Lymphoglandular complexes of the colon: structure and distribution

O'Leary, Allison; Sweeney, E. C.

doi:10.1111/j.1365-2559.1986.tb02481.x

Cited by 181 publications

(115 citation statements)

References 13 publications

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“…Thus, on the basis of these findings, we believe that misplacement of crypt epithelium into the submucosa of hyperplastic polyps may occur via a mechanism similar to that observed in adenomas with so-called pseudoinvasion. In fact, we agree with Sobin (12,14), who first suggested that misplacement of epithelium may occur secondary to tissue damage from torsion, or twisting, of the polyp followed by protrusion of glands through inherently weak regions of the muscularis mucosae, such as those that occur normally adjacent to lymphoid aggregates. Although none of the hyperplastic polyps in our study were pedunculated, it is possible that minor trauma may occur due to other factors, such as vigorous peristalsis or bulky intraluminal material.…”

Section: Discussionsupporting

confidence: 91%

Hyperplastic Polyp with Epithelial Misplacement (Inverted Hyperplastic Polyp): A Clinicopathologic and Immunohistochemical Study of 19 Cases

2001

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Hyperplastic polyps of the colon are the most common type of benign colonic polyp. Rarely, these polyps may show misplaced epithelium within the submucosa, thereby simulating an adenoma with pseudoinvasion or even an adenocarcinoma. In this study, we describe the clinical, pathologic, and immunophenotypic features of 19 hyperplastic polyps with misplaced epithelium to identify potential diagnostic pitfalls and gain insight into their pathogenesis. Routinely processed polypectomy specimens from 12 patients with 19 hyperplastic polyps containing foci of misplaced epithelium were evaluated for a variety of morphologic features including pattern and extent of submucosal involvement, continuity of the submucosal epithelium with the mucosa, presence of recent or remote hemorrhage, inflammation, association of misplaced epithelium with lymphoid aggregates, inflammation, and defects in the muscularis mucosae. Clinical and endoscopic data were obtained and correlated with the histologic findings. Immunoperoxidase stains (ABC method) for collagen IV (basement membrane marker), MIB-1 (proliferation marker), and E-cadherin (intercellular adhesion protein) were performed in all cases. The study group consisted of five males and seven females ranging in age from to 52 to 73 years (mean: 63 y). All of the polyps were located in the rectum or sigmoid colon, and their mean size was 0.5 cm (range: 0.2 to 1.0 cm). Most showed misplaced epithelium in a lobular (26%) or a mixed pattern consisting of lobules and irregularly distributed crypts (63%) that, upon deeper levels, was almost always continuous with the mucosal portion of the polyps (95%). Defects in the muscularis mucosae and splaying of the muscle fibers around misplaced epithelium were seen in all cases. Lymphoid aggregates were present adjacent to foci of misplaced epithelium in 37% of cases. Fresh hemorrhage, vascular congestion, and hemosiderin deposits were present in 79, 53, and 42% of cases, respectively. Strong and uniform staining of the misplaced epithelium for MIB-1 and E-cadherin was demonstrated in all cases, similar to that seen in the lower third of the mucosal portion of the polyps. A continuous collagen IV basement membrane pattern of staining was noted around all foci of misplaced epithelium. Hyperplastic polyps with misplaced epithelium probably occur secondary to trauma-induced protrusion of glands through breaks in the muscularis mucosae. Pathologists should be aware of this entity to avoid diagnostic confusion with other, more serious lesions, such as adenomas with pseudoinvasion or well-differentiated adenocarcinoma.

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Section: Discussionsupporting

confidence: 91%

Hyperplastic Polyp with Epithelial Misplacement (Inverted Hyperplastic Polyp): A Clinicopathologic and Immunohistochemical Study of 19 Cases

2001

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“…[1][2][3][4] The comparable density obtained with acetic acid staining and with H&E histology in our study suggest that the latter method is reliable, reproducible, and permits to evaluate the lymphoid aggregate density as well as additional parameters in conditions of active inflammation also. A wide range of 'normal' densities (from 3 to 25 aggregates/cm 2 ) has been obtained in necropsy specimens, [1][2][3] whereas the data on 'normal' diameter are scarce, being limited to an approximate range between 0.5 and 2 mm.…”

Section: Discussionmentioning

confidence: 53%

“…Even their frequency in healthy individuals is obscure, and, since the pioneeristic study of Dukes and Bussey, 1 a wide range of values has been reported. 2,3 Although sporadic papers have described the lymphoid aggregate features in several large bowel diseases, 2,4-6 their pathogenic role in common colorectal diseases is largely unexplored. Nonetheless, a transmural distribution of lymphoid aggregates is considered a histological peculiarity of Crohn's disease, 7 and the clinical implementation of lymphoid aggregate analysis has been proposed, as they may be detected both on double-contrast barium enema 8 and on colonoscopy.…”

mentioning

confidence: 99%

Morphology of colorectal lymphoid aggregates in cancer, diverticular and inflammatory bowel diseases

et al. 2005

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“…Colonic patches are also very likely to be involved in the pathogenesis of IBD. Lymphoid follicles with an M cell-containing follicle-associated epithelium have been reported to be abundant in the human colon, although they are smaller in size than Peyer's patches of the small intestine (42,43). These findings suggest that colonic patches are a functional type of GALT for Ag uptake and presentation and for T and B cell interactions.…”

Section: Discussionmentioning

confidence: 95%

Elimination of Colonic Patches with Lymphotoxin β Receptor-Ig Prevents Th2 Cell-Type Colitis

Dohi

Rennert

Fujihashi

et al. 2001

The Journal of Immunology

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Past studies have shown that colonic patches, which are the gut-associated lymphoreticular tissues (GALT) in the colon, become much more pronounced in hapten-induced murine colitis, and this was associated with Th2-type T cell responses. To address the role of GALT in colonic inflammation, experimental colitis was induced in mice either lacking organized GALT or with altered GALT structures. Trinitrobenzene sulfonic acid was used to induce colitis in mice given lymphotoxin-β receptor-Ig fusion protein (LTβR-Ig) in utero, a treatment that blocked the formation of both Peyer’s and colonic patches. Mice deficient in colonic patches developed focal acute ulcers with Th1-type responses, whereas lesions in normal mice were of a diffuse mucosal type with both Th1- and Th2-type cytokine production. We next determined whether LTβR-Ig could be used to treat colitis in normal or Th2-dominant, IFN-γ gene knockout (IFN-γ−/−) mice. Four weekly treatments with LTβR-Ig resulted in deletion of Peyer’s and colonic patches with significant decreases in numbers of dendritic cells. This pretreatment protected IFN-γ−/− mice from trinitrobenzene sulfonic acid-induced colitis; however, in normal mice this weekly treatment was less protective. In these mice hypertrophy of colonic patches was seen after induction of colitis. We conclude that Th2-type colitis is dependent upon the presence of colonic patches. The effect of LTβR-Ig was mediated through prevention of colonic patch hypertrophy in the absence of IFN-γ. Thus, LTβR-Ig may offer a possible treatment for the Th2-dominant form of colitis.

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Lymphoglandular complexes of the colon: structure and distribution

Cited by 181 publications

References 13 publications

Hyperplastic Polyp with Epithelial Misplacement (Inverted Hyperplastic Polyp): A Clinicopathologic and Immunohistochemical Study of 19 Cases

Hyperplastic Polyp with Epithelial Misplacement (Inverted Hyperplastic Polyp): A Clinicopathologic and Immunohistochemical Study of 19 Cases

Morphology of colorectal lymphoid aggregates in cancer, diverticular and inflammatory bowel diseases

Elimination of Colonic Patches with Lymphotoxin β Receptor-Ig Prevents Th2 Cell-Type Colitis

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