ࡱ> .0)*+,-jprt#`bjbjmm ,w""""$$$4$ޗޗޗhFZ$iv ֩M Yeeeeeee$lhne$h?lhhe""SUGi'''h"V$e'he''pX$$^ YBCBޗ2 [J_ei<if[>So"So^So$^ ' Yee&^ihhhh$$$Dm$$$$$$"""""" SVEU ILI`TE U ZAGREBU MEDICINSKI FAKULTET Stipe `kara Rituksimab u lije enju refraktornih ili relapsirajuih agresivnih limfoma DIPLOMSKI RAD  Zagreb, 2012. SVEU ILI`TE U ZAGREBU MEDICINSKI FAKULTET Stipe `kara Rituksimab u lije enju refraktornih ili relapsirajuih agresivnih limfoma DIPLOMSKI RAD Zagreb, 2012. Ovaj diplomski rad izraen je na Zavodu za hematologiju Klinike za unutarnje bolesti Klini kog bolni kog centra Zagreb pod vodstvom prof. dr. sc. Igora Aurera i predan je na ocjenu u akademskoj godini 2011./2012. Mentor rada: prof. dr. sc. Igor Aurer Popis kratica ACB  eng. activated B-cell like, sli ni aktiviranim B-stanicama ACVBP  kemoterapijski protokol: doksorubicin, ciklofosfamid, vindezin, bleomicin, i prednizon ADCC  eng. antibody-dependent cellular cytotoxicity, citotoksi nost ovisna o protutijelima ATKS - transplantacija autolognih mati nih krvotvornih stanica CDC  eng. complement-dependent cytotoxicity, citotoksi nost ovisna o komplementu CHOEP  kemoterapijski protokol: ciklofosfamid, doksorubicin, etopozid, vinkristin i prednizon CHOP  kemoterapijski protokol: ciklofosfamid, doksorubicin, vinkristin, prednizon DHAP  kemoterapijski protokol: deksametazon, citarabin i cisplatina DLBCL  eng. diffuse large B-cell lymphoma, difuzni B-velikostani ni limfom EBV  Epstein-Barr virus ECOG  eng. eastern cooperative oncology group ESHAP  kemoterapijski protokol: etopozid, metilprednizolon, citarabin, cisplatina FDG  fluordeoksiglukoza FL  folikularni limfom GCB  eng. germinal centar B-cell like, sli an stanicama germinativnog centra HHV8  humani herpes virus 8 HLA  eng. human leukocyte antigen, humani leukocitni antigen ICE - kemoterapijski protokol: ifosfamid, karboplatina, etopozid IPI  eng. international prognostic index, meunarodni prognosti ki indeks KLL  kroni na limfocitna leukemija KR  kompletna remisija LDH  laktat dehidrogenaza miniBEAM  kemoterapijski protokl: karmustin, etopozid, cytarabine, melfalan NHL  ne-Hodginov limfom nKR  nepotvrena kompletna remisija NOS  eng. not otherwise specified, nespecificirani OS  eng. overall survival, ukupno pre~ivljenje PET  pozitronska emisijska tomografija PFS  eng. progression free survival, pre~ivljenje bez progresije bolesti PR- parcijalna remisija R-DHAP  kemoterapijski protokol: rituksimab + deksametazon, citarabin i cisplatina R-ICE - kemoterapijski protokol: rituksimab + ifosfamid, karboplatina, etopozid SB- stabilna bolest US - FDA  eng. United States food and drug administration, Ameri ka agencija za lijekove i hranu SADR}AJ 1. SA}ETAK 2. SUMMARY TOC \o "1-3" \h \z \u   HYPERLINK \l "_Toc326505119" 3. UVOD  PAGEREF _Toc326505119 \h 1  HYPERLINK \l "_Toc326505120" 3.1. Difuzni B-velikostani ni limfom (DLBCL)  PAGEREF _Toc326505120 \h 1  HYPERLINK \l "_Toc326505121" 3.1.1. Definicija  PAGEREF _Toc326505121 \h 1  HYPERLINK \l "_Toc326505122" 3.1.2. Epidemiologija  PAGEREF _Toc326505122 \h 2  HYPERLINK \l "_Toc326505123" 3.1.3. Etiologija  PAGEREF _Toc326505123 \h 2  HYPERLINK \l "_Toc326505124" 3.1.4. Patologija  PAGEREF _Toc326505124 \h 3  HYPERLINK \l "_Toc326505125" 3.1.5. Klini ka slika  PAGEREF _Toc326505125 \h 4  HYPERLINK \l "_Toc326505126" 3.1.6. Dijagnosti ka obrada  PAGEREF _Toc326505126 \h 5  HYPERLINK \l "_Toc326505127" 3.1.7. Procjena odgovora na lije enje  PAGEREF _Toc326505127 \h 6  HYPERLINK \l "_Toc326505128" 3.1.8. Klini ki prognosti ki imbenici  PAGEREF _Toc326505128 \h 8  HYPERLINK \l "_Toc326505129" 3.1.9. Lije enje DLBCL  PAGEREF _Toc326505129 \h 9  HYPERLINK \l "_Toc326505130" 3.2. Rituksimab  PAGEREF _Toc326505130 \h 12  HYPERLINK \l "_Toc326505131" 3.2.1. Mehanizmi djelovanja rituksimaba  PAGEREF _Toc326505131 \h 13  HYPERLINK \l "_Toc326505132" 3.3. Rituksimab u lije enju relapsirajuih/refraktornih DLBCL  PAGEREF _Toc326505132 \h 14  HYPERLINK \l "_Toc326505133" 4. HIPOTEZA  PAGEREF _Toc326505133 \h 17  HYPERLINK \l "_Toc326505134" 5. CILJEVI  PAGEREF _Toc326505134 \h 18  HYPERLINK \l "_Toc326505135" 6. BOLESNICI I METODE  PAGEREF _Toc326505135 \h 19  HYPERLINK \l "_Toc326505136" 6.1. Dizajn istra~ivanja  PAGEREF _Toc326505136 \h 19  HYPERLINK \l "_Toc326505137" 6.2. Bolesnici PAGEREF _Toc326505137 \h Error! Bookmark not defined...............................................................................................................19  HYPERLINK \l "_Toc326505138" 6.3. Lije enje i procjena odgovora  PAGEREF _Toc326505138 \h 19  HYPERLINK \l "_Toc326505139" 6.4. Statisti ka analiza  PAGEREF _Toc326505139 \h 20  HYPERLINK \l "_Toc326505140" 7. REZULTATI  PAGEREF _Toc326505140 \h 21  HYPERLINK \l "_Toc326505141" 7.1. Zna ajke bolesnika i bolesti  PAGEREF _Toc326505141 \h 21  HYPERLINK \l "_Toc326505142" 7.2. Odgovor na terapiju  PAGEREF _Toc326505142 \h 22  HYPERLINK \l "_Toc326505143" 7.3. Prikupljanje transplantata  PAGEREF _Toc326505143 \h 30  HYPERLINK \l "_Toc326505144" 7.4. Nehematoloake nuspojave i toksi nost terapije  PAGEREF _Toc326505144 \h 30  HYPERLINK \l "_Toc326505145" 7.5. Uzroci smrti  PAGEREF _Toc326505145 \h 31  HYPERLINK \l "_Toc326505146" 8. RASPRAVA  PAGEREF _Toc326505146 \h 32  HYPERLINK \l "_Toc326505150" 9. ZAKLJU CI 35  HYPERLINK \l "_Toc326505151" 10. ZAHVALE 36  HYPERLINK \l "_Toc326505152" 11. LITERATURA  PAGEREF _Toc326505152 \h 37  HYPERLINK \l "_Toc326505153" 12. }IVOTOPIS  PAGEREF _Toc326505153 \h 40  Naslov rada: Rituksimab u lije enju refraktornih ili relapsirajuih agresivnih limfoma Autor: Stipe `kara 1. SA}ETAK Difuzni B  velikostani ni limfom (DLBCL) je naj eaa vrsta non-Hodgkinovog limfoma (NHL). Na DLBCL otpada oko 1/3 svih non-Hodginovih limfoma (NHL) odraslih ato ga ini naj eaom B-stani nom neoplazmom. Bolesnici s novootkrivenom bolesti se lije e kombinacijom rituksimaba i CHOP (ili sli ne) kemoterapije. Oni koji ne odgovore na ovakvo lije enje ili u kojih se bolest ponovno pojavi se lije e agresivnim kemoterapijskim protokolima i, ako povoljno odgovore, autotransplantacijom. Uloga rituksimaba u ovoj skupini bolesnika nije posve definirana. Cilj ovog rada bio je retrospektivnom anlizom podataka iz povijesti bolesti pokuaati utvrditi kako dodatak rituksimaba ICE protokolu djeluje na ishod lije enja bolesnika s refraktornim ili relapsirajuim DLBCL. Analizirali smo ishod 54 bolesnika, 32 lije enih samo ICE kemoterapijom i 22 lije enih i rituksimabom (RICE). Bolesnici lije eni ICE kemoterapijom imali su ukupni odgovor na terapiju od 26% a bolesnici u RICE skupni 54 % (p=0,05, 2 test). Bolesnici lije eni rituksimabom su u multivarijatnoj analizi imali bolje pre~ivljavanje od onih lije enih samo kemoterapijom (medijan pre~ivljavanja 40 vs. 20%, p=0,031, Coxova regresijska analiza). Drugi nepovoljni prognosti ki imbenici bili su prethodno lije enje rituksimabom, kratko trajanje remisije i nepovoljan meunarodni prognosti ki indeks (IPI). ini se da u skupini bolesnika koji nisu prethodno lije eni rituksimabom, svi imaju koristi od rituksimaba, a u skupini onih koji su prethodno primali rituksimab, samo oni u kasnom relapsu. Izgleda da dodatk rituksimaba ICEu ne nosi poviaeni rizik od nuspojava niti negativno utje e na uspjeanost prikupljanja mati nih stanica. Klju ne rije i: Difuzni B-velikostani ni limfom, relaps, refraktorna bolest; rituksimab. Title: Rituximab in the treatment of refractory or relapsed aggressive lymphomas Author: Stipe kara 2. SUMMARY Diffuse large B - cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphomas (NHL). DLBCL acccounts for about 1/3 of all NHLs in adults which makes it the most common B-cell neoplasm. Patients with newly diagnosed disease are treated with a combination of rituximab and CHOP (or similar) chemotherapy. Those who do not respond to such treatment or whose disease recurrs are treated with aggressive chemotherapy regimens and, if they respond, autotransplantation. The role of rituximab in this patient group is not completely defined. The aim of this study was to retrospectively analyse the data from patient medical histories to try to determine the effect of the addition of rituximab to ICE chemotherapy on the outcome of patients with relapsing or refractory DLBCL. We analyzed the outcome of 54 patients, 32 treated with ICE chemotherapy alone and 22 treated with ICE and rituximab (RICE). The response of patients treated with ICE only was 26% and those treated with RICE 54% (p = 0.05, 2 test). In a mul tivariate analysis patients treated with rituximab had a better overall survival than those treated only with chemotherapy (40% vs. 20%, p=0.031, Cox regression analysis). Other adverse prognostic factors were prior treatment with rituximab, short remission duration and an unfavorable international prognostic index (IPI). It seems that in the group of patients not previously treated with rituximab all benefit from rituximab, but in the group previously treated with rituximab, only those in a late relapse. The addition of rituximab to ICE dose not seem carry an increased risk of toxicity or stem cell collection failure. Key words: diffuse large B-cell lymphoma, relapse, refractory; rituximab. 3. UVOD 3.1. Difuzni B-velikostani ni limfom (DLBCL) 3.1.1. Definicija Difuzni B  velikostani ni limfom (DLBCL) je skupina limfoma graena od velikih transformiranih stanica B-limfocitne loze ije su jezgre jednako velike ili vee od jezgara makrofaga, odnosno dvaput vee od malih limfocita (Aurer I et al, 2007; Swerdlow SH i sur, 2008). Tumorsko tkivo se sastoji od difuznog infiltrata velikih limfocita. Postoji nekoliko varijanti. Najzastupljeniji oblik DLBCL je nespecificrani DLBCL ili engleski DLBCL-NOS (not otherwise specied). Naj eai patohistoloaki podtipovi unutar DLBCL-NOS, su centroblasti ni, imunoblasti ni te anaplasti ni tip. Tumorske stanice na svojoj povraini izra~avaju B-stani ne biljege, naj eae CD19, CD20, CD22, PAX5 i CD79a. Osim navedenih izra~avaju i CD45 stani ni biljeg te neato rijee CD10 ili CD5. Posotje naznake da su CD5+ tumori agresivnije prirode i imaju loaiju prognozu. Difuzni B  velikostani ni limfom nije jedinstven entitet, ve heterogena grupa tumora B-stani ne loze. Istra~ivanja genske ekspresije tumorskih stanica su pokazala da postoje barem tri razli ita entiteta s razli itim genskim profilima. Tako razlikujemo stanice s genskim profilom sli nim stanicama germinativnog centra (eng. germinal center B-cell-like or GCB), zatim stanice s genskim izra~ajom sli nim aktiviranim B-stanicama (eng. activated B-cell-like or ABC) te intermedijarni koji se ne mo~e svrstati niti u GCB ni u ABC. Izmeu navedenih skupina postoje razlike u odgovoru na terapiju i ishodu lije enja pa tako GCB tumori bolje odgovaraju na terapiju i imaju bolju prognozu u usporedbi s ostale dvije skupine. DLBCL se naj eae nalazi u limfnim vorovima, mo~e se javljati i u ekstrafimfati kim organima, a rijetko s leukemijskom slikom bolesti. U trenutku dijagnoze koatana sr~ je zahvaena u 10-20% slu ajeva. Otprilike 50-60% novodijagnosticiranih bolesnika se prezentira u uznapredovalom stadiju bolesti (Ann Arbor III i IV). Bolest eae nastaje de novo iako mo~e nastati i transformacijom iz limfoma niskog stupnja malignosti poput limfoma malih limfocita ili folikularnog limfoma. 3.1.2. Epidemiologija Na DLBCL otpada oko 1/3 svih non-Hodginovih limfoma (NHL) odraslih ato ga ini naj eaom B-stani nom neoplazmom. Incidencija u Europskoj Uniji i Hrvatskoj je 3-4 slu aja na 100 000 stanovnika godianje. Incidencija raste sa ~ivotnom dobi (Tilly H et al, 2010) a medijan pojavljivanja bolesti je u dobi od 65 godina. DLBCL se javlja eae u muakog spola i to 1.5 puta u estalije. U SAD-u i drugim razvijenim zemljama je pojavnost NHL-a, uklju ujui i DLBCL bila u stalnom porastu od 3-4% svake godine izmeu 1973. do sredine 90-ih kad se stabilizirala. To poveanje incidencije je neovisno o spolu ili rasi, a javlja se u svim dobnim skupinama osim kod jako mladih osoba. Razlog za takav porast incidencije pokuaavao se protuma iti boljim dijagnosti kim metodama, promjenama u klasifikaciji limfoproliferativnih bolesti te sve u estalijim infekcijama virusom HIV-a, ali nakon iscrpnih analiza zaklju eno je da se ni jedan od spomenutih faktora ne mo~e sa sigurnoau povezati s tako velikim porastom incidencije NHL-a (Friedberg JW, 2008). 3.1.3. Etiologija To na etiologija DLBCL kao i veine ostalih limfoma nije poznata. Poznati su nam samo odreeni rizi ni imbenici za nastanak NHL-a. Rizik za nastanak DLBCL je povien u osoba koje u obiteljskoj anamnezi u prvom koljenu imaju osobu oboljelu od NHL-a, Hodgkinovog limfoma, leukemije te bilo koje druge hematoloke maligne bolesti. Povieni rizik za nastanak DLBCL je povezan s dijagnozom reumatoidnog artritisa (OR, 1.4), Sjogrenovog sindroma (OR, 2.0) te autoimune hemoliti ke anemije (OR, 3.3). Osobe oboljele od sistemskog eritematoznog lupusa imaju takoer poviaeni rizik za nastanak NHL-a. Pacijenti kojima je dijagnosticiran neki indolentni limfom su pod poviaenim rizikom za nastanak DLBCL zbog ve spomenute sklonosti transformaciji. Osim autoimunih bolesti, primarne i sekundarne imunodeficijencije nose poviaen rizik za nastanak NHL-a. Poznato je da osobe oboljele od AIDS-a imaju eae maligne bolesti pa tako i NHL. Imunosupresija nakon transplantacije organa je takoer rizi ni imbenik za nastanak limfoma. Infekcije EBV-om su povezane s nastankom DLBCL, posebno s primarnim limfomom CNS-a. Osim EBV-a, HHV8 se dovodi u vezu s nastankom nekih oblika DLBCL dok se infekcije s H. pylori i C. psittaci eae povezuju s indolentnim limfomima (Flowers CR et al, 2010). 3.1.4. Patologija DLBCL je neoplazma velikih transformiranih B-stanica koje svojom klonalnom proliferacijom i difuznim rastom potpuno naruaavaju normalnu arhitekturu limfnog vora (Hunt KE, Reichard KK, 2008). DLBCL je klini ki, molekularno i patohistoloaki heterogen zbog ega je u klasifikaciji Svjetske Zdravstvene Organizacije iz 2008. godine podijeljen u nekoliko entiteta (tablica1) (Jaffe ES, Pittaluga S, 2011). TABLICA 1. Klasifikacija svjetske zdravstvene organizacije zrelih B-velikostani nih neoplazmi KLASIFIKACIJADifuzni B-velikostani ni limfom, nespecificirani DLCL-B, NOS T-stanicama/histiocitima bogat B-velikostani ni limfom Primarni DLBCL CNS-a Primarni ko~ni DLBCL, no~ni tip EBV+ DLBCL starijihDLBCL povezan s kroni nom upalomLimfomatoidna granulomatozaPrimarni medijastinalni B-velikostani ni limfomIntravaskularni B-velikostani ni limfomALK+ B-velikostani ni limfomPlazmablasti ni limfomDLBCL povezan s Castelmanovom bolestiPrimarni efuzijski limfom  3.1.5. Klini ka slika Pacijenti oboljeli od difzuznog B-velikostani nog limfoma se obi no prezentiraju simptomima koji ovise o lokalizaciji tumora. Tako naj eae bolesnik dolazi s brzo rastuim, bezbolnim, vratnim ili supraklavikularnim limfnim vorovima. Osim nodalne varijante bolesti, 40% bolesnika se inicijalno prezentira ekstranodalnim lokalizacijama tumora. Naj eae ekstralimfati ke lokalizacije su gastrointestinalni trakt, ko~a, CNS, kosti te plua. Kako je ve spomenuto, simptomi ovise o lokalizaciji bolesti, tako npr. medijastinalni tumor mo~e uzrokovati sindrom gornje auplje vene, a primarni limfom CNS-a neuroloake ispade. Osim simptoma specifi nih za pojedine organe kod limfoma se javljaju i tzv. B-simptomi (vruica, nono znojenje, gubitak na tjelesnoj masi) koji su uzrokovani otpuatanjem citokina iz tumorskih stanica. Oko jedne treine bolesnika na po etku bolesti ima neki od B-simptoma. Otprilike 15% bolesnika se prezentira na po etku bolesti sa zahvaenom koatanom sr~i, gotovo polovina ima stadij bolesti III/IV, a isto toliko bolesnika ima poviaen serumski LDH (Friedberg JW, Fisher RI, 2008). 3.1.6. Dijagnosti ka obrada Dijagnosti ka obrada bolesnika s limfomom ima nekoliko ciljeva. Prvi je ustanoviti koju vrstu tumora bolesnik ima. Drugi je ustanoviti koliko je bolest proairena. Trei cilj je procijeniti vrijednost prognosti kih pokazatelja te pokazatelja aktivnosti bolesti kako bi se odlu ili za vrstu lije enja koje bolesnik mo~e podnijeti. Prva pretraga koja treba biti u injena kod sumnje na limfom jest citoloaka punkcija limfnog vora. Ukoliko citoloaki nalaz upuuje na limfom potrebno je u initi kiruaku biopsiju limfnog vora ili zahvaenog organa. Umjesto kiruake biopsije, mo~e se napraviti i biopsija iglom, ali tada hematopatolog ima slabiji uvid u arhitekturu limfnog vora. Za postavljanje dijagnoze nu~na je imunohistokemijska analiza tumora, a danas se sve viae koriste i citogenetske i molekulske tehnike. Proairenost limfoma procjenjuje se CTom (odnosno PET-CTom) i biopsijom kosti. Biopsija ima veu dijagnosti ku vrijednost od aspiracije koatane sr~i. Stupanj proairenosti odreuje se prema modificiranoj Ann Arborskoj klasifikaciji (tablica 2). Stadij I smatra se lokaliziranom, a ostali stadiji proairenom boleau. Uobi ajeno se tijekom obrade bolesnika naprave i krvne pretrage: SE, KKS, GuK, kreatinin, urati, urea, bilirubin, AF, AST, ALT, GGT, LDH, elektroforeza proteina seruma i Ig. (Aurer I et al, 2007). TABLICA 2  3.1.7. Procjena odgovora na lije enje Procjena odgovora na lije enje DLBCL provodi se obi no nakon polovine do treine lije enja i na kraju lije enja. Nakon prvih nekoliko ciklusa trebalo bi postii najmanje parcijalnu, a na kraju lije enja kompletnu remisiju. Godine 1999. je meunarodna radna skupina, koju su inili klini ari, patolozi i radiolozi, objavila smjernice za procjenu odgovora na lije enje bolesnika s limfomima (Cheson BD i sur, 1999) . Preporuke su uskoro airoko prihvaene od strane klini ara diljem svijeta. Te smjernice temeljile su se na upotrebi CT-a. Godine 2007. objavljene su nove upute temeljene na upotrebi PET-CT-a (Cheson BD i sur, 2007). Pozitronska emisijska tomografija FDG-om (PET) je najbolja metoda za procjenu proairenosti bolesti te za procjenu odgovora na antitumorsko lije enje. Prednost pozitronske emisijske tomografije u odnosu na CT ili NMR je u sposobnosti da razlikuje prisutnost tumora od nekroze ili fibroznih promjena u rezidualnim masama koje su esto prisutne nakon lije enja. Nedostaci pozitronske emisijske tomografije su la~no-pozitivni rezultati kod hiperplazije timusa, sarkoidoze te nekih infekcija. Poja ano nakupljanje FDG-a mo~e se vidjeti i u koatanoj sr~i nakon lije enja kod davanja hematopoetskih faktora rasta. Prema smjernicama radne skupine PET-CT je preporu ljivo napraviti prije lije enja DLBCL-a da se utvrdi stupanj proairenosti bolesti i nakon zavraenog lije enja kako bi se utvrdio odgovor na protutumorsko lije enje. PET-CT treba napraviti nakon minimalno tri tjedna od zadnje kemoterapije, a najbolje nakon 6-8 tjedana. 3.1.7.1. Kompletna remisija (KR) Kompletna remisija zna i nestanak svih klini kih znakova bolesti i simptoma povezanih s bolesti. Ako se odgovor procjenjuje CT-om, rezidualni limfni vorovi koji su prije po etka lije enja bili > 1,5 cm, moraju se smanjiti na 1,5 cm ili manje. vorovi koji su prije lije enja bili veliki 1,1-1,5 cm u duljoj osi i vei od 1cm u kraoj osi moraju nakon terapije biti d" 1,0 cm u kraoj osi. Jetra i slezena, ukoliko su bile poveane prije lije enja, ne smiju biti palpabilne. Ako se koristi PET-CT, veli ina rezidualnih promjena nije va~na, ali moraju biti PET negativne. U oba slu aja se u biopsiji koatane sr~i ne smije nai tumorskih stanica. 3.1.7.2. Nepotvrena kompletna remisija (nKR) Kriteriji za nKR su isti kao i za KR osim ato ostatni limfni vorova smiju biti vei od 1,5 cm, ali moraju biti za najmanje 75% manji od po etnog nalaza. Veli ina limfnih vorova se ra una tako da se pomno~e dva meusobno okomita najvea promjera izmjerena na aksijalnoj CT snimki. nKR kategorija ne postoji ako se za procjenu odgovora koristi PET. Na elno se nKR smatra ekvivalentnom KR. 3.1.7.3. Parcijalna remisija (PR) Parcijalna remisija zna i smanjenje tumorske mase za najmanje 50% bez da su ispunjeni svi kriteriji za KR ili nKR. 3.1.7.4. Stabilna bolest (SB) Smatra se da bolesnik ima SB ako ne ispunjava kriterije za KR, nKR, PR niti za progresivnu bolest (PB). 3.1.7.5. Progresivna bolest (PB) PB zna i pojavu bilo koje nove lezije tokom ili nakon terapije bez obzira jesu li se ostali vorovi smanjili ili poveanje neke tumorske mase za najmanje 50% u odnosu na najmanju opa~enu veli inu. Ako se koristi PET, lezije moraju biti pozitivne. 3.1.8. Klini ki prognosti ki imbenici Kod predvianja ishoda lije enja oboljelih od DLBCL slu~imo se meunarodnim prognosti kim indeksom (IPI) koji je orginalno razvijen 1993. godine te se bazira na klini kim i radioloakim pokazateljima aktivnosti bolesti (The international non-Hodgkin s lymphoma prognostic factors project, 1993). Stadij III/IV, LDH iznad granice normale, dob > 60 godina, ECOG performance status > 1 te zahvaenost viae od jedne ekstranodalne lokalizacije nose po jedan bod za svaki zadovoljeni uvjet. IPI sistem bodovanja dijelio je bolesnike u 4 skupine s prosje nim petogodianjim pre~ivljenjem od 26% do 73%. U dobi prilagoen IPI ulaze isti imbenici kao i u IPI osim broja ekstranodalnih lokalizacija. Uvoenje rituksimaba u standardnu terapiju DLBCL dovelo je do promjena u prognozi, tako da se danas koristimo i revidiranim meunarodnim prognosti kim indeksom (R-IPI) (tablica 3) (Flowers CR et al, 2010). TABLICA 3O ekivani ishodi za bolesnike ovisno o rizi nim skupinama kojima pripadaju po meunarodnom prognosti kom indeksu (IPI) i revidiranom prognosti kom indeksu (R- IPI) za bolesnike lije ene po shemi R-CHOP RIZI NA GRUPAZBROJ BODOVAKR (%)5-godianji OS (%) Meunarodni prognosti ki indeks bolesnika svih dobnih skupina Niski rizik 0-1 87 73Srednj niski 2 67 51Srednje visoki 3 55 43Visoki 4-5 44 26Godinama prilagoen IPI za bolesnike d" 60 godina Niski rizik 0 92 83Srednj niski 1 78 69Srednje visoki 2 57 46Visoki 3 46 32Revidirani meunarodni prognosti ki indeks (r-ipi)RIZI NA GRUPAZBROJ BODOVA4-godianj PFS (%)4- godianji OS (%)Vrlo dobra 0 94 94Dobra 1-2 80 79Loaa 3-5 53 55 KR  kompletna remisija, OS  eng. overall survival (ukupno pre~ivljenje), PFS  progression free survival (pre~ivljenje bez progresije bolesti).  3.1.9. Lije enje DLBCL DLBCL je agresivni limfom te, ukoliko se ne lije i, medijan pre~ivljenja iznosi manje od 1 godine (Fisher RI et al, 2004). Algoritmi lije enja se razlikuju prema fazi bolesti, proairenosti, IPI i starosti bolesnika (Zelenetz AD et al, 2010). Za uspjeano lije enje je, osim antineoplasti nog lije enja, od velike va~nosti i potporno lije enje kojim se nastoje suzbiti komplikacije osnovne blesti, ali i nuspojave protutumorske terapije 3.1.9.1. Lije enje novootkrivenog DLBCL Standardna prva linija kemoterapije je CHOP (ciklofosfamid, doksorubicin, vinkristin, prednizon). U pojedinim zemljama uobi ajene su ina ice CHOPa (npr. u Njema koj CHOEP, u Francuskoj ACVBP itd), ali nema konsenzusa o tome da je bilo koji od ovih protokola uistinu bolji. Dodatak rituksimaba, kimeri nog protu-CD20 monoklonskog protutijela CHOPu ili ina icama zna ajno poveava odgovor, vrijeme bez progresije bolesti (eng. progression free survival, PFS) i ukupno pre~ivljenje (eng. overall survival, OS) bolesnika s DLBCL i to bez zna ajnijeg poveanja toksi nosti terapije. Uloga zra enja nije tako dobro definirana. ini se da zra enje zahvaenog polja s 30-36 Gy u bolesnika s inicijalno velikom tumorskom masom ili u parcijalnoj remisiji nakon lije enja poboljaava u najmanju ruku PFS, a mogue i OS. Bolesnici u stadiju I bez nepovoljnih prognosti kih imbenika imaju izvrsnu prognozu. S 3 ciklusa CHOPa i zra enjem zahvaenog polja, izlije enje se posti~e u preko 90% slu ajeva. Preko 80% bolesnika bez nepovoljnih prognosti kih imbenika mo~e se izlije iti sa 6 ciklusa CHOPa i 8 ciklusa rituksimaba. Uz 8 R-CHOP ciklusa mo~e se izlije iti oko 60% DLBCL srednjeg rizika. Nema konsenzusa o optimalnom lije enju visoko rizi nih mlaih bolesnika, R-CHOPom se izlije i manje od 50% takvih (Aurer I et al, 2007). 3.1.9.2. Relapsirajui / refraktorni DLBCL Unato  velikom napretku u lije enju DCBLC postignutom dodatkom rituksimaba standardnoj terapiji, oko 40% bolesnika je refraktorno na lije enje ili do~ivljava relaps nakon zavraene terapije. Relaps se naj eae dogaa unutar 2-3 godine od dijagnoze, no mo~e se javiti i nakon 5 ili viae godina. Bolesnicima iji CT ili PET/CT nalaz upuuje na relaps bolesti, treba u initi istu obradu kao i kod novootkrivene bolesti uklju ujui, ako je mogue, biopsiju suspektne mase. Biopsiju je dobro napraviti jer neke druge bolesti poput sarkoidoze, infekcija te karcinoma mogu na nekoj od slikovnih metoda dati isti nalaz kao DLBCL. Bolesnici, koji nisu izlije eni prvom linijom, mogu se podijeliti na primarno refraktorne, one u ranom relapsu i one u kasnom relapsu. Primarno refraktorni su bolesnici kod kojih se prvom linijom lije enja ne uspije postii remisija. Rani relaps nastupa unutar godinu dana od dijagnoze (ili unutar 6 mjeseci od zavraetka lije enja), a kasni nakon toga. Potonji imaju najbolju, a prvi naloaiju prognozu. Osnova lije enja DLBCL u relapsu je agresivna kemoterapija i, ukoliko je limfom kemosenzitivan, transplantacija autolognih mati nih krvotvornih stanica (ATKS). Uloga ATKS dokazana je u multicentri noj studiji poznatoj pod imenom PARMA (Philip T i sur, 1995). Studija je obuhvatila 215 bolesnika s relapsirajuim kemosenzitivnim DLBCL. Bolesnici su randomizirani u dvije skupine, jednu koja je primala kemoterapiju po shemi DHAP (deksametazon, cisplatina, citarabin) te drugu koja je nakon iste kemoterapije podvrgnuta ATKS. PFS i OS su zna ajno bili vei u DHAP + ATKS skupini nego u skupini lije enoj samo kemoterapijoma (46% i 53% vs 12% i 22%). Za drugu liniju lije enja koristi se nekoliko razli itih kemoterapijskih protokola. Naj eae su koriateni: DHAP, ICE (ifosfamid, karboplatina, etopozid), ESHAP (etopozid, cisplatina, citarabin, metilprednizolon) i miniBEAM (karmustin, etopozid, citarabin, melfalan). Svakom od navedenih protokola se mo~e dodati i rituksimab koji poboljaava ishod lije enja. Nema dokaza da je jedan protokol bolji od drugog. Jedina randomizirana studija nije naala razlike izmeu R-ICE i R-DHAP-a (Gisselbrecht C i sur, 2010). Prije upotrebe rituksimaba je na 2. liniju kemoterapije odgovaralo oko 50% bolesnika. Oko polovice njih se moglo izlije iti autotransplantacijom. U onih koji su u 1. liniji lije eni rituksomabom se sli ni rezultati mogu postii samo u bolesnika s kasnim relapsom. Prognoza onih s ranim relapsom je loaija, dok rijetko koji refraktorni bolesnik odgovori na 2. liniju lije enja. Bolesnici koji ne reagiraju na drugu liniju kemoterapije ili uu u relaps nakon autotransplatacije na raspolaganju ostaje alotransplatacija od HLA identi nog srodnog davatelja, radioimunoterapija i palijativni postupci. Otprilike 30% alotransplatiranih bolesnika bude izlje eno. Na radioimunoterapiju odgovori 30% bolesnika ali je trajanje remisije kratko (Aurer I et al, 2007). 3.2. Rituksimab Rituksimab je kimeri no IgG1 monoklonsko protutijelo usmjereno protiv CD20 antigena. Graen je od ljudske konstantne regije i miaije varijabilne regije. Antigen CD20 izra~en je na povraini stanica B-limfocitne loze svih stupnjeva diferencijacije, osim nezrelih limfoblasta i plazma stanica (Aurer I et al, 2007). Osim na normalnim stanicama B-limfocitne loze, molekula CD20 nalazi se i na viae od 90% B-limfocitnih zloudnih novotvorina (Jakai B et al, 2008). FDA (Food and Drug Administration, dio vlade SAD odgovoran za odobravanje lijekova) je 1997. odobrila upotrebu rituksimaba za lije enje CD20+ folikularnog limfoma refraktornog ili u relapsu (Scott SD, 1998). Uskoro potom je lijek odobren i u drugim zemljama, prvo za tu, a onda i za druge indikacije, prvenstveno DLBCL. Rituksimab se danas, osim za lije enje B-stani nih limfoma, koristi i u lije enju nekih autoimunih bolesti poput reumatoidnog artritisa i sistemskog lupusa (Jakai B et al, 2008). Rituksimab smanjuje broj CD20 pozitivnih stanica i to razli itim mehanizmima: citotoksi noau ovisnom o protutijelima (ADCC), citotoksi noau posredovanom komplementom (CDC), indukcijom programirane stani ne smrti, poja avanjem kemosenzitivnosti i radiosenzitivnosti tumorskih stanica. Osim navedenog, kao mogui mehanizam djelovanja navodi se i pasivna imunizacija (Lim SH et al, 2010). 3.2.1. Mehanizmi djelovanja rituksimaba Citotoksi nost ovisna o komplementu (CDC) Viae studija je pokazalo da rituksimab izaziva lizu razli itih stanica B-stani ne loze, kako normalnih, tako i malignih. CDC potaknuta rituksimabom je dokazana u pokusima  in vitro i  in vivo na ~ivotinjskim modelima. Istra~ivanja su pokazala da se kaskada aktivacije komplementa potaknuta rituksimabom dogaa i u ekstravaskularnim prostorima npr. u ascitesu i pleuralnoj tekuini. Dakako, u navedenim prostorima je manja koncentracija komponenti komplementa nego u serumu, ali dovoljna za protutumorsku aktivnost rituksimaba. Neke tumorske stanice, poput onih kod KLL, izra~avaju na svojoj povraini CD55 i CD59, molekule koje inhibiraju djelovanje komplementa. Blokadom navedenih molekula mo~e se poja ati osjetljivost na CDC. Bitno je napomenuti kako svi tumori B-stani ne loze ne eksprimiraju CD20 u istoj koli ini na svojoj stani noj povraini. Upravo o stupnju ekspresije CD20 ovisi CDC potaknuta rituskimabom. Tako su na CDC najosjetljivije stanice folikularnog limfoma (FL), slijede stanice DLBCL-a te stanice KLL-a koje najmanje izra~avaju CD20 te su time i najmanje osjetljive na CDC. Programirana stani na smrt Pokazalo se da rituksimab mo~e vezanjem na CD20 potaknuti unutarstani ne puteve koji dovode do apoptoze. Apoptoza se tada najvjerojatnije dogaa mitohondrijskim putem koji zavraava aktivacijom kaspaze-9 i efektorske kaspaze-3. Citotoksi nost ovisna o protutijelima (ADCC) Interakcija Fc fragmenta gamaglobulina i molekule FcR igra va~nu ulogu u lije enju protu-CD20 imunoterapijom. Molekula FcR nalazi se na povraini monocita, makrofaga, NK-stanica i neutrofila pa se te stanice mogu aktivirati nakon Fc:FcR interakcije. Do sada je otkriveno osam FcR molekula. Aktivacijom navedenih stanica dolazi do otpuatanja upalnih medijatora i/ili direktne fagocitoze opsoniziranih stanica ato se naziva ADCC (Weiner GJ, 2010). 3.3. Rituksimab u lije enju relapsirajuih/refraktornih DLBCL Unato  velikom napretku u lije enju, oko 40% bolesnika s DLBCL je i dalje primarno refraktorno ili do~ivljava relaps nakon zavraenog lije enja (Jonathan W. Friedberg 2011). Obzirom da se rituksimab mo~e kombinirati s kemoterapijom, pokuaava ga se koristiti i u ovih bolesnika. Dodatak rituksimaba drugoj liniji kemoterapije ispitivan je u viae studija. Jedna od prvih je ona Kewalramanija i sur koji su 2004. godine objavili rezultate skupine lije ene R-ICEom (n=36) i usporedili je s rezultatima povijesne kontrolne skupine lije ene ICE protokolom (n=147). Dodatak rituksimaba ICE-u je gotovo udvostru io KR (53% vs 27%). R-ICE se pokazao osobito u inkovitim za DLBCL u relapsu. U toj skupini je 65% bolesnika lije enih R-ICEom i 34% onih lije enih ICEom postiglo KR. Studija je pokazala i da bolesnici u R-ICE skupini s umjereno-visokim rizikom prema IPI imaju identi an postotak kompletnih remisija (53%) kao i bolesnici s niskim ili umjereno-niskim rizikom. Rezultat govori u prilog tomu da dodatak rituksimaba ICE protokolu mo~e  poniatiti negativne prognosti ke parametre unutar IPI. Bolesnici koji su povoljno odgovorili su potom autotransplantirani. PFS bolesnika koji su podvrgnuti autotransplataciji nakon R-ICE protokola bio je neato vei u odnosu na one koji su primili ICE (24% vs 43% u dvije godine praenja), no ta razlika nije bila statisti ki zna ajna. Dodatak rituksimaba nije imao zna ajne ne~eljene u inke, naprotiv bolesnici koji su primili rituksimab uz ICE imali su manji postotak febrilnih neutropenija (Kewalramani T et al, 2004). Nakon ovoga je objavljeno joa nekoliko istra~ivanja 2. faze sa sli nim rezultatima. Povoljan u inak rituksimaba u lije enju relapsirajuih/refraktornih limfoma dokazan je i u jednoj randomiziranoj studiji. Vellenga E et al su u multicentri noj randomiziranoj studiji istra~ili ulogu rituksimaba u drugoj liniji lije enja oboljelih od CD20+ DLBCLa. Bolesnici su randomizirani u skupinu koja je primala DHAP (cisplatina. citarabin, deksametazon) i VIM (etopozid, ifosfamid, metotreksat) protokol (n=112) i skupinu koja je uz to dobivala i rituksimab u standardnim dozama od 375mg/m2 (n=113) po ciklusu. Bolesnici koji su postigli najmanje PR su autotransplantirani. Na terapiju je odgovorilo 75% bolesnika koji su primali rituksimab i 54% onih lije enih samo kemoterapijom. ATKS je provedena u 46% bolesnika iz skupine lije ene samo kemoterapijom i 63% onih lije enih i rituksimabom. Medijan praenja bolesnika nakon ATKS je iznosio 31 mj (9-67). Nakon 2 godine je PFS u skupini koja je primala rituksimab bio 52%, a u skupini lije enoj samo kemoterapijom 31%, a OS 59% naprema 52%. Razlika u PFS je bila statisti ki zna jna, a u OS ne (Vellenga E et al, 2008). Iako bi se na temelju iznesenog moglo zaklju iti da je uloga rituksimaba u 2. liniji lije enja DLBCL nedvojena, treba imati na umu da su u obje studije uklju eni uglavnom bolesnici koji u 1. liniji nisu dobili rituksimab. Kao ato je ve ranije navedeno, rezultati 2. linije lije enja bolesnika koji su u 1. liniji lije enja dobivali rituksimab su zna ajno slabiji. Najvee randomizirano istra~ivanje (CORAL) u kojem su usporeeni R-ICE i R-DHAP je pokazalo da svega oko 50% bolesnika prethodno lije enih rituksimabom odgovore na 2. liniju lije enja te da je PFS nakon 3 godine tih bolesnika oko 20% (Gisselbrecht C et al, 2010). Nema studije koja bi usporeivala lije enje bolesnika s refraktornim ili relapsirajuim DLBCL s i bez rituksimaba u bolesnika koji su ve ranije primali rituksimab. 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Stoga ga ne dobivaju svi bolesnici s DLBCL u relapsu. Odlu ili smo analizirati naae rezultate lije enja bolesnika s DLBCL ICE kemoterapijom s i bez dodatka rituksimaba kako bismo pokuaali ustanoviti njegovu ulogu u ovoj indikaciji. 4. HIPOTEZA Dodatak rituksimaba kemoterapiju poboljaava ishod lije enja bolesnika s rezistentnim ili relapsirajuim B-velikostani nim limfomom bez zna ajnijeg poveanja toski nosti. 5. CILJEVI Cilj ovog rada bio je utvrditi rezultate dodavanja rituksimaba ICE protokolu u lije enju rezistentnih i relapsirajuih difuznih B-velikostani nih limfoma. Analizirali smo utjecaj rituksimaba na postizanje odgovora na lije enje, OS i EFS. Osim navedenog, cilj rada bio je pokazati kako lije enje rituksimabom u ovoj indikaciji ne pridonosi veoj toksi nosti terapije. 6. BOLESNICI I METODE 6.1. Dizajn istra~ivanja Ovo istra~ivanje temelji se na retrospektivnom pregledu i analizi podataka iz povijesti bolesti pacijenata lije enih pod dijagnozom refraktornog ili relapsirajueg difuznog B-velikostani nog limfoma. Istra~ivanje je provedeno u Zavodu za hematologiju Klinike za unutarnje bolesti Klini kog bolni kog centra Zagreb. 6.2. Bolesnici U istra~ivanje su uklju eni bolesnici oboljeli od refraktornog/relapsirajueg DLBCL lije eni kemoterapijskim protokolom ICE na Zavodu za hematologiju KBC Zagreb (Moskowitz CH i sur, 1992). Jedna skupina bolesnika je lije ena samo kemoterapijom dok dok je druga uz to dobila i rituksimab. 6.3. Lije enje i procjena odgovora ICE se sastojao od etopozida 100 mg/m2 dnevno u infuziji od 1. do 3. dana, ifosfamida i uromiteksana 5 g/m2 u kontinuiranoj 24-satnoj infuziji 2. dan i karboplatine AUC 5 (ali ne viae od 800 mg) u infuziji 2. dan. Bolesnici su terapiju primali u bolnici, a 4. dan su, ako nije bilo komplikacija, otpuateni u kunu njegu. Bilo je planirano dati dva ciklusa u razmaku od 2-3 tjedna. Za profilaksu i lije enje mu nine i povraanja su koriateni antagonisti serotinina (obi no ondansetron ili granisetron) i deksametazon. Bolesnici su primali profilakti ke antibiotike, antifungike, filgrastim i transfuzije krvnih pripravaka kako je uobi ajeno. Odgovor je procjenjivan nakon 2 ciklusa terapije. Ako su terapiju zadovoljavajue podnijeli, a bolest je bila kemosenzitivna, dobili su 3. ciklus agresivne kemoterapije (s ili bez rituksimaba) nakon kojeg je pokuaano iz krvi prikupiti CD34+ stanice za autotransplantaciju. Bolesnici koji su nakon 3 ciklusa postigli najmanje PR su potom autotransplantirani nakon kondicioniranja BEAMom (karmustin, etopozid, citarabin, melfalan). Podru ja koja prije ATKS nisu bila u KR su, nakon oporavka od ATKS, ozra ena s 30-40 Gy. 6.4. Statisti ka analiza Promatrani ishodi su odgovor na lije enje, pre~ivljavanje bez dogaaja (EFS) te ukupno pre~ivljenje (OS). Ishodi su definirani prema uobi ajenim kriterijima (Cheson BD i sur, 1999). Kao povoljan odgovor na lije enje smatrali smo postizanje najmanje PR nakon 2 ciklusa ICE-a. U EFS analizi kao dogaaji su smatrani smrt, progresija bolesti i izostanak odgovora nakon 2 ciklusa terapije. Za usporedbu kategorijskih zna ajki bolesnika koristio se 2 test. Vrijeme bez dogaaja i pre~ivljenje bolesnika prikazano je Kaplan-Meierovom metodom. Za usporedbu pre~ivljenja izmeu pojedinih skupina koristio se log-rank test, a za multivarijatnu analizu Coxova regresijska analiza. 7. REZULTATI 7.1. Zna ajke bolesnika i bolesti Pregledom dostupne medicinske dokumentacije, u istra~ivanje je uklju eno 54 bolesnika oboljelih od DLBCL, 32 muakaraca i 22 ~ene. Prosje na dob bolesnika iznosila je 44 godine. Prosje no trajanje bolesti od dijagnoze do po etka terapije iznosilo je 17 mjeseci. 32 bolesnika lije eno je kemoterapijom po shemi ICE a 22 je uz navedeni protokol dobilo i rituksimab (R-ICE). Razlozi za po etak terapije su podjeljeni u 3 skupine: primarno refraktorna bolest, rani relaps i kasni relaps. U trenutku prikupljanja podataka je u skupini lije enoj ICEom bilo joa 10 ~ivih bolesnika, a u skupini lije enoj RICEom 9. Medijan praenja za sve bolesnike iznosio je 7 mjeseci a za ~ive 35 mjeseci. Izmeu ICE i RICE skupine nije bilo razlika u zna ajkama, osim u trajanju remisje u emu je RICE skupina bila nepovoljnija zbog veeg udjela bolesnika s primarno-refraktornom bolesti (p=0,009, 2 test). Zna ajke svih 54 bolesnika kao i karakteristike bolesti prikazane su u tablici 4. TABLICA 4 Zna ajke bolesnika ICE (n=32)RICE (n=22)UKUPNO (n=54)Dob u vrijeme primanja terapije raspon medijan 26-63 42 23-65 45 23-65 44Spol m ~ 18 14 14 8 32 22Status bolesti refraktoran rani relaps kasni relaps 9 12 11 15 2 5 24 14 16Stadij pri po etku protokola I-II III-IV 12 20 6 16 18 36IPI pri po etku protokola 0-1 2 3 4 11 9 9 3 8 4 4 6 19 13 13 9Ranije lije eni rituksimabom da ne 16 16 10 12 26 28Trajanje bolesti do po etka primanja protokola (mj.) raspon medijan 4-83 12  1-60 12 1-83 12 7.2. Odgovor na terapiju Kemoterapijom po shemi ICE postignuta je kompletna remisija (KR) u 1 pacijenta (3%) parcijalna remisija (PR) u 8 (23%), a 23 ih nije odgovorilo na terapiju (74%). Ukupan odgovor na terapiju iznosi 26%. U skupini bolesnika koja je primala uz navedeni protokol i rituksimab (R-ICE), ukupan odgovor na terapiju iznosi 54% (27% KR i 27% PR). Na terapiju nije odreagiralo 10 bolesnika (45%). Skupina lije ena RICEom je bolje odgovorila na terapiju (p=0,05, 2 test). Ovi rezultati su prikazani na slici 1.  EMBED Excel.Chart.8 \s   EMBED Excel.Chart.8 \s  Slika 1. Grafi ki prikaz ishoda terapije Nakon medijana praenja od 35 mjeseci za ~ivue pacijente, ukupno pre~ivljenje (OS) u RICE vs. ICE skupinama iznosi 40% vs. 20%. Vrijeme pre~ivljavanja bez dogaaja (EFS) u RICE skupini iznosi 32% dok u ICE skupini iznosi 15%. OS i EFS prikazani su slici br.2.  OS mjeseci EFS mjeseci Slika 2. Grafi ki prikaz ukupnog pre~ivljenja (OS) i pre~ivljenja bez dogaaja (EFS) Ispitan je utjecaj ranijeg lije enja rituksimabom na OS i EFS. OS kod bolesnika koji su ranije primali rituksimab iznosi 18%, a bolesnika koji nisu 44%. EFS je u ranije lije enih rituksimabom 6%, a 35% u bolesnika koji nisu ranije primali rituksimab. Rezultati su prikazani na slici br. 3. OS  mjeseci EFS mjeseci Slika 3. Grafi ki prikaz utjecaja ranijeg lije enja rituksimabom na OS i EFS Utjecaj trajanja remisije (refraktorna bolest vs. rani relaps vs. kasni relaps) na OS i EFS prikazan je na slici br. 4. OS  mjeseci EFS mjeseci Slika 4. Grafi ki prikaz utjecaja trajanja remisije na OS i EFS Poznato je da je IPI prognosti ki imbenik u ishodu lije enja limfoma, kako kod novodijagnosticiranih, tako i kod limfoma relapsu. Ispitao sam i utjecaj IPIa na ukupno pre~ivljenje (OS) i pre~ivljavanje bez dogaaja (EFS). Bolesnici su grupirani u dvije skupine, jednu iji IPI iznosi od 0-2, i drugu gdje IPI iznosi 3-4. Slika br. 5 prikazuje utjecaj IPIa na promatrane ishode. OS  mjeseci EFS mjeseci Slika 5. Grafi ki prikaz utjecaja IPIa na OS i EFS Analizirao sam i utjecaj davanja RICEa u odnosu na trajanje remsije posebno za skupinu prethodno lije enu i nelije enu rituksimabom. Prema analizi, mogue je da dodatak RICEa koristi svim bolesnicima prethodno nelije enim rituksimabom, a onima koji su lije eni ranije rituksimabom samo ako se radi o kasnom relapsu. Razlike, meutim zbog malog broja bolesnika nisu statisti ki zna ajne. Navedeni rezultati su prikazani na slici br. 6 OS mjeseci Bolesnici refraktorni ili u ranom relapsu koji su ranije dobivali rituksimab OS mjeseci Bolesnici refraktorni ili u ranom relapsu koji nisu ranije dobivali rituksimab OS mjeseci Bolesnici u kasnom relapsu koji su ranije primali rituksimab OS mjeseci Bolesnici u kasnom relapsu koji nisu ranije primali rituksimab Slika 6. Utjecaj davanja RICEa u odnosu na trajanje remisije kod bolesnika koji su prethodno primali, odnosno nisu primali rituksimab U multivarijantnoj analizi za OS, sva etiri imbenika koja smo ispitali su statisti ki zna ajna. Statisti ka zna ajnost prikazana je u tablici br. 5. TABLICA 5 Rezultati multivarijantne analize za OS imbenikStatisti ka zna ajnostRanije lije eni rituksimabom0,036Refraktorni/rani relaps/kasni relaps0,017IPI 0,01ICE vs. RICE0,031 7.3. Prikupljanje transplantata Bolesnici koji postignu KR ili najmanje PR mogu se podvrgnuti autolognoj transplantaciji mati nih stanica. U skupini koja je primala RICE kod 11 bolesnika je prikupljanje mati nih stanica bilo uspjeano, jedan pacijent nije prikupio dovoljno. U ICE skupini 7 bolesnika je prikupilo dovoljno mati nih stanica, a jedan nije. 7.4. Nehematoloake nuspojave i toksi nost terapije U skupini koja je primala protokol ICE, 42% bolesnika je imalo neku infekciju kao nuspojavu lije enja. U RICE skupini je u estalost infekcija bila 47%. Za 6 bolesnika u ICE i 3 bolesnika u RICE skupini nemamo podatke o infektivnim nuspojavama. U obje skupine je zabilje~en velik broj teakih mukozitisa. Zabilje~ene su po jedna tromboembolija i sr ana aritmija u svakoj skupini. Evidentiran je i slu aj perforacije duodenuma u ICE skupini te pleuralni izljev u RICE skupini. 7.5. Uzroci smrti U ICE skupini vodei uzrok smrti je bila osnovna bolest. Na drugom mijestu su infekcije kao komplikacija lije enja. U RICE skupini je osnovna bolest takoer bila glavni uzrok smrti. U ICE skupini jedan je pacijent umro mjesec dana nakon primanja terapije, a u RICE su 2 pacijenta umrla u navedenom vremenskom razdoblju od posljedica lije enja. 8. RASPRAVA Ovo istra~ivanje u injeno je na uzorku od 54 bolesnika lije enih u Klini kom bolni kom centru Zagreb pod dijagnozom difuznog B-velikostani nog limfoma u relapsu ili primarno refraktornim na terapiju. U uvodu je spomenuto da je medijan pojavljivanja ove bolesti u dobi od 65 godina (Friedberg JW, 2008). Medijan pojave bolesti kod bolesnika uklju enih u ovo istra~ivanju je u dobi od 42 godine. Usporedimo li navedene medijane pojave limfoma, mogli bi smo rei da smo u istra~ivanje imali uklju enu relativno mlau populaciju te da medijan kod naaih bolesnika ne odgovara stvarnom stanju u populaciji. To se mo~e objasniti injenicom da su ICE dobivali bolesnici koji su kandidati za ATKS, dakle stariji bolesnici koji zbog dobi ne mogu podnijeti agresivno lije enje, nisu ovu terapiju niti dobivali. Ukupni odgovor na terapiju po shemi RICE iznosi 54%, od toga kompletna remisija (KR) iznosi 27%. Ukupni odgovor na terapiju u ICE skupini iznosi 26% s 3% kompletnih remisija (KR). Naai rezultati su usporedivi s rezultatima CORAL studije (Gisselbrecht C et al. 2009) gdje je na RICE ili RDHAP odgovorili 63% bolesnika. Postotak kompletnih remisija je takoer usporediv (27% vs. 24%) s rezultatima navedene studije. Kewalramani T et al. (Kewalramani T et al. 2004) su usporedili RICE (n=36) i ICE (n=147) protokol u svojoj studiji 2004. godine. Medijan dobi pojave bolesti u navedenoj studiji je prili no blizak medijanu u ovom radu te je iznosio 45 za RICE skupinu i 48 godina za ICE skupinu. Ukupan odgovor na terapiju u RICE skupini iznosio je 78% s 53% kompletnih remisija. Odgovor na terapiju u ICE skupini je iznosio 71% s 27 kompletnih remisija. Ako usporedimo odgovor na terapiju RICEom u navedenoj studiji s rezultatima u ovom radu, naa rezultat od 54% je vidno manji. Slabiji postotak odgovora mo~emo protuma iti time ato je u naaoj RICE skupini bilo dvostruko viae primarno refraktornih bolesnika ato je negativan prognosti ki imbenik odgovora na terapiju. To je vjerojatno posljedica selekcije bolesnika. Faktori iji smo utjecaj na OS ispitali bili su: ICE vs. RICE, ranije lije enje rituksimabom, IPI i duljina trajanja prve remisije. Prema naaim analizama sva etiri faktora su imala statisti ki zn ajan utjecaj na OS. Naaa analiza meutim sugerira da dodatak rituksimaba ICE protokolu poboljaava OS i EFS u onih bolesnika koji ranije nisu primali rituksimab. Bolesnici koji su ranije dobivali rituksimab, a eventualno bi mogli imati koristi od RICE protokola su oni u kasnom relapsu. Meutim, zbog malog broja bolesnika koji ovaj rad obuhvaa, potrebna su daljnja istra~ivanja u smislu primjene rituksimaba u kasnim relapsima kod bolesnika koji su ranije lije eni CD20 monoklonskim antitijelom. Iz rezultata je vidljivo kako bolesnici s primarno refraktornom bolesti imaju najloaiji OS i EFS dok oni u kasnom relapsu imaju vidno bolje prosje no pre~ivljenje i vrijeme bez dogaaja. Takoer je vidljivo da bolesnici s ija je vrijednosi IPIa viaa od 2 imaju loaiji OS i EFS. Navedena zapa~anja se uklapaju u saznanja iz literature. Iz navedenog proizlazi da bolesnici u kasnom relapsu koji nisu primali rituksimab ranije imaju najveu korist od dodatka rituksimaba. ini se da rituksimab koristi i onima u kasnom relapsu iako su ranije bili lije eni rituksimabom. Da je rituksimab koristan u lije enju pacijenata u kasnom relapsu pokazali su i Kewalramani T i sur. u svojoj studiji. Jedan od ciljeva ovoga rada bio je i pokazati kako dodatak rituksimaba ICEu ne pridonosi zna ajnijoj toksi nosti terapije. Kako je navedeno, glavni uzrok smrti u obje skupine je bila osnovna bolest, infekcije su na drugom mjestu. Jedan bolesnik je umro mjesec dana nakon primanja ICEa a dva nakon RICEa. Iz navedenog je vidljivo da dodatak rituksimaba ne poveava toksi nost terapije ato se uklapa i u opa~anja iz ranije spomenutog istra~ivanja koje su proveli Kewalramani T i sur. Dodavanje rituksimaba ICEu nije imalo negativnog utjecaja na uspjeanost prikupljanja mati nih stanica za autolognu transplantaciju. Ograni enja ovog istra~ivanja mo~emo pronai u injenici da se radi o retrospektivnom istra~ivanju i to na malom uzorku (n=54). Potrebna su daljnja istra~ivanja o uporabi rituksimaba u lije enju relapsirajuih i refraktornih DLBCL u koje bi se uklju io vei broj bolesnika kako bi dobili relevantnije podatke. 9. ZAKLJU CI Dodatak rituksimaba ICE kemoterapiji (ifosfamid, karboplatina, etopozid) u lije enju refraktornih i relapsirajuih DLBCL poboljaava ukupnu u estalost odgovora na lije enje Bolesnici ranije lije eni rituksimabom imaju manji OS i EFS od bolesnika koji nisu lije eni rituksimabom u prvoj liniji Bolesnici s primarno refraktornom bolesti imaju najloaiju a oni s kasnim relapsom najbolju prognozu nakon zavraenog lije enja Visok IPI je negativan prognosti ki imbenik ishoda u lije enju refraktornih i relapsirajuih limfoma Dodatak rituksimaba ICEu poboljaava OS u bolesnika s refraktonrim i relapsirajuim DLBCL Dodatak rituksimaba ne poveava toksi nost terapije i ne smanjuje uspjeanost prikupljanja autotransplantata ini se da rituksimab povoljno djeluje na ishod lije enja bolesnika koji nisu ranije primali rituksimab te onih u kasnom relapsu koji su ranije primali rituksimab Ishod lije enja bolesnika koji su ve primali rituksimab i refraktorni su ili u ranom relapsu je vrlo loa. Ovi bolesnici su stoga kandidati za nove metode lije enja. 10. ZAHVALE Zahvaljujem mentoru prof. dr. sc Igoru Aureru na predlo~enoj temi, stru noj pomoi, savjetima i strpljivosti tijekom izrade diplomskog rada. Hvala prijateljici i kolegici Tei Lovri na tehni koj pomoi u izradi ovog rada. Najveu zahvalu upuujem svojim roditeljima, Anelu i Dragici. Hvala Vam na bezuvjetnoj potpori i podraci tokom mog akolovanja. 11. LITERATURA Aurer I, Radman I, Serti D, Mikuli M, Labar B (2007) Zloudni tumori limfocita. U: Labar B, Hauptmann E, Hematologija, Zagreb: `kolska knjiga, 234-300.  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(2010) NCCN clinical practice guidelines in oncology: non-Hodgin lymphomas. J Natl Compar Canc Netw 8:288-334. 12. }IVOTOPIS Roen sam u Zadru 21. studenog 1987. godine. Osnovnu akolu i srednju Medicinsku akolu Ante Kuzmania pohaao sam u Zadru. Nakon polo~ene mature, 2006. godine upisao sam Medicinski fakultet Sveu iliata u Rijeci te sam se nakon zavraene prve godine studija prebacio na Medicinski fakultet Sveu iliata u Zagrebu      PAGE \* MERGEFORMAT 40 p= 0,359 p= 0,132 p= 0,029 p= 0,010 p= 0,04 p= 0,042 p= 0,000 p= 0,07 p= 0,821 p= 0,821 p= 0,087 p= 0,087 |~ $da$gdmdgdm $da$gdH7&( <FƷ}q}bTh+CJOJQJ^JaJh4hH7B*OJQJphhTB*OJQJphh4h4B*OJQJph h+h+hmB*OJQJphh+B*OJQJphhH7B*OJQJphhmhmB*OJQJphhmCJOJQJ^JaJhTCJOJQJ^JaJhH7CJOJQJ^JaJhmhH7B*OJQJph NPRNZlngd1dhgd1dhgd+dhgd+ $da$gd4dgd4 $da$gdmgd+dgdmdgdm $da$gdH7 j:>$LNPRT(*`XZ\ָււtg\han6mHnHsH h(h1mHnHsH hanCJOJQJ^JaJh1CJH*OJQJ^JaJh1h+ h+h+h1B*OJQJphhanB*OJQJphh1h1B*OJQJphh16CJOJQJ^JaJh1CJOJQJ^JaJhTCJOJQJ^JaJhH7CJOJQJ^JaJ\jjln&(*.6~йph\N\h;hH7CJH*\aJh;hH7CJ\aJh;hH7\han6CJOJQJ^JaJhH7CJOJQJ^JaJh+CJOJQJ^JaJhihH7B*OJQJphhihiB*OJQJph,h1h1CJOJQJ^JaJmHnHsH  hanh1CJOJQJ^JaJhanCJOJQJ^JaJ hanhanCJOJQJ^JaJnVXB $da$gdH7 $da$gd7dgd7dgd7gd+dgd7$d`a$gdan $da$gdiGdgdiTVX.  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