Study on histogenesis of enterochromaffin-like carcinoid in autoimmune atrophic gastritis associated with pernicious anemia

Lana Macukanovic-Golubovic, Vuka Katic, Gorana Rancic, Mladen Milenovic, Goran Marjanovic, Zoran Golubovic
2007 Vojnosanitetski Pregled  
Medicinski fakultet, *Klinika za hematologiju, † Institut za patologiju, ‡ Institut za histologiju sa embriologijom, Niš Apstrakt Uvod/Cilj. Autoimunski atrofijski gastritis korpusne sluznice (Agastritis) dovodi do perniciozne anemije (PA) i promena u epitelnim i endokrinim ćelijama sluznice želuca. Najvažnije komplikacije su: ahlorhidrija, hipergastrinemija, želudačni karcinom i karcinoidni tumori porekla enterohromafinolikih ( ECL) endokrinih ćelija. Cilj rada bio je citohemijsko i
more » ... mijsko proučavanje histogeneze ECL karcinoida u autoimunskom atrofijskom gastritisu udruženim sa pernicioznom anemijom. Metode. Ispitivanje je obuhvatilo 65 bolesnika sa PA i 30 bolesnika kontrolne grupe u periodu 2000−2006. godine. Patohistološka proučavanja vršena su na endoskopskim biopsijama sluznice želuca (po četiri iz korpusa i antruma želuca) fiksiranim u 10% rastvoru formaldehida. Parafinski preseci debljine 4 μm bojeni su sledećim metodama: klasičnom − hematoksilin-eozin (HE), histohemijskom AB-PAS (pH 2,5), citohemijskom argirofilnom metodom po Sevier-Mungeru za otkrivanje ECL ćelija i imunocitohemijskom PAP tehnikom za otkrivanje G ćelija u antrumu želuca i antitela na hromogranin A − specifični marker za neuroendokrine ECL ćelije. G i ECL ćelije kvantifikovane su na 20 vidnih polja, površine od 0,0245312 mm 2 po jednom vidnom polju. U serumu bolesnika određivane su bazalne vrednosti gastrina radioimmunoassay (RIA) metodom. Dobijeni rezultati su statistički obrađivani Studentovim t testom. Rezultati. Ustanovljena je hiperplazija gastrinskih ćelija u antrumu želuca i ECL ćelija u korpusu želuca bolesnika sa PA koja je bila različite forme od proste, linearne, mikronodusne, do slike intramukoznog ECL karcinoida. Prosečan broj G ćelija bio je statistički značajno viši u grupi sa PA u odnosu na kontrolnu grupu (p < 0,05), kao i prosečan broj ECL ćelija (p < 0,001). Zaključak. Hipergastrinemija indukuje hiperplaziju ECL ćelija i nastajanje korpusnih ECL karcinoida, a njihova histogeneza ide preko proste, linearne i adenomatoidne hiperplazije. Ključne reči: gastritis, atrofijski; anemija, perniciozna; autoimunske bolesti; karcinoid; enterohromafine ćelije; histološke tehnike. Abstract Background/Aim. Autoimmune atrophic fundic gastritis induces the pernicious anemia (PA), as well as the changes in both epithelium and endocrine cells of gastric mucosa. The most important complications are: achlorhydria, hypergastrinemia, gastric cancer and enterochromaffin-like ( ECL) carcinoid.The aim of this study was to examine ECL carcinoid histogenesis in A-gastritis associated with PA. Methods. During the period from 2000−2006, 65 patients with PA and 30 patients of the control group were examined. Histopathological examination was done in endoscopical biopsies of gastric mucosa fixed in 10% formaldehyde. Paraffin sections were stained with classic hematoxylin-eosin (HE); histochemical AB-PAS (pH 2.5), cytochemical argyrophilic Servier-Munger′s and immunocytochemical PAP methods for G cell identification and chromogranin A antibodies -specific marker for neuroendocrine ECL cells. Both G and ECL cells were counted per 20 fields, of surface 0.0245312 mm 2 by a field. Basal gastrin serum levels were also examined by using radioimmunoassay (RIA) method. The obtained results were statisticaly calculated by using Student΄s t test. Results. Marked antral G cell hyperplasia associated with corporal ECL hyperplasia was found. ECL cell hyperplasia was of simplex, linear, adenomatoid type to the pattern of intramucous ECL cell carcinoid. An average number of G cells was statistically significant in the patients with PA as compared to the control group (p < 0.05) as well as an average number of ECL cells. Conclusion. We concluded that antral G cell hyperplasia accompanied by gastrinemia induces ECL hyperplasia and ECL corporal carcinoid in A-gastritis and that their histogenesis develops trough simple, linear and adenomatoide hyperplasia.
doi:10.2298/vsp0708543m pmid:17874722 fatcat:h724g3msdrb7vhfct7mesn6iwa