CELIJAČNA BOLEST KOD DECe: SAVREMENI DIJAGNOSTIČKI PRISTUP
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1 PREGLEDI LITERATURE BIBLID: , 136(2008) Suppl 2, p CELIJAČNA BOLEST KOD DECe: SAVREMENI DIJAGNOSTIČKI PRISTUP Nedeqko RADLOVIĆ Univerzitetska dečja klinika, Beograd KRATAK SADRŽAJ C e l i j ačn a b ol e s t j e n as l e dn i p or em eć aj p o d n o š e w a gl u t e n a, o d n o s n o gl i j a d i n a i s r o d n i h p r o l a m i n a p š e n i c e, ra ži i ječ ma. Pri mar no se ja vqa kod pri pad ni ka be le ra se (1: ), dok je kod qu di dru gih ra sa znat no re đa ili iz u zet no ret ka. Po seb no je če sta kod bli skih srod ni ka obo le lih, oso ba s uro đe nim ne do stat kom imu no glo bu li na A (IgA) i bo le sni ka s auto i mu nim i ne kim hro mo zom skim obo qe wi ma. Osno vu bo le sti i kquč ni na laz u we noj di jag nosti ci čini zapaqewe sluznice tankog creva, ko je iš če za va na di je ti bez glu te na. Po red en te ro pa ti je, kli nič ki ma ni fest ne ili nemanifestne, česte su i promene na dru gim or ga ni ma i si ste mi ma. Di jag no za ma ni fest nog ob li ka bo le sti se zasniva na tipičnom patohistološkom na la zu pri pre gle du slu zni ce tan kog cre va kod bo le sni ka na stan d a r d n oj i sh r an i i w eg ov o m k l in ičko m o p or a vk u n a d i j e t i b e z gl u t e n a. Z a p o t v r d u n e m a n i f e s t n o g o b l i k a b o l e s t i, me đu tim, neo phod na je i kon trolna en terobi op si ja, ko jom se do ka zu je nor ma li za ci ja iz gle da slu zni ce tan kog cre va na eli mi na ci o noj di je ti. Kod de ce s glu tenskom en te ro pa ti jom di jag no sti ko va nom to kom pr ve dve go di ne po rođe wu, kao i u slučajevima gde uzorci sluznice pri pr voj en te ro bi op si ji ni su ima li ti pi čan iz gled ili su bi li ne a de kvatni za pouzdano tumačewe, konačna dijag no za se za sni va na bi op sij skom na la zu to kom pro vo ka ci je pod no še wa glu tena. Pošto može da ugrozi kvalitet stal nih zu ba, ovaj po stu pak se ne pre po ru ču je pre na vr še ne še ste go di n e, a z b o g n ež eq en i h e f ek at a n a r a s t i r a zv oj d e t e t a, n i t o ko m p u b e r t e t a. Te s t o v i n a se r o l o š ke p o k a z a t e q e b o l e s t i, zbog nepotpune osetqivosti i specifičnosti, ne ma ju di jag no stič ku vred nost. Otu da se pri mar no ko ri ste u ot kri va wu asimptomatskih i netipičnih oblika celi jač ne bo le sti, kao i u pro ce ni do sled no sti eli mi na ci o ne di je te ka da je bolest već potvrđena. Pored toga, primena ovih te sto va olak ša va do no še we od lu ke za pa to hi sto lo ški pre gled sluznice tankog creva kod bolesnika na pro vo ka ci ji pod no še wa glu te na i da je pot pu ni ji uvid u re mi si ju bo le sti to kom po čet ne fa ze le če wa. Kqučne reči: celijačna bolest; gluten; enteropatija; enterobiopsija; serološki testovi UVOD Celijačna bolest je trajni oblik nepodnošewa glutena, odnosno glijadina i srodnih prolamina koji se nalaze u endospermu zrna pšenice, raži i ječma [1]. Iako je, prema zapisima Areteusa (Are ta e- us) iz Kapadokije, poznata još od prvog veka pre nove ere, wen prvi detaqan opis dao je Semjuel Xi (Samuel Gee), engleski lekar iz 19. veka [1]. Povezanost kliničke slike bolesti i konzumirawa pšeničnog brašna uočio je Vilijem Dik (Wil li am D ic ke) godine. Tipične morfološke promene na sluznici tankog creva, koje predstavqaju osnovu bolesti, kod odrasle osobe dokazao je Poli (Pa ul le y) godine, dok su ove promene kod deteta dokazali Sakula (Sakula) i Šajner (Shi ner) godine [1, 2]. I pored toga što se za celijačnu bolest dugo zna, tek posledwih decenija je ustanovqeno da se ona ubraja u red najčešćih hroničnih oboqewa čoveka i da se, s promenqivom učestalošću, nalazi kod svih rasa i u celom svetu [2-6, 7]. Primarno se javqa kod pripadnika bele rase, posebno u određenim grupacijama, dok je kod osoba drugih rasa znatno ređa ili izuzetno retka [1, 3-6]. Velike razlike u incidenciji bolesti zavise ne samo od genetskih faktora i navika u ishrani, već i od dostupnosti savremenih dijagnostičkih metoda [1, 3]. Na osnovu seroloških ispitivawa obavqenih u zemqama zapadne Evrope i Sjediwenim Američkim Državama, celijačna bolest se javqa kod jednog na stanovnika [3-6, 8-12]. Učestalost bolesti s klasičnom kliničkom slikom je, međutim, višestruko niža; u evropskim zemqama je od 1:300 (Irska) do 1:4000 (Portugal), dok je kod dece uzrasta do 15 godina u našoj zemqi 1:1000 [1, 13, 14]. KLINIČKA OBELEŽJA BOLESTI Celijačna bolest je hronično zapaqewsko oboqewe multifaktorske etiologije, a nastaje kao posledica poligenske predispozicije i izloženosti glutenu. Posmatrana s patogenetskog aspekta, ona je u svojoj suštini autoimuno oboqewe u kojem je gluten pokretač autoimunog procesa [1-7, 13, 15]. U prilog naslednoj sklonosti govori i velika promenqivost incidencije bolesti u različitim populacijama, kao i visoka stopa prevalencije kod jednojajčanih blizanaca (80%) i srodnika prvog reda (10%) [1]. Istraživawa obavqena tokom posledwe dve decenije su pokazala da glavnu ulogu u naslednoj sklonosti bolesti imaju HLA geni klase II, ali uz bitno učešće i drugih gena [1, 16-19]. Više od 90% ispitanika s trajnim oblikom nepodnošewa glutena ima HLA DQ2 haplotip, dok se kod ostalih gotovo u potpunosti beleži HLA DQ8 haplotip [3, 4, 16, 17]. Značaj glikoproteina HLA klase II koji postoje na antigen-prezentujućim ćelijama ogle 152
2 da se u svojstvu da, posle spoja s peptidnim hidrolizatom glijadina sačiwenim od 33 aminokiseline i modifikovanom tkivnom transglutaminazom, aktiviraju intestinalne CD4+ T-limfocite, koji lučewem proinflamatornih citokina dovode do infiltrativnog ili infiltrativno-destruktivnog zapaqewa sluznice tankog creva, te do promena na drugim organima [15, 20]. Pored T-ćelijskog imunog odgovora, bitno učešće u patogenezi bolesti ima i humoralni imunitet qudskog organizma, o čemu govore antiglijadinska antitela, kao i autoantitela na retikulin, endomizijum, tkivnu transglutaminazu i druge telesne strukture [1, 4, 15, 21, 22]. Stepen zapaqewa sluznice tankog creva je najizraženiji u proksimalnom delu jejunuma i progresivno se smawuje ka ileumu [1, 2, 7, 23]. Morfološke promene na sluznici tankog creva u celijačnoj bolesti nisu specifične, ali su u manifestnom obliku bolesti, u odnosu na druge enteropatije izazvane nepodnošewem proteina, obično više izražene [1]. Prema navodima Marša (Marsh) [24], oštećewe sluznice tankog creva se klasifikuje u dva osnovna oblika: lakši ili infiltrativni i teži ili destruktivni oblik. U prvom obliku mukoznog oštećewa utvrđuje se povećan broj intraepitelnih limfocita sa γ/δ receptorskim svojstvom i visoka limfoplazmocitna infiltracija strome, dok visina crevnih resica i dubina kripti ostaju očuvane. Kod destruktivnog oblika, osim izraženih infiltrativnih promena u lamini epitelijalis i stromi, dolazi do skraćewa, odnosno gubitka resica i hiperplazije kripti. U najtežem obliku oštećewa sluznice tankog creva, koji retko nastaje, tipične infiltrativne promene, kao i hiperplazija krpiti mogu i da izostanu. Na osnovu kliničko-seroloških i patohistoloških promena, celijačna bolest se deli na dva osnovna tipa: simptomatski i asimptomatski [1-6, 13, 23]. U okviru simptomatskog vida bolesti razlikuju se oblici s klasičnom i netipičnom (monosimptomatskom i oligosimptomatskom) kliničkom slikom. Klasični oblik bolesti se uglavnom javqa kod odojčadi i male dece, a netipični u kasnijem uzrastu [1]. Kod asimptomatskog oblika bolesti, koji može biti latentni i potencijalni, beleže se samo serološki parametri nepodnošewa glutena. Pored toga, kod potencijalnog oblika celijačne bolesti, za razliku od latentnog, pri patohistološkom pregledu sluznice tankog creva uočava se i povećana intraepitelna infiltracija limfocita [1, 3, 23]. Klasični oblik celijačne bolesti se uglavnom javqa u uzrastu od devet do 36 meseci, a odlikuje se postepenim početkom koji je praćen hroničnom dijarejom, anoreksijom, poremećajem napredovawa u telesnoj težini, apatijom i razdražqivošću (Slike 1a i 1b) [1, 25]. U kasnijem toku javqaju se gubitak telesne težine, smawewe kostno-mišićne mase i uvećawe trbuha, a kod zapuštenog oblika bolesti hipoproteinemijski edemi i zaostajawe u longitudinalnom rastu. Najteži oblik bolesti, tzv. celijačna kriza, nastaje veoma retko, uglavnom tokom prve godine po rođewu, a odlikuje se potpunom gastrointestinalnom insuficijencijom koja je praćena teškim hidroelektrolitnim i acidobaznim poremećajem, drastičnim gubitkom telesne težine i eksudativnom enteropatijom [7]. Iako je klasični oblik bolesti najčešće opisivan i najboqe proučen entitet, danas se zna da predstavqa samo vrh celijačnog brega i da najveći broj bolesnika, kako dece, tako i odraslih, jesu oni sa netipičnim ili asimptomatskim oblikom bolesti [1, 3-7, 13]. Simptomi i znaci celijačne bolesti posle treće godine po rođewu, a posebno u predškolskom i školskom uzrastu, obično su netipični i često neprimetni [1-5, 22, 25]. Gastrointestinalne smetwe uglavnom nisu naglašene. Povremeno se javqaju opstipacija ili dijareja, nekada rekurentni bol u abdomenu, a često anemija, zastoj u rastu i razvoju i promene u ličnosti deteta [1, 3-5, 22]. U odraslom dobu, međutim, poremećaj podnošewa glutena, bilo da se dotad ispoqavao ili ne, može biti uzrok steriliteta kod mladih qudi, a kod starijih osoba uzrok osteoporoze, nehočkinskog (non-hod gkin) limfoma tankog creva i karcinoma usne dupqe, ždrela i jedwaka [3, 4, 13, 23]. U sklopu celijačne bolesti, pored simptomatskog ili asimptomatskog oštećewa sluznice tankog creva, javqaju se i različite autoimune, odnosno nutritivne promene na drugim organima i sistemima organa [4, 7, 13, 26-28]. To se, pre svega, odnosi na neke neurološke poremećaje, kao što su ataksija, polineuro a SLIKA 1. Dvogodišwak s enteropatijom osetqivom na gluten tokom postavqawa dijagnoze (a) i posle dva i po meseca dijete bez glutena (b). FIGURE 1. A two-year-old boy with gluten sensitive enteropathy in the phase of diagnostics (a) and after two and a half months on gluten-free diet (b). b 153
3 patija, Myast he nia gra vis, epilepsija, miopatija i shizofrenija, zatim na sideropenijsku anemiju otpornu na oralnu primenu gvožđa, oštećewa gleđi na stalnim zubima, osteopeniju, rekurentni aftozni stomatitis, izolovanu hipertransaminazemiju, steatozu jetre, sklonost krvarewu usled nedostatka faktora koagulacije koji zavise od vitamina K i druge [7, 28]. Takođe, celijačnu bolest, pored značajne učestalosti među bliskim srodnicima obolelog, naročito srodnika prvog reda, obeležava i visoka udruženost s nekim imunim i neimunim oboqewima, kao što su: dijabetes melitus tip I, autoimuni tireoiditis, autoimuni hepatitis, Sjegrenov (Sjögren) sindrom, nedostatak imunoglobulina A (IgA), IgA nefropatija, dermatitis herpetiformis, Daun Tarner Vilijemsov (Down Tur ner Wil li ams) sindrom i druga oboqewa [15, 27, 29-40]. a b DIJAGNOSTIKA a b SLIKA 2. Stereomikroskopski (a) i patohistološki izgled (b) najtežeg oštećewa sluznice tankog creva kod deteta s celijačnom bolešću. FIGURE 2. Stereomicroscopic (a) and pathohistological aspect (b) of the most severe disorder of small bowel mucosa in a child with celiac disease. SLIKA 3. Normalan stereomikroskopski (a) i patohistološki izgled (b) sluznice tankog creva. FIGURE 3. Normal stereomicroscopic (a) and pathohistological aspect (b) of small bowel mucosa. Postavqawe dijagnoze celijačne bolesti se zasniva na kriterijumima koje je definisalo Evropsko udružewe za dečju gastroenterologiju, hepatologiju i nutriciju (Euro pean So ci ety of Pa e di a tric Ga stro en tero logy, He pa to logy and Nu tri tion ESPGHAN) [41]. Prema ovim opšteprihvaćenim kriterijumima, patohistološki pregled sluznice tankog creva predstavqa ne samo osnovu, već i obavezu u dijagnostikovawu celijačne bolesti [39, 42]. Važan doprinos dijagnozi ima i stereomikroskopija, koja omogućava trodimenzionalnu vizuelizaciju i idealnu pripremu uzoraka sluznice tankog creva za patohistološku analizu [1, 43, 44-46]. Kod bolesnika na ishrani sa glutenom sluznica pokazuje tipične patohistološke promene koje se na dijeti bez glutena povlače (Slike 2a,b i 3a,b). U manifestnom obliku bolesti na eliminacionoj dijeti iščezavaju i tegobe bolesnika. Serološki pokazateqi bolesti, kao što su IgA autoantitela na endomizijum i tkivnu transglutaminazu, visoko su osetqivi i specifični, ali nemaju i apsolutnu dijagnostičku vrednost [39, 41, 42, 46]. Ovo se, pre svega, odnosi na osobe s nedostatkom IgA i decu sa glutenskom enteropatijom u uzrastu do dve godine. Otuda se ovi testovi primarno koriste u otkrivawu asimptomatskih i netipičnih oblika celijačne bolesti, koji se često javqaju kod najbližih srodnika obolelih i bolesnika s različitim imunim i neimunim oboqewima, kao i u proceni doslednosti eliminacione dijete kada je bolest već potvrđena [33, 42, 46, 47]. Takođe, primena seroloških testova olakšava donošewe odluke o patohistološkom pregledu sluznice tankog creva kod bolesnika na provokaciji 154
4 podnošewa glutena i omogućava potpuniji uvid u remisiju bolesti tokom početne faze dijetetskog tretmana [33, 34, 41, 42]. Endoskopska ili aspiraciona enterobiopsija s patohistološkom analizom uzoraka sluznice tankog creva pre uvođewa dijete bez glutena ostaje i daqe tzv. zlatni standard u dijagnostikovawu celijačne bolesti. Prema prvim dijagnostičkim kriterijumima ESPGHAN, usvojenim u Interlakenu godine, pored početne, bilo je neophodno obaviti još najmawe dve enterobiopsije, jednu posle 2-4 godine dijete bez glutena i drugu tokom 3-6 meseci provokacije podnošewa glutena [48]. Ispitanici bez dokazanog recidiva bolesti zahtevali su treću biopsiju, koja je vršena u preostalom periodu do pune dve godine normalne ishrane, a neki od wih i četvrtu ukoliko su se simptomi i znaci bolesti primetili kasnije. Zahvaqujući iskustvima stečenim u međuvremenu, kao i uvođewu seroloških pokazateqa specifičnih za celijačnu bolest, ovi kriterijumi su na sastanku ESPGHAN u Budimpešti godine značajno korigovani i dopuweni [41]. U sklopu novih preporuka provokacija podnošewa glutena s ponovnom enterobiopsijom zadržana je, praktično, samo kod dece kod koje je glutenska enteropatija utvrđena pre navršene druge godine. Ovo je neophodno zbog iskqučewa prolaznog oblika nepodnošewa glutena, koje je moguće u ovom uzrastu, kao i izdvajawa drugih oboqewa koja su, prema svojim kliničkim i patohistološkim osobinama, mogla odgovarati glutenskoj enteropatiji. Pored toga, primena dijagnostičkih principa iz Interlakena indikovana je i kada uzorci sluznice tankog creva pri prvoj biopsiji nisu imali tipičan izgled ili su bili neadekvatni za pouzdano tumačewe i gde je bezglutenska dijeta data bez prethodne enterobiopsije. Provokacija podnošewa glutena se ne savetuje pre navršene šeste godine i tokom puberteta; u prvom slučaju zbog visokog rizika od oštećewa stalnih zuba, a u drugom zbog nežeqenog dejstva na rast i razvoj deteta. U okviru provokacije podnošewa glutena vrše se dve enterobiopsije: prva pred samu provokaciju i druga tokom normalne ishrane, tj. sa najmawe grama glutena dnevno. Prvom biopsijom se dokazuje oporavak sluznice tankog creva posle dosledno primewene dijete, a drugom postojawe ili izostanak morfoloških parametara tipičnih za podnošewe glutena. Pored kliničkog ispitivawa bolesnika, dragocenu ulogu u precizirawu termina za enterobiopsiju tokom opterećewa glutenom ima određivawe seroloških parametara specifičnih za celijačnu bolest. Međutim, kod bolesnika starijih od dve godine kod kojih je patohistološki pregled sluznice tankog creva ukazao na tipične promene i koji su se oporavili na dijeti bez glutena ponovna enterobiopsija nije potrebna. Značajan doprinos postavqawu dijagnoze u ovim slučajevima ima i gubitak prethodno potvrđenih seroloških parametara važnih za celijačnu bolest. Ponovna (kontrolna) enterobiopsija u uzrastu starijem od dve godine neophodna je samo kod bolesnika koji se ne oporavqaju na striktnoj dijeti bez glutena, kao i kod onih kod kojih je bolest otkrivena u asimptomatskom obliku. U prvom slučaju biopsija se vrši radi revizije dijagnoze, a u drugom radi uvida u normalizaciju izgleda sluznice tankog creva posle odgovarajućeg perioda eliminacione dijete. LEČEWE I PROGNOZA Celijačna bolest zahteva doživotnu dijetu bez glutena [39, 41, 42]. Kod većine bolesnika sa simptomatskim oblikom obolesti, posebno odojčadi i male dece, neophodna je korekcija nedostatka mikroelemenata i vitamina, naročito gvožđa i folata, a kod 5-10% bolesnika i privremena restrikcija laktoze [1, 4, 34, 49]. Kod najtežih oblika bolesti, pored intravenske nadoknade vode i elektrolita, primewuje se elementarna, odnosno dodatna parenteralna ishrana, a nekad i glikokortikoidna terapija [4, 33, 34, 49]. Uz striktnu dijetu celijačna bolest ima dobru prognozu. Zapravo, ukoliko poštuju odgovarajući režim ishrane, osobe s trajnim poremećajem podnošewa glutena i nisu bolesnici. Ukoliko se ne pridržavaju dijete bez glutena, međutim, može doći do različitih nutritivnih, odnosno autoimunih komplikacija, koje su nekada i veoma teške [4, 33, 34, 39, 42]. Takođe, osobe s nelečenom celijačnom bolešću, u odnosu na pripadnike matične populacije, imaju znatno veći rizik od nastanka T-ćelijskog limfoma tankog creva i karcinoma usne dupqe, ždrela i jedwaka [4, 23, 27, 39, 42, 49, 50]. ZAKQUČAK Celijačna bolest ili trajni oblik nepodnošewa prolamina pšenice, raži i ječma ubraja se u red najčešćih hroničnih oboqewa čoveka. Nastaje kao rezultat autoimunog procesa kod genski predisponiranih osoba izloženih glutenu. Primarno se javqa kod pripadnika bele rase, a posebno često kod srodnika prvog reda obolelih osoba i bolesnika s različitim autoimunim i nekim neimunim oboqewima. Osnovu bolesti, kao i kqučni nalaz u wenoj dijagnostici, čini tipičan patohistološki nalaz pri pregledu sluznice tankog creva, koji se povlači na dijeti bez glutena. Pored enteropatije, klinički manifestne ili nemanifestne, moguća su oštećewa i drugih organa i sistema organa, nekada i vrlo teška. Serološka ispitivawa nemaju dijagnostičku vrednost, ali su, zbog visoke osetqivosti i specifičnosti, od izuzetne koristi u otkrivawu asimptomatskih i netipičnih oblika bolesti, kao i u proceni doslednosti eliminacione dijete kada je bolest već potvrđena. 155
5 LITERATURA 1. Walker-Smith JA. Celiac disease. In: Walker AW, Durie PR, Hamilton RJ, Walker-Smith JA, Watkins JB, editors. Pediatric Gastrointestinal Disease. Hamilton: BC Decker Inc; p Walker-Smith JA. Food sensitive enteropathies. Clin Gastroenterol 1986; 15: Catassi C, Fabiani E, Fasano A. A journey around the coeliac disease. Annales Nestle 2004; 62: Troncone R, Auricchio S. Celiac disease. In: Wyllie R, Hymas J, editors. Pediatric Gastrointestinal Disease. Philadelphia: WB Saunders Comp; p Catassi C, Ratsch IM, Fabiani E, at al. Coeliac disease in the year 2000: exploring the iceberg. Lancet 1994; 343: Not T, Horvath K, Hill ID, et al. Celiac disease risk in the USA: high prevalence of antiendomysium antibodies in helthy blood donors. Scand J Gastroenterol 1988; 33: Walker-Smith JA, Murch S. Gastrointestinal food allergy. In: Walker-Smith JA, Murch S, editors. Diseases of the Small Intestine in Childhood. Oxford: Isis Medical Media; p Maki M, Mustalahti K, Kokkonen J, et al. 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Beograd: Medicinski fakultet Univerziteta u Beogradu; Finkel Y. Celiac disease in children and adolescents. In: Gouma DJ, Krejs GJ, Tytgat GN, Finkel Y, editors. New Developments and Management of Benign Gastrointestinal Disorders. Paris: JL Eurotext; p Zubillaga P, Vidales MC, Zubillaga I, et al. HLA-DQA1 and HLA- DQB1 genetic markers and clinical presentation in celiac disease. J Pediatr Gastroenterol Nutr 2002; 34: Kaukinen K, Partanen J, Maki M, Kollin P. HLA-DQ typing in the diagnosis of celiac disease. Am J Gastroenterol 2002; 97: Naluai AT, Nilsson S, Gudjonsdottir AH, et al. Genome-wide linkage analysis of Scandinavian affected sib-pairs supports presence of susceptability loci for celiac disease on chromosomes 5 and 11. Eur J Hum Genet 2001; 9: Woolley N, Holopainen P, Ollikainen V, et al. A new locus for coeliac disease mapped to chromosome 15 in a population isolate. Hum Genet 2002; 111: Holmes G, Catassi C, editors. Coeliac Disease. Oxford Health Press; Dietrich W, Laag E, Schopper H, et al. Autoantibodies to tissue transglutaminase as predictors of celiac disease. Gastroenterology 1998; 115: Auricchio S. Pathogenetic mechanisms in coeliac disease. In: Farthing MJG, Bianchi-Porro G, editors. New horizons in gastrointestinal and liver disease: mechanisms and management. Paris: John Libbey Eurotext; p Kumar PJ. Management of coeliac disease. In: Farthing MJG, Bianchi-Porro G, editors. New Horzons in Gastrointestinal and Liver Disease: Mechanisms and Management. Paris: John Libbey Eurotext; p Marsh MN. Gluten, major histocompatibility complex and the amall intestine. A molecular and immunologic approach to the spectrum of gluten sensitivity (celiac sprue). Gastroentrology 1992; 102: Radlović N. Intolerancija proteina hrane. In: Stepanović R, editor. Pedijatrija. Beograd: Savremena administracija; p Biagi F, Distephano M, Jorizzo RA, et al. Pathophysiology of coeliac disease. In: Gaslmiche JP, Gournay J, editors. Paris: John Libbey Euroterxt; p Mody RJ, Brown PI, Wechsler DS. Refractory iron deficiency anemia as the primary clinical manifestation of celiac disease. J Pediatr Hematol Oncol 2003; 25: Kalayci AG, Kansyu A, Girgin N, et al. Bone mineral density and importance of a gliadin-free diet in patients with celiac disease in childhood. Pediatrics 2001; 108: Hadjivassiliou M, Grunewald RA, Davies-Jones GAB. Gluten sensitivity as a neurological illness. J Neurol Neurosurg Psychiatr 2002; 72: Schober E, Rami B, Granditsh G, Crone J. Coeliac disease in children and adolescents with type I diabetes mellitus: to screen or not, to treat or not. Horm Res 2002; 57(Suppl 1): Barera G, Bonfani R, Viscardi M, et al. Occurence of celiac disease after onset of type I diabetes: A 6-year prospective longitudinal study. Pediatriucs 2002; 109: Mackey J, Treem WR, Woley G, et al. Frequency of celiac disease in individuals with Down syndrome in the United States. Clin Pediatr 2001; 40: Fasano A, Catassi C. Current approaches to diagnosis and treatment of celiac disease: An evolving spectrum. Gastroenterol 2001; 120: Farrell RJ, Kelly CP. Celiac spru. N Engl J Med 2002; 346: Srivastava A, Abboud T, Fritzler M, et al. Evaluation of celiac disease screening methods in first-degree relatives. J Pediatr Gastroenterol Nutr 2004; 39(1): Hill I, Horvath K, Fasanoano A, et al. Prevalence of celiac disease in at risk groops of children in the USA. J Pediatr Gastroenterol Nutr 1997; 25(4): Vitoria JC, Castano L, Luis I, et al. Association of insulin-dependent diabetes mellitus and celiac disease: A study based on serologic markers. J Pediatr Gastroenterol Nutr 1998; 27(1): Barera G, Bonfanti R, Viscardi M, et al. Occurrence of celiac disease after onset of type 1 diabetes: A 6-year prospective longitudinal study. Pediatrics 2002; 109: Hill ID, Bhatnagar S, Cameron D, et al. Celiac disease: Working Group Report of the First World Congress of Pediatric Gastroienterilogy, Hepatology and Nutrition. J Pedaitr Gastroenterol Nutr 2002; 35(2): Neri E, Not T, Kryszak D, et al. Follow up in an USA adult celiac population: The role of the gluten in autoimmunity. J Pediatr Gastroenterol Nutr 2004; (1): Walker-Smith JA, Guandalini S, Schmitz J, et al. Revised criteria for diagnosis of coeliac disease. Arch Dis Child 1990; 65: Guideline for the Diagnosis and Treatment of Celiac Disease in Children: Recommendation of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition. J Pediatr Gastroenterol Nutr 2005; 40: Radlović N, Milosavljević S, Nestorović B, et al. Značaj stereomikroskopije u dijagnostici hroničnih dijareja kod dece. Gastroenterološki arhiv 1988; 7(3): Thompson M, Kitching P, Alison J, et al. Are endoscopic biopsis of small bowel as good as suction biopsis for diagnosis of enteropathy. J Pediatr Gastroenterol Nutr 1999; 29(4): Radlović N. Značaj stereomikroskopije u dijagnostici hroničnih enteropatija. In: Bogdanović R, Radlović N, editors. 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6 CELIAC DISEASE IN CHILDREN MODERN DIAGNOSTIC APPROACH Nedeljko RADLOVIĆ University Children s Hospital, Belgrade ABSTRACT Celiac disease presents a hereditary disorder of gluten tolerance, i.e. of gliadin and related prolamins of wheat, rye and barley. It primarily occurs in Caucasians (1: ), while it is considerably or exceptionally rare in colored races. It is particularly frequent in close relatives of the patient, as well as in persons with congenital IgA deficiency and in patients with autoimmune and some chromosomal diseases. The basis of the disease, as well as the key finding in its diagnostics, lies in small bowel inflammation, which withdraws on gluten free diet. Beside clinically manifest or non-manifest enteropathy, changes involving other organs and systems are also frequently seen. The diagnosis of the manifest form of the disease is based on characteristic pathohistological finding detected by the examination of small bowel mucosa in patients on standard diets and their clinical improvement after the introduction of gluten free diet. However, in the diagnosis of the asymptomatic form of the disease, it is necessary to perform enterobiopsy, which confirms the normalization of the appearance of small bowel mucosa in patients on the elimination diet. In children with gluten sensitive enteropathy detected in the first two years of life, as well as in cases in which mucosa samples taken on the first enterobiopsy do not have typical appearance or are inadequate for a reliable interpretation, a definite diagnosis is made based on biopsy finding during the provocation of gluten tolerance. As the quality of permanent teeth can be disturbed, this procedure is not suggested to be done before the completed age of 6 years, and due to adverse effects on the growth and development of the child, it should not be done during puberty. Due to incomplete sensitivity and specificity, the serological indicators of the disease do not have diagnostic value. Therefore, they are primarily used in the disclosure of asymptomatic and atypical forms of celiac disease, as well as in the assessment of the consistency of elimination diet in cases with already verified disease. In addition, the application of these tests makes easier passing the decision to perform pathohistological examination of small bowel mucosa in patients with provoked gluten tolerance, which also gives a more complete understanding into the remission of the disease during the initial phase of treatment. Key words: celiac disease; gluten; enteropathy; enterobiopsy; serological tests Nedeljko RADLOVIĆ Univerzitetska dečja klinika Tiršova 10, Beograd Tel.: vladar@beotel.yu * Pristupno predavawe je održano 12. marta godine. 157
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