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Multiple lymphomatous polyposis (MLP) is an uncommon type of primary non-Hodgkin gastrointestinal (GI) B-cell lymphoma characterized by the presence of multiple polyps along the GI tract. Malignant cells of MLP have mantle cell characteristics and thus are considered to be the counterpart of the mantle cell lymphoma (MCL) in the GI tract. Since 1961, no more than 70 well-documented cases have been published. We report the case of 53-year-old man diagnosed as having MLP. The patient presented with diffuse abdominal pain, chronic lower GI bleeding, peripheral lymphadenopathy, and weight loss. The lymphomatous polyps extended from the esophagus to the rectum, with bone marrow infiltration. Immunohistologic findings were characteristic of MCL. The patient was treated with a combined cyclophosphamide, vincristine, and prednisone chemotherapy regimen, resulting in a partial response. [ABSTRACT FROM AUTHOR]

Context: Atypical regeneration can mimic carcinoma in various epithelia. On endoscopic biopsies, atypical regenerative hyperplasia of the esophagus may show pleomorphism and atypia, simulating esophageal squamous cell carcinoma., Objective: To establish the most useful histologic features to distinguish atypical regenerative hyperplasia from esophageal carcinoma in endoscopic biopsies., Design: To study the frequency and histologic appearance of atypical regenerative hyperplasia, which simulate carcinoma, we reviewed 600 endoscopic biopsies (555 with chronic esophagitis and 45 with carcinomas of the esophagus). We selected those cases in which the differential diagnosis included regenerative atypical hyperplasia versus esophageal carcinoma and cases of atypical regenerative hyperplasia that were mistaken for carcinoma. For comparative purposes, we studied 10 cases of esophageal carcinoma from endoscopic biopsies that were confirmed by esophagectomy., Results: Among the cases with chronic esophagitis, we found 10 biopsies (1.8%) in which atypical regenerative hyperplasia mimicked carcinoma. In 7 cases, there were 4 to 12 years of follow-up, and no patient developed esophageal neoplasm. The remaining 3 patients were submitted to esophagectomy. None of these patients had carcinoma or dysplasia in the esophageal resection (false-positive biopsies). The most useful architectural changes in squamous carcinoma included stromal infiltration by nests, cords, or thin prongs of neoplastic keratinocytes, palisading desmoplasia, and in situ carcinoma in the adjacent epithelium. Malignant keratinocytes showed variable degrees of differentiation with differently shaped and sized cells, squamous epithelial pearls, individual keratinization, and atypical mitosis. In contrast, biopsies with atypical hyperplasia showed detached nests or irregular fragments without stroma and were made up of immature and relatively monotonous medium or small keratinocytes that were intermixed with inflammatory cells. Individual keratinization was rare, and no squamous pearls were seen. Other features of atypical hyperplasia included granulated tissue with atypical endothelial cells, nonatypical mitosis, lymphoid hyperplasia, and the absence of dysplasia or carcinoma in situ. Two biopsies showed stromal pseudoinfiltration as a result of tangential sectioning and were characterized by thick, round prongs composed of keratinocytes that penetrated regions with granulation or the inflamed tissues of esophageal ulcers., Conclusions: Atypical esophageal regenerative hyperplasia may mimic carcinoma in a small percentage of esophageal biopsies. If the histologic changes are not sufficient to establish an accurate diagnosis, medical treatment and subsequent biopsies should be performed, particularly if there are no endoscopic or radiologic data to support the presence of a neoplasm.

Context: Recently, we have observed intestinal metaplasia, atrophy, and dysplasia in the mucosa adjacent to primary gastric lymphoma (PGL) in gastrectomy specimens., Objective: To determine the frequency and type of epithelial disorders at the histopathologic level in the mucosa adjacent to PGL in endoscopic specimens., Design: We studied 54 endoscopic biopsies from patients harboring PGL. We searched for the following morphologic changes in the gastric mucosa: intestinal metaplasia; atrophy; dysplasia; epithelial erosion; and atypical regeneration of the glandular epithelium. Other nonepithelial findings such as lymphoid follicles, Helicobacter pylori, and lymphoma grade, were also recorded. For comparative purposes, 50 endoscopic biopsies with gastric adenocarcinoma and 50 biopsies with chronic gastritis associated with H pylori infection were also studied., Results: The 54 biopsies included 28 (52%) low-grade and 26 (48%) high-grade PGLs. We found intestinal metaplasia in 32 biopsies (59%), atrophy in 20 biopsies (37%), dysplasia in 2 biopsies (4%), erosion of the epithelium in 33 biopsies (61%), and atypical regenerative changes of the glandular epithelium in 10 biopsies (19%). Lymphoid follicles were found in 21 biopsies (39%), and H pylori was demonstrated in 31 biopsies (57%). When groups were compared, the frequency of epithelial changes in biopsies from patients with PGL and adenocarcinoma was similar. Intestinal metaplasia or atrophy were present in only 10% of biopsies from patients with gastritis, and dysplastic glands were not identified., Conclusions: Biopsies from patients with PGL showed chronic damage of the gastric mucosa at diagnosis, including precancerous conditions. Intestinal metaplasia and atrophy were among the most frequent disorders, but dysplasia was also occasionally present. Endoscopists and pathologists must be acquainted with such changes and look for them in the initial biopsy, as well in subsequent samples. This practice is particularly important when reviewing biopsies from patients with low-grade mucosa-associated lymphoid tissue (MALT)-lymphomas who are eligible for eradication treatment for H pylori.

Objective: To describe the morphologic characteristics of neoplastic lymphocytes with shrinkage artifact of cytoplasm secondary to formalin fixation and/or necrosis, which simulate carcinoma signet-ring cells in endoscopic biopsy., Design: Sixty-eight endoscopic biopsies with gastric lymphoma were studied retrospectively. We selected those biopsies in which artifactual signet-ring-like cells were the main histologic feature and were confused with adenocarcinoma. Mucin stains were performed on all specimens. To support their B-cell phenotype, immunohistochemical study with leukocyte common antigen (CD45), pan B-cell marker L26, keratin, and carcinoembryonic antigens were performed. The diagnosis of gastric lymphoma was confirmed in gastrectomy specimens., Setting: The distinction between poorly differentiated adenocarcinoma and gastric lymphoma in endoscopic biopsies is sometimes difficult owing to the morphologic similarities that these neoplasias can share and the small amount of tissue obtained by this technique. An additional factor that may contribute to this confusion is the presence of artifactual lymphocytes resembling signet-ring cells., Results: Three (4%) of the 68 biopsies showed artifactual lymphocytes in most or all the tissue fragments that resembled carcinoma signet-ring cells. These biopsies showed massive substitution of gastric glands by lymphomatous infiltrate. Crush artifact of neoplastic lymphocytes was observed in many fields. Necrosis, inflammation, and epithelial erosion were prominent findings. Mucin stains were negative, and immunohistochemical studies were positive for leukocyte common antigen and B-cell marker L26 in two of the three cases., Conclusions: We conclude that if a poorly differentiated neoplasm consistent with signet ring adenocarcinoma is found in an endoscopic biopsy with artifactual changes, the diagnosis of gastric lymphoma must be excluded using histochemical and immunohistochemical studies.

We describe the clinicopathologic characteristics of three patients with chronic intestinal pseudo-obstruction and malabsorption. The patients were young women (average age, 25 years) who presented with abdominal pain, nausea, vomiting, diarrhea, and weight loss that led to extreme inanition and death in two patients despite multiple treatment schemes. The evolution of the process averaged 8 years. No case manifested evidence of malignant lymphoproliferative progression. Histologically, a diffuse lymphoplasmacytic infiltrate that affected all the layers of the intestinal wall was observed in full-thickness biopsy specimens. The proliferating lymphocytes were small and mixed with mature plasma cells that proved to be polyclonal on immunohistochemical analysis. An outstanding finding in all three cases was extensive damage to submucosal and myenteric nerve plexus associated with a lymphoid infiltrate. Quantification of the myenteric plexus by using immunohistochemical and morphometric techniques also revealed a marked reduction in their number. We concluded that diffuse lymphoplasmacytic infiltration of the small intestine associated with damage to the intestinal nerve plexus constitutes a specific disorder that is different from other diseases that produce intestinal pseudo-obstruction.