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Chest Department,AssiutUniversity,Assiut,Egypt Abstract Purpose: Encouraging positive diagnosticyieldsin malignantpleuraleffusion couldbeobtainedbypleuralbrushingperformedthroughtwotechniques,thefirstwasclosedandthesecondwasthoracoscopic.Untilnowtheultrasoundguidedpleuralbrushingisnotincludedwithinthesetechniquesanditsdiagnosticyield therefore is notevaluated.Sotheaim of thisstudywasto evaluatethe diagnosticyield of thisprocedureanditscontributionsasatechniquenotusedpreviouslyintheinterventionalpulmonologypracticetoobtainpleuralspecimenforcytologicalexaminationinmalignantpleuraleffusion.Methods:ThisprospectiveinterventionalstudywasconductedintheChestDepartment–AssiutUniversityHospitalduringtheperiod from July2014to September2015.Patientswhohadhighlysuspiciousmalignantpleural effusion(clinical,radiological,andlaboratory)werehospitalizedandenrolledinthisstudy.Patientswithbleedingtendencyorcoagulationprofileabnormalitieswereexcludedfromthestudy.Patientswerealsoexcludedfromthisstudyiftheetiologyofeffusionwasprovedtobebenign.Informedwrittenconsentwasobtainedfromallpatients.Theequipmentusedinourstudywereultrasoundapparatus(ALOKA–Prosound–SSD–3500SV),biopsyforceps(KARL–STORZ–Germany10329L–BS),thebronchoscopiccleaningbrush(PENTAX CS6002SN) trocar andcannula of Cope’sneedle and the semirigidthoracoscope(LTF; Olympus;Tokyo,Japan).Thoracentesis,pleuralbrushingandbiopsyforcepsofthepleurawereperformedforallenrolledpatientsintheultrasoundunitoftheChestDepartmentwhilethoracoscopywasdoneintheendoscopyunitonlyforpatientsinwhomthediagnosiscouldnotbeachievedbytheseprocedures.Results:Among22patientswhowerefinallydocumentedtohavemalignancy,theultrasoundguidedpleuralbrushingprovideddiagnosisin9(41%)/22cases,itwasexclusivelydiagnosticin3patients.Interestingly,theyieldof thisprocedurehad its contributionsregardingthefinalpathologicaldiagnosisof ourcases,itcouldaugmentthepositiveyieldtobe55%insteadof41%(forpleuralfluidcytologyalone),82%insteadof68%(forbiopsyforcepsalone)and86%insteadof72%(forbothfluidcytologyandforcepsbiopsy).Therecordedcomplicationsinourstudywereminimalandnotassociatedwithanymortality.Conclusions:Ultrasound-guidedpleuralbrushingisanewmethodforobtainingpleuralspecimens.Itisasimpleandrelativelysafeprocedure.Thistechniqueprovidesadditionaldiagnosticyieldin malignantpleuraleffusion.Werecommend itbesideothersin our diagnosticpracticeforsuspiciousmalignanteffusionespeciallywhenthoracoscopy is notavailable.

Chest Department,AssiutUniversity,Assiut,Egypt Abstract Purpose: Encouraging positive diagnosticyieldsin malignantpleuraleffusion couldbeobtainedbypleuralbrushingperformedthroughtwotechniques,thefirstwasclosedandthesecondwasthoracoscopic.Untilnowtheultrasoundguidedpleuralbrushingisnotincludedwithinthesetechniquesanditsdiagnosticyield therefore is notevaluated.Sotheaim of thisstudywasto evaluatethe diagnosticyield of thisprocedureanditscontributionsasatechniquenotusedpreviouslyintheinterventionalpulmonologypracticetoobtainpleuralspecimenforcytologicalexaminationinmalignantpleuraleffusion.Methods:ThisprospectiveinterventionalstudywasconductedintheChestDepartment–AssiutUniversityHospitalduringtheperiod from July2014to September2015.Patientswhohadhighlysuspiciousmalignantpleural effusion(clinical,radiological,andlaboratory)werehospitalizedandenrolledinthisstudy.Patientswithbleedingtendencyorcoagulationprofileabnormalitieswereexcludedfromthestudy.Patientswerealsoexcludedfromthisstudyiftheetiologyofeffusionwasprovedtobebenign.Informedwrittenconsentwasobtainedfromallpatients.Theequipmentusedinourstudywereultrasoundapparatus(ALOKA–Prosound–SSD–3500SV),biopsyforceps(KARL–STORZ–Germany10329L–BS),thebronchoscopiccleaningbrush(PENTAX CS6002SN) trocar andcannula of Cope’sneedle and the semirigidthoracoscope(LTF; Olympus;Tokyo,Japan).Thoracentesis,pleuralbrushingandbiopsyforcepsofthepleurawereperformedforallenrolledpatientsintheultrasoundunitoftheChestDepartmentwhilethoracoscopywasdoneintheendoscopyunitonlyforpatientsinwhomthediagnosiscouldnotbeachievedbytheseprocedures.Results:Among22patientswhowerefinallydocumentedtohavemalignancy,theultrasoundguidedpleuralbrushingprovideddiagnosisin9(41%)/22cases,itwasexclusivelydiagnosticin3patients.Interestingly,theyieldof thisprocedurehad its contributionsregardingthefinalpathologicaldiagnosisof ourcases,itcouldaugmentthepositiveyieldtobe55%insteadof41%(forpleuralfluidcytologyalone),82%insteadof68%(forbiopsyforcepsalone)and86%insteadof72%(forbothfluidcytologyandforcepsbiopsy).Therecordedcomplicationsinourstudywereminimalandnotassociatedwithanymortality.Conclusions:Ultrasound-guidedpleuralbrushingisanewmethodforobtainingpleuralspecimens.Itisasimpleandrelativelysafeprocedure.Thistechniqueprovidesadditionaldiagnosticyieldin malignantpleuraleffusion.Werecommend itbesideothersin our diagnosticpracticeforsuspiciousmalignanteffusionespeciallywhenthoracoscopy is notavailable.

Chest Department,AssiutUniversity,Assiut,Egypt Abstract Purpose: Encouraging positive diagnosticyieldsin malignantpleuraleffusion couldbeobtainedbypleuralbrushingperformedthroughtwotechniques,thefirstwasclosedandthesecondwasthoracoscopic.Untilnowtheultrasoundguidedpleuralbrushingisnotincludedwithinthesetechniquesanditsdiagnosticyield therefore is notevaluated.Sotheaim of thisstudywasto evaluatethe diagnosticyield of thisprocedureanditscontributionsasatechniquenotusedpreviouslyintheinterventionalpulmonologypracticetoobtainpleuralspecimenforcytologicalexaminationinmalignantpleuraleffusion.Methods:ThisprospectiveinterventionalstudywasconductedintheChestDepartment–AssiutUniversityHospitalduringtheperiod from July2014to September2015.Patientswhohadhighlysuspiciousmalignantpleural effusion(clinical,radiological,andlaboratory)werehospitalizedandenrolledinthisstudy.Patientswithbleedingtendencyorcoagulationprofileabnormalitieswereexcludedfromthestudy.Patientswerealsoexcludedfromthisstudyiftheetiologyofeffusionwasprovedtobebenign.Informedwrittenconsentwasobtainedfromallpatients.Theequipmentusedinourstudywereultrasoundapparatus(ALOKA–Prosound–SSD–3500SV),biopsyforceps(KARL–STORZ–Germany10329L–BS),thebronchoscopiccleaningbrush(PENTAX CS6002SN) trocar andcannula of Cope’sneedle and the semirigidthoracoscope(LTF; Olympus;Tokyo,Japan).Thoracentesis,pleuralbrushingandbiopsyforcepsofthepleurawereperformedforallenrolledpatientsintheultrasoundunitoftheChestDepartmentwhilethoracoscopywasdoneintheendoscopyunitonlyforpatientsinwhomthediagnosiscouldnotbeachievedbytheseprocedures.Results:Among22patientswhowerefinallydocumentedtohavemalignancy,theultrasoundguidedpleuralbrushingprovideddiagnosisin9(41%)/22cases,itwasexclusivelydiagnosticin3patients.Interestingly,theyieldof thisprocedurehad its contributionsregardingthefinalpathologicaldiagnosisof ourcases,itcouldaugmentthepositiveyieldtobe55%insteadof41%(forpleuralfluidcytologyalone),82%insteadof68%(forbiopsyforcepsalone)and86%insteadof72%(forbothfluidcytologyandforcepsbiopsy).Therecordedcomplicationsinourstudywereminimalandnotassociatedwithanymortality.Conclusions:Ultrasound-guidedpleuralbrushingisanewmethodforobtainingpleuralspecimens.Itisasimpleandrelativelysafeprocedure.Thistechniqueprovidesadditionaldiagnosticyieldin malignantpleuraleffusion.Werecommend itbesideothersin our diagnosticpracticeforsuspiciousmalignanteffusionespeciallywhenthoracoscopy is notavailable.

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-αwithp0.0001foreach)andthelevelsofmeasuredTNF-αweresignificantlyincreasedwiththeincreaseddegreeandseverityofCOPDandincreasedseverityofsmokingstatus.RegardingthesmokingstatusofCOPDpatients,therewasahighlysignificantlydifferencefor the measuredTNF-α(53.74±9.52versus12.73±1.20withp0.0001)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.

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-αwithp0.0001foreach)andthelevelsofmeasuredTNF-αweresignificantlyincreasedwiththeincreaseddegreeandseverityofCOPDandincreasedseverityofsmokingstatus.RegardingthesmokingstatusofCOPDpatients,therewasahighlysignificantlydifferencefor the measuredTNF-α(53.74±9.52versus12.73±1.20withp0.0001)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.

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-αwithp0.0001foreach)andthelevelsofmeasuredTNF-αweresignificantlyincreasedwiththeincreaseddegreeandseverityofCOPDandincreasedseverityofsmokingstatus.RegardingthesmokingstatusofCOPDpatients,therewasahighlysignificantlydifferencefor the measuredTNF-α(53.74±9.52versus12.73±1.20withp0.0001)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.

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-αwithp0.0001foreach)andthelevelsofmeasuredTNF-αweresignificantlyincreasedwiththeincreaseddegreeandseverityofCOPDandincreasedseverityofsmokingstatus.RegardingthesmokingstatusofCOPDpatients,therewasahighlysignificantlydifferencefor the measuredTNF-α(53.74±9.52versus12.73±1.20withp0.0001)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.

AbstractContinuouspositiveairwaypressure(CPAP)isastandardtreatmentofmoderateandsevereobstructive sleepapnea syndrome.However, itseffect inpatients with coexistingobstructiveandcentralapneasiscontroversial. Objectives:TodeterminetheimmediateresponsetoCPAPincombinedobstructiveandcentralsleepapneapatientswithoutheartfailure. Methods:Thirty sevenconsecutivepatients with moderateandsevere coexisting obstructive andcentralapneas(combinedgroup)wereprospectivelyenrolledinthiscrosssectionalanalyticstudy.Allpatientsunderwentafullnight-attendedandafullnightCPAPtitrationpolysomnography.TitrationwasconsideredsuccessfulifAHI 10andthetitrationstudyincludedatleast15 min inREMstage. Results:OnCPAPtitration,thecombinedgroupshowedsignificantimprovementinsleepandrespiratorypolysomnographicparameters.MeanAHIwasreducedfrom71.9±30.3to 8.39±5.15(P=0.000).WhereasCPAPsignificantlyreducedthecentralapneaindexfrom 12.8±6.67to3.1±2.86(P=0.000),theresponsetocentraleventswasvariable(rangedfrom20%to100%).Overallresults,25(67.6%)hadsuccessfultitrationwithsignificantbetterresponseinfemalesthanmalestoCPAPthanmales(88.9%vs.60.7%,P=0.019). Conclusion:CPAPcanbeeffectiveincombinedobstructiveandcentralapneapatientswithoutheartfailurewithconsiderationofindividualvariability.AtrialofCPAPtitrationshouldbedoneinthosepatients. 2016TheEgyptianSocietyof ChestDiseasesandTuberculosis.Productionandhostingby ElsevierB.V.Thisisanopenaccessarticle under theCCBY-NC-ND license (http://creativecommons.org/licenses/by-nc-