Abstract
Simple SummaryCeliac disease (CeD) is an multiorgan autoimmune disease precipitated by the ingestion of gluten in genetically predisposed individuals. After the initiation of a gluten-free diet, CeD generally has a benign course, with the complete remission of symptoms and a normal life expectancy; however, robust evidence suggests that subjects with CeD are at increased risk of developing malignancies compared to the general population. Peculiar associations with lymphomas, including enteropathy-associated T-cell lymphoma (EATL), and small bowel carcinoma (SBC), as well as correlations with other cancers, have been thoroughly investigated. In this review, we will examine the risk of developing malignancies in patients with CeD, as well as clinical aspects of and therapeutic options for EATL and SBC.Celiac disease (CeD) is an immune-mediated enteropathy precipitated by ingestion of gluten in genetically predisposed individuals. Considering that CeD affects approximately 1% of the Western population, it may be considered a global health problem. In the large majority of cases, CeD has a benign course, characterized by the complete resolution of symptoms and a normal life expectancy after the beginning of a gluten-free-diet (GFD); however, an increased risk of developing malignancies, such as lymphomas and small bowel carcinoma (SBC), has been reported. In particular, enteropathy-associated T-cell lymphoma (EATL), a peculiar type of T-cell lymphoma, is characteristically associated with CeD. Moreover, the possible association between CeD and several other malignancies has been also investigated in a considerable number of studies. In this paper, we aim to provide a comprehensive review of the current knowledge about the associations between CeD and cancer, focusing in particular on EATL and SBC, two rare but aggressive malignancies.
Highlights
Celiac disease (CeD) is an immune-mediated disease precipitated by the ingestion of gluten in genetically predisposed individuals [1]
In contrast to the increase in awareness of the pathogenesis of CeD that occurred in the last decade, as well as the reduction of the diagnostic delay, we still have poor knowledge of the risk factors that may contribute to the development of CD-associated neoplasms
Based on the available literature, we can report that CeD patients have a modestly increased risk of developing lymphomas, in particular the characteristic enteropathy-associated T-cell lymphoma (EATL), as well as small bowel carcinoma (SBC), as compared to the general population
Summary
Celiac disease (CeD) is an immune-mediated disease precipitated by the ingestion of gluten in genetically predisposed individuals [1]. Considering that many patients remain undiagnosed for many years before being correctly diagnosed and receiving an appropriate treatment, the exact prevalence of CeD is unknown [2]. According to recently published data, the worldwide serological and histological prevalence rates of CeD are 1.4% and 0.7%, respectively [3]. The prevalence is higher in females compared to males and in children compared to adults. The clinical spectrum of CeD is highly variable, from asymptomatic to severe malabsorptive form [2]. A strict lifelong gluten-free diet (GFD) is the only proven, asymptomatic to severe malabsorptive form [2]. A strict lifelong gluten-free diet (GFD) is the only proven, globally accepted treatment for CeD; since it can negatively imgploabcatlolynaqcuceaplitteydotfrleiafetm, tehnetcfoomr CpeliDan; cheowiseovfeter,nsdinifcfeiciut lctatnonmegaiantitvaeinly[4im,5p].act on quality of life,Tthhee cgoremapt lmiaanjcoeriitsyooftfenpadtiifefinctuslrtetsopmonadinttaoina [G4,F5D]. S-IoIm) aenpdruenlceeorpatliavsetijcejcuonnodiilteiiotinss(,UsuJIc),haasswreeflrlaacstoseryveCraelD tytpyepse o1famndaltiygpnean2c(iResC, Dm-aI yancdomRCplDic-aItIe) atnhde udlicseeraasteivceoujerjsuen.oAilmeitoins g(UtJhIe),ma,s nwoenll-Hasosdegvkeirnal lytmyppehsoomf ams a(NligHnLa)n,ciinecsl,umdianygctohme pchliacraatcetethriestdiciseenatseerocpouatrhsye.-aAssmocoinagtedthTem-ce, lnl olynm-Hpohdogmkain (ElyAmTLp)hoamndasth(Ne HsmLa),llinbcolwudeilncgartchienochmaara(cStBerCis),tihcaevnetebreoepnatthyyp-iacsaslolyciaastesodcTia-cteedll wlyimthphCoemDa [1(,E7A].TInL)CaenDd pthaetisemntasl,lmboowrteallictayrcfrinomomaall(cSaBuCs)e,shsaeveembseeton btyep2ic-faolllyd ahsisgohceiartceodmwpiathreCdetDo [t1h,e7]. gatfchohsewpIeoccesnanovnouoiremitaCpcasdhlrvyiuceapeaamtmDillnlteniaieclrcapptpadeiailosbhoaiptrgtwpltinoeaienincugemriga[ttnealm8hinaavrctC–tstdsauimi1,eddloil(2imnDaeaangi]sgrnml,.noeic[gatraao8ohetnnnsa–nneedacrl1gsiaeni2teagsly[tt]ys8sha,drofm–creeraic1odomlspni0emeimahdn,vat1Epiogasa3oAaemlnl]nitls;cTthractba[Lceehas8teol)uiu–teannw(sas1vsgate,n0saermswo,Cdine1bscnote3eeSuina]DeCacBt;tgmiio.ieCtmoohnDsn,ntutehtwrdastoibeon,bhtbmewduoittechwtcechi2iaoEose-ananfmAeioircmnnelTpetdcorerLCtredhhre)ehtieiashDtgeaksoicnhesn.hacseddWaniorivnrmddceeacSoelwrcpcBymaetareCitarenlphrels,hciaevfsreerodiwtiernecsidcwkushrdiimsitvesicotsikaehhanttl.aelhyhpisWageasarrvrnogereeiaatvcseiiwnkincilateaucehtiwbiirlleesealaldesrl
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