenceforthemeasuredhs-CRP(3.87±0.29versus 3.58±0.27withp˃0.05).Interestingly,therewere significant negativecorrelationsbetweenthelevelsofTNF-αand hs-CRP,andFEV1instagesII,III,IVofCOPD.
Conclusions:Thecirculatinglevelsoftheinflammatorymarkershs-CRPandTNF-alphaaresignificantlyelevatedinpatientswithstableCOPDandthesebiomarkerscouldbeusedaspredictorfactorsforseverityofinflammationinCOPDpatients..Longitudinalstudiesevaluatingtheeffectsofsmokingcessationonbronchialandsystemicinflammationareneededtoallowbetterunderstandingoftheserelationshipsandtheirconsequences.
Keywords:COPD,FEV1,inflammatorymarkers;hs-CRPandTNF-alpha.