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42 P Fecal calprotectin: A marker of intestinal inflammation
Inflammatory bowel diseases
41 P
43 P
“ITAMTN 86 DEFICIENCY, A RISK FACTOR FOR THROMBOSIS, IS FREQUENT fN THE ACTlVE PHASESOF INnAMMATGRY BOWEL “TSEASES S Saibeoi’,M Veccbi”, M Cattaneo*,R Lombard?,ML Zighetti’, L Spine’, A I.ecchi”. R de Franchis’
LAMINA PROPRIA MONONUCLEAR CELL (LPMC) EXPRESSION OF METALLOPROTEINASE-I m-1) IN INFLAMED AREAS OF CROHN’S DISEASE A Di Sabatioo*,R Cwzocioppo”, L IDcewt~*, F P Tinoti”, MC Ciione§, G R Coraza*
‘Univerriti degli St& di Mdano, ‘IRCCS OspedaleMaggtoredi Milano
‘GastroenterologyUmt, IRCCS Policlioico SanMatteo, University of Pawa,‘Dept oflnterna, Medicine,Lhiversity ofL’Aquila, “Dept of Surgery, LRCCSPoliclinico SanMatteo, University of P&a, SDeptof ExperimentalMedicine,University of L’Aquila
BACKGROUND: intlammatorybowel diseases(IBD) are et increasedrisk for thrombosis andvitamin deficienciesFew dataexist aboutthe relatianshiobetweenIBD andvitamin B6status Vitamin B6 de6nency is an independentrisk factor for thrombosispet se and by the inductionof hyperhomocystebtemia,which is frequentlyobservedin IBD AIM to evehts,tevitmtin 86 plasmalevelsin IBD patientsandtheir possiblecorrelationswith oatieots’clinicalfeatures.acuteobesereactantsandhvoerbomocvsteieemiaPATIENTS ~METHODS: we &died il IBD patients 32 C’&t’s d&se (IS tttw mean age37 3 + 1I I years) and29 tdcemtivecolitis (IS mea,mean age45.5 + 17 8 years) For each patient,3 gender-and age-matchedhealthycontrols were studied Plasmahomocysteinewas determinedby meansof HPLC. Vitamin B6 levelswere evaluatedby meansof a radiougrmatic asnay Statisticalanalysiswas performedby meansofMann-Whitney, Pishdr exact andSpearmancorrelationtests RESULTS medianwtaedn86 levelswere sigdicdy lower in IBD patients(22 0 pm&, range3 6-231 0 pm&l) than in controls (31.1 pmoVI,range3 7-363.4 pmol/l),(p
Background & Aims Sinceit hasbeat shown m in vitro studiesthat the disruptmnof celhetrk interactionscausese raoid onset ofawotoas in human coloruc cells.we tried to mvestigatethe possiblerole of M&-I, anenddpebtidatethat degradesthe e&cellular matrix, in moduletingenterocyte apoptosisin Crobn ‘s disease(CD). Patients& Methods:Endoscopicileal and c&mic biopsy specimenswere collectedfrom macroscopic& iovolvedand uninvolvedintestinalareasof 20 CD patientsandfrom 20 subjectswho proved to have functionaldiamhoeaDiagnosiswes establishedby clinicaland oatholoticalctiteria. MMF-I exoressionwes evaluatedbv immuwbistochemistw with the mouse&ti-human MMP-I Moib at a concentrationof i2S “g/ml (Gocogene).Apoptosts detectionwes assessedby TUNEL technique(ApopTag kit, Oocor) Tissue macrophages andftbrob,astswere identifiedby processingseriatesections with anti-CD68MoAb (DAKO) and anti-anin smooth mu& MoAb (Chemicon),respectively.Results The perceetagesofMMl-l+ LPMCs were signiticantlyincreased(p
42 P FECAL CALPRGTECTM A MARKER OF MTESTINAL INFLAMMATION F COSTA, M G M”MOL0, P ARPE, M R ROMANO, F CRISTIANI, L CECCARELLI,. C STERPI , M BELLMI, S MARCHI, G MALTINTI S 0 GASTROENTEROLOGIA UNIVERSITA’ DI PISA Calprotectin (C) is a 36.kD calcium and zinc binding protein that accounts for about 60% of solublecytosolic protem in neutropbilgrarulocytes An increaseof fecal C has beenreported in innammatorybowel disease(JBD) andcolorectal catxer in patientsfrom North Europe and USA Our study aimed to evaluatethe diagnosticaccuracy of fecal C measurementto discrbmnating orattic thorntimctiotwJchronic intestinaldisorders. Stool sampleswere collected from 99 patientswith IBD (40 CD, 59 UC), 20 with intestinal neoplasticlesions(12 adenwarcinoma, 6 adenoma,2 lymphoma),32 patientswith irritable bowel syndrome (IBS) and 18healthy vokmteers ON) Fecal C was measuredby a quantitativecommercially availableenzyme-linkedimmwtoassey(Calprest, Eurosp~tal, Trieste, Itake) andexpressed es ,,g,g of stoo,; according to the menufacmre?sinstruction., the normalC value wes < 50 ps/B, while strongly positive results were >I00 ,t& Values between 50and lo0 pglg were consideredindetemtinateatd,in ibis study,were not usedfor the performanceevaluationofthe test Statisticalanalysiswas carried out by using the Kroskai-Wellis test and the Fish& exact test The medianC coocentrationr were the following 257 p& (CD), 234 &p/p (UC), 130 flk+d (neoplesia),20 pg/g @BS),25 Kg/g (HV) Valuesfrom patientswith organic disorders (IBD, neoplasta)tomed out to be significantlyhigherthan values from IBS andHV (p
SERUM BASIC FIBROBLAST GROWTH FACTOR (bFGF) AND VASCULAR ENDOTHELIAL GROWTH FACTOR (VEGF) IN CROHN’S DISEASE PATENTS TREATED WIT?, lNFLLK,MAB A Di Sabatino’, R Ciccoctoppo9 B Cinqueg,L Benauato”, R. Morera, M G CifoneB. G C Stur”iolo”, G R Corawa* ‘GestroenterologyUnit, IRCCS Policlinico SanManeo, University of Pavia,“Dept of Internal Medicine.University of L.’Aquila: SDeetof ExperimentalMedicine,Umversity of ,‘Aqui,a *GastroemerologyUnit, University of Padova;%GestroeoterolagyUnit, IRCCS Policlinico SanMatteo, University ofPwia. Background & Aims.locreased levelsofbFGF and VEGF have beendemonstratedin inflammatorybowel diseases,suggestinga role ofbFGF in inducingan excessive fibrotic changein Croho ‘s disease(CD), and aninvolvementof VEGF in promoting gut iotlammatiooby increasingvascular permeabilityandmediatingangiogeoesirWe measured serumbFGF and VEGF levelsin CD patientstreatedwith the anti-TNF-a cbimeric antibody, irdliximab,to investigatethe effect of this treatment on processesof fibrogeoesisand angiogeoesnin CD. Patients&Methods Serumsampleswere obtamedfrom 12 fistuliziog CD patientsbefore andafter three consecutiveinfusionsof iotlmimah(Remicede. ScheringPlougb),administeredet week 0, 2 and 6 in a singlemtravenousdose(5 mgikg), and from 12 healthyvolunteers.Diagnosiswas establishedby clinicaland pathologicalcriteria Diseaseactivity was assewedby Crobn ‘s diseaseactivity index(CDAI) SerumbFGF and VEGF levelswere measuredby ELISA assaywith the QuantikineHS Human bFGF mmunoessey(R&D Systems) andthe QuantikineHS HumanVEGF immunoassay (R&D Systems) Serumcontents were determinedaccordingto the manufacturer‘s instructionand expressedas pdmg protein Resuhs:In untreatedCD patients,serum bFGF levelswere signitiuntly tugher(mean 38 4 p@) comparedto treated CD patients(mean I9 6 pg!nd, p
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41 P
43 P
“ITAMTN 86 DEFICIENCY, A RISK FACTOR FOR THROMBOSIS, IS FREQUENT fN THE ACTlVE PHASESOF INnAMMATGRY BOWEL “TSEASES S Saibeoi’,M Veccbi”, M Cattaneo*,R Lombard?,ML Zighetti’, L Spine’, A I.ecchi”. R de Franchis’
LAMINA PROPRIA MONONUCLEAR CELL (LPMC) EXPRESSION OF METALLOPROTEINASE-I m-1) IN INFLAMED AREAS OF CROHN’S DISEASE A Di Sabatioo*,R Cwzocioppo”, L IDcewt~*, F P Tinoti”, MC Ciione§, G R Coraza*
‘Univerriti degli St& di Mdano, ‘IRCCS OspedaleMaggtoredi Milano
‘GastroenterologyUmt, IRCCS Policlioico SanMatteo, University of Pawa,‘Dept oflnterna, Medicine,Lhiversity ofL’Aquila, “Dept of Surgery, LRCCSPoliclinico SanMatteo, University of P&a, SDeptof ExperimentalMedicine,University of L’Aquila
BACKGROUND: intlammatorybowel diseases(IBD) are et increasedrisk for thrombosis andvitamin deficienciesFew dataexist aboutthe relatianshiobetweenIBD andvitamin B6status Vitamin B6 de6nency is an independentrisk factor for thrombosispet se and by the inductionof hyperhomocystebtemia,which is frequentlyobservedin IBD AIM to evehts,tevitmtin 86 plasmalevelsin IBD patientsandtheir possiblecorrelationswith oatieots’clinicalfeatures.acuteobesereactantsandhvoerbomocvsteieemiaPATIENTS ~METHODS: we &died il IBD patients 32 C’&t’s d&se (IS tttw mean age37 3 + 1I I years) and29 tdcemtivecolitis (IS mea,mean age45.5 + 17 8 years) For each patient,3 gender-and age-matchedhealthycontrols were studied Plasmahomocysteinewas determinedby meansof HPLC. Vitamin B6 levelswere evaluatedby meansof a radiougrmatic asnay Statisticalanalysiswas performedby meansofMann-Whitney, Pishdr exact andSpearmancorrelationtests RESULTS medianwtaedn86 levelswere sigdicdy lower in IBD patients(22 0 pm&, range3 6-231 0 pm&l) than in controls (31.1 pmoVI,range3 7-363.4 pmol/l),(p
Background & Aims Sinceit hasbeat shown m in vitro studiesthat the disruptmnof celhetrk interactionscausese raoid onset ofawotoas in human coloruc cells.we tried to mvestigatethe possiblerole of M&-I, anenddpebtidatethat degradesthe e&cellular matrix, in moduletingenterocyte apoptosisin Crobn ‘s disease(CD). Patients& Methods:Endoscopicileal and c&mic biopsy specimenswere collectedfrom macroscopic& iovolvedand uninvolvedintestinalareasof 20 CD patientsandfrom 20 subjectswho proved to have functionaldiamhoeaDiagnosiswes establishedby clinicaland oatholoticalctiteria. MMF-I exoressionwes evaluatedbv immuwbistochemistw with the mouse&ti-human MMP-I Moib at a concentrationof i2S “g/ml (Gocogene).Apoptosts detectionwes assessedby TUNEL technique(ApopTag kit, Oocor) Tissue macrophages andftbrob,astswere identifiedby processingseriatesections with anti-CD68MoAb (DAKO) and anti-anin smooth mu& MoAb (Chemicon),respectively.Results The perceetagesofMMl-l+ LPMCs were signiticantlyincreased(p
42 P FECAL CALPRGTECTM A MARKER OF MTESTINAL INFLAMMATION F COSTA, M G M”MOL0, P ARPE, M R ROMANO, F CRISTIANI, L CECCARELLI,. C STERPI , M BELLMI, S MARCHI, G MALTINTI S 0 GASTROENTEROLOGIA UNIVERSITA’ DI PISA Calprotectin (C) is a 36.kD calcium and zinc binding protein that accounts for about 60% of solublecytosolic protem in neutropbilgrarulocytes An increaseof fecal C has beenreported in innammatorybowel disease(JBD) andcolorectal catxer in patientsfrom North Europe and USA Our study aimed to evaluatethe diagnosticaccuracy of fecal C measurementto discrbmnating orattic thorntimctiotwJchronic intestinaldisorders. Stool sampleswere collected from 99 patientswith IBD (40 CD, 59 UC), 20 with intestinal neoplasticlesions(12 adenwarcinoma, 6 adenoma,2 lymphoma),32 patientswith irritable bowel syndrome (IBS) and 18healthy vokmteers ON) Fecal C was measuredby a quantitativecommercially availableenzyme-linkedimmwtoassey(Calprest, Eurosp~tal, Trieste, Itake) andexpressed es ,,g,g of stoo,; according to the menufacmre?sinstruction., the normalC value wes < 50 ps/B, while strongly positive results were >I00 ,t& Values between 50and lo0 pglg were consideredindetemtinateatd,in ibis study,were not usedfor the performanceevaluationofthe test Statisticalanalysiswas carried out by using the Kroskai-Wellis test and the Fish& exact test The medianC coocentrationr were the following 257 p& (CD), 234 &p/p (UC), 130 flk+d (neoplesia),20 pg/g @BS),25 Kg/g (HV) Valuesfrom patientswith organic disorders (IBD, neoplasta)tomed out to be significantlyhigherthan values from IBS andHV (p
SERUM BASIC FIBROBLAST GROWTH FACTOR (bFGF) AND VASCULAR ENDOTHELIAL GROWTH FACTOR (VEGF) IN CROHN’S DISEASE PATENTS TREATED WIT?, lNFLLK,MAB A Di Sabatino’, R Ciccoctoppo9 B Cinqueg,L Benauato”, R. Morera, M G CifoneB. G C Stur”iolo”, G R Corawa* ‘GestroenterologyUnit, IRCCS Policlinico SanManeo, University of Pavia,“Dept of Internal Medicine.University of L.’Aquila: SDeetof ExperimentalMedicine,Umversity of ,‘Aqui,a *GastroemerologyUnit, University of Padova;%GestroeoterolagyUnit, IRCCS Policlinico SanMatteo, University ofPwia. Background & Aims.locreased levelsofbFGF and VEGF have beendemonstratedin inflammatorybowel diseases,suggestinga role ofbFGF in inducingan excessive fibrotic changein Croho ‘s disease(CD), and aninvolvementof VEGF in promoting gut iotlammatiooby increasingvascular permeabilityandmediatingangiogeoesirWe measured serumbFGF and VEGF levelsin CD patientstreatedwith the anti-TNF-a cbimeric antibody, irdliximab,to investigatethe effect of this treatment on processesof fibrogeoesisand angiogeoesnin CD. Patients&Methods Serumsampleswere obtamedfrom 12 fistuliziog CD patientsbefore andafter three consecutiveinfusionsof iotlmimah(Remicede. ScheringPlougb),administeredet week 0, 2 and 6 in a singlemtravenousdose(5 mgikg), and from 12 healthyvolunteers.Diagnosiswas establishedby clinicaland pathologicalcriteria Diseaseactivity was assewedby Crobn ‘s diseaseactivity index(CDAI) SerumbFGF and VEGF levelswere measuredby ELISA assaywith the QuantikineHS Human bFGF mmunoessey(R&D Systems) andthe QuantikineHS HumanVEGF immunoassay (R&D Systems) Serumcontents were determinedaccordingto the manufacturer‘s instructionand expressedas pdmg protein Resuhs:In untreatedCD patients,serum bFGF levelswere signitiuntly tugher(mean 38 4 p@) comparedto treated CD patients(mean I9 6 pg!nd, p
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