Introduction: Benign esophageal tumors are uncommon; most are detected by chance upon endoscopy. Lymphoid polyps, like those of the small and large intestine, have not been reported to occur in the esophagus. We describe an esophageal benign lymphoid polyp. Case Report: A 7.5-year-old girl was referred with dysphagia. Upper endoscopy demonstrated and removed a single small pedunculated polyp in the upper third of the esophagus. The polyp consisted of two hyperplastic lymphoid aggregates in the lamina propria covered by stratified non-keratinizing squamous epithelium. Discussion: Esophageal polyps may be produced by hyperplastic lymphoid tissue and may be a cause of dysphagia.

A 69-year-old man underwent endoscopic mucosal resection of a solitary polyp located in the cecum. After the procedure, a fecal mass and appendiceal orifice appeared under the cut surface. A diagnosis of reactive lymphoid hyperplasia was made based on the results of an immunostaining analysis, which revealed a segregated population of T cells and B cells in multiple lymphoid follicles. The aggregation of adipocytes forming a lipomatous area and granulation tissue was also observed. We speculate that the compaction of the fecal mass in the appendix triggered mucosal inflammation, resulting in the formation of the polyp, which concealed both the feces and appendiceal orifice.

The rectal tonsil (RT), a localized reactive proliferation of lymphoid tissue occurring in the rectum, can cause diagnostic difficulty; and awareness of this entity can prevent a misdiagnosis of lymphoma. A clinicopathologic analysis of 11 cases of RT was performed to determine the features that can aid in the recognition of this entity. The patients (6 males and 5 females) were middle-aged adults, except for 1 case affecting a young boy (age range, 1 to 62 y; mean, 49 y). All presented with either rectal bleeding or abdominal pain, or had the lesion found on routine screening. Endoscopic descriptions, available in all cases, reported a raised, polypoid lesion in 8 cases, a nodule in 2 cases, and a "mass" in 1 case. Histologically, all cases were composed of a lymphoid proliferation involving the lamina propria or submucosa. Lymphoid follicles could be identified in all cases, although some were difficult to appreciate without immunostains for follicular dendritic cells. Five cases showed overlying cryptitis and mild architectural distortion, but no cases showed crypt obliteration or crypt abscesses. Intraepithelial lymphocytes were present in 9 cases, and 5 cases showed nondestructive lymphoepithelial lesions. During a mean follow-up of 5.8 years, none showed a recurrence or developed lymphoma. In conclusion, RT, with its distinctive features, is an important entity to recognize. Familiarity with the range of histologic features characteristic of the RT is critical in avoiding misinterpretation as lymphoma.

Various nonneoplastic entities may manifest as submucosal abnormalities at colorectal evaluation, and it may be difficult to distinguish between those with an intramural origin and those with an extramural origin on the basis of optical colonoscopy alone. Cross-sectional radiologic imaging, which allows evaluation of the entire bowel wall and the surrounding tissues, plays an important role in the localization and characterization of these abnormalities. However, some superficial submucosal lesions that are initially detected at computed tomographic colonography or barium enema studies may be better characterized with colonoscopy; thus, it is important to recognize the complementary uses of these diagnostic tests. In addition, modalities such as transrectal ultrasonography and magnetic resonance imaging may be useful for the identification and characterization of some abnormalities. For timely and effective management, it is especially important that submucosal neoplasms of the large intestine be accurately distinguished from nonneoplastic entities such as lymphoid polyps, vascular lesions, and cystic lesions, as well as from extracolonic abnormalities (eg, endometriosis, uterine fibroids) and normal extracolonic structures (eg, uterus, vasculature).

An early adenocarcinoma of the ascending colon was confined to a mass of gut-associated lymphoid tissue (GALT). The first description of an adenocarcinoma of colon differentiating as dome epithelium is presented.

A plaque-like carcinoma was identified opposite the ileocaecal valve in an asymptomatic 56-year-old man with a family history of colorectal cancer. Malignant epithelium was confined to a mass of GALT filling but limited to the submucosa. Characterization of the neoplasm was undertaken by means of mucin histochemistry, immunohistochemistry, electron microscopy and assessment of DNA microsatellite instability status. The malignant epithelium comprised well differentiated columnar cells with a microvillous brush border and expressing MUC1, but no goblet cells or expression of MUC2. The demonstration of focal clusters of intraepithelial B-lymphocytes supported the presence of functioning M-cells within the malignant neoplasm. The cancer was DNA microsatellite stable despite the finding of tumour infiltrating lymphocytes.

There is evidence for the origin of colorectal neoplasia from dome epithelium in both experimental models and microreconstruction studies of early adenomas in nonpolypotic human colorectal mucosa. It is suggested that the lymphocyte-rich subset of colorectal cancer that expresses MUC1 but not MUC2 may be differentiating as dome epithelium of gut-associated lymphoid tissue.