BACKGROUND AND AIM: Colorectal Paneth cell metaplasia (PCM) is known to be a sign of idiopathic inflammatory bowel disease (IBD), although its distribution and histogenesis are not fully understood. Objectives of this research were to investigate the spatial distribution of PCM in IBD and other forms of colitis (non-IBD), and to find stimuli causing PCM. METHODS: We studied multiple biopsy specimens from 181 patients with ulcerative colitis (UC), 159 with Crohn's disease (CD), 448 with non-IBD, and 78 normal controls. Paneth cell metaplasia frequency, at each colorectal site, was evaluated to find possible differences among diseases, phases of activity, and extents of disease. RESULTS: In non-IBD and controls, PCM was rarely (0-1.9%) seen at distal sites, but frequently (up to 48.7%) found at the ascending colon and cecum (P < 0.001). Paneth cell metaplasia frequency was significantly higher in IBD than in non-IBD patients and controls at distal sites (P < 0.001), but did not differ significantly between UC and CD, or among active, resolving, and quiescent phases. In UC, proctitis and left-sided colitis rarely displayed PCM at unaffected sites. Multiple logistic regression analysis revealed that PCM was positively associated with crypt distortion and mononuclear cell infiltration (P < 0.005), but negatively or not significantly associated with crypt atrophy, mucin depletion, acute inflammation, or phase of activity. CONCLUSIONS: Paneth cell metaplasia is a non-specific phenomenon in the proximal colon, but distal PCM, which occurs exclusively in affected mucosa, is a useful marker indicating IBD, even in the inactive phase. Regression analysis suggests that repair and regeneration may be the most potent stimuli causing PCM.
BACKGROUND AND AIM: Colorectal Paneth cell metaplasia (PCM) is known to be a sign of idiopathic inflammatory bowel disease (IBD), although its distribution and histogenesis are not fully understood. Objectives of this research were to investigate the spatial distribution of PCM in IBD and other forms of colitis (non-IBD), and to find stimuli causing PCM. METHODS: We studied multiple biopsy specimens from 181 patients with ulcerative colitis (UC), 159 with Crohn's disease (CD), 448 with non-IBD, and 78 normal controls. Paneth cell metaplasia frequency, at each colorectal site, was evaluated to find possible differences among diseases, phases of activity, and extents of disease. RESULTS: In non-IBD and controls, PCM was rarely (0-1.9%) seen at distal sites, but frequently (up to 48.7%) found at the ascending colon and cecum (P < 0.001). Paneth cell metaplasia frequency was significantly higher in IBD than in non-IBD patients and controls at distal sites (P < 0.001), but did not differ significantly between UC and CD, or among active, resolving, and quiescent phases. In UC, proctitis and left-sided colitis rarely displayed PCM at unaffected sites. Multiple logistic regression analysis revealed that PCM was positively associated with crypt distortion and mononuclear cell infiltration (P < 0.005), but negatively or not significantly associated with crypt atrophy, mucin depletion, acute inflammation, or phase of activity. CONCLUSIONS: Paneth cell metaplasia is a non-specific phenomenon in the proximal colon, but distal PCM, which occurs exclusively in affected mucosa, is a useful marker indicating IBD, even in the inactive phase. Regression analysis suggests that repair and regeneration may be the most potent stimuli causing PCM.
Authors: Dana Almohazey; Yuan-Hung Lo; Claire V Vossler; Alan J Simmons; Jonathan J Hsieh; Edie B Bucar; Michael A Schumacher; Kathryn E Hamilton; Ken S Lau; Noah F Shroyer; Mark R Frey Journal: Cell Death Differ Date: 2017-03-17 Impact factor: 15.828
Authors: Shiyan Yu; Iyshwarya Balasubramanian; Daniel Laubitz; Kevin Tong; Sheila Bandyopadhyay; Xiang Lin; Juan Flores; Rajbir Singh; Yue Liu; Carlos Macazana; Yanlin Zhao; Fabienne Béguet-Crespel; Karuna Patil; Monica T Midura-Kiela; Daniel Wang; George S Yap; Ronaldo P Ferraris; Zhi Wei; Edward M Bonder; Max M Häggblom; Lanjing Zhang; Veronique Douard; Michael P Verzi; Ken Cadwell; Pawel R Kiela; Nan Gao Journal: Immunity Date: 2020-08-18 Impact factor: 31.745
Authors: Eric B Nonnecke; Patricia A Castillo; Malin E V Johansson; Edward J Hollox; Bo Shen; Bo Lönnerdal; Charles L Bevins Journal: FASEB J Date: 2022-03 Impact factor: 5.834
Authors: Philip J Smith; Adam P Levine; Jenny Dunne; Paul Guilhamon; Mark Turmaine; Gavin W Sewell; Nuala R OʼShea; Roser Vega; Jennifer C Paterson; Dahmane Oukrif; Stephan Beck; Stuart L Bloom; Marco Novelli; Manuel Rodriguez-Justo; Andrew M Smith; Anthony W Segal Journal: Inflamm Bowel Dis Date: 2014-10 Impact factor: 5.325