Endoscopic management of non-ampullary duodenal adenomas

Duodenal polyps are found in 0.1 % to 0.8 % of all upper endoscopies. Duodenal adenomas account for 10 % to 20 % of these lesions. They can be sporadic or occur in the setting of a hereditary predisposition syndrome, mainly familial adenomatous polyposis. Endoscopy is the cornerstone of management of duodenal adenomas, allowing for diagnosis and treatment, primarily by endoscopic mucosal resection. The endoscopic treatment of duodenal adenomas has a high morbidity, reaching 15 % in a prospective study, consisting of bleeding and perforations, and should therefore be performed in expert centers. The local recurrence rate ranges from 9 % to 37 %, and is maximal for piecemeal resections of lesions > 20 mm. Surgical resection of the duodenum is flawed with major morbidity and considered a rescue procedure in cases of endoscopic treatment failures or severe endoscopic complications such as duodenal perforations. In this paper, we review the existing evidence on endoscopic diagnosis and treatment of non-ampullary duodenal adenomas.

Carbonic Anhydrases II and IX in Non-ampullary Duodenal Adenomas and Adenocarcinoma

Non-ampullary duodenal adenocarcinoma (DAC) is a rare malignancy. Little information is available concerning the histopathological prognostic factors associated with DAC. Carbonic anhydrases (CAs) are metalloenzymes catalyzing the universal reaction of CO2 hydration. Isozymes CAII, CAIX, and CAXII are associated with prognosis in various cancers. Our aim was to analyze the immunohistochemical expressions of CAII, CAIX, and CAXII in normal duodenal epithelium, duodenal adenomas, and adenocarcinoma and their associations with clinicopathological variables and survival. Our retrospective study included all 27 DACs treated in Oulu University Hospital during years 2000–2020. For comparison, samples of 42 non-ampullary adenomas were collected. CAII expression was low in duodenal adenomas and adenocarcinoma. CAIX expression in adenomas and adenocarcinoma was comparable with the high expression of normal duodenal crypts. Expression patterns in carcinomas were largely not related to clinicopathological features. However, low expression of CAII associated with poorer differentiation of the tumor ( p=0.049) and low expression of CAIX showed a trend for association with nodal spread, although statistical significance was not reached ( p=0.091). CAII and CAIX lost their epithelial polarization and staining intensity in adenomas. CAXII expression was not detected in the studied samples. CAs were not associated with survival. The prognostic value of CAII and CAIX downregulation should be further investigated. Both isozymes may serve as biomarkers of epithelial dysplasia in the duodenum. (J Histochem Cytochem XX: XXX–XXX, XXXX)

Feline pyloric and duodenal adenoma: A histological and immunohistochemical study

Although pyloric and duodenal adenomas occasionally occur in cats, limited information is currently available on their phenotypes and molecular features. The present study investigated the pathological features of these tumors and the mechanisms underlying their tumorigenesis. Biopsy samples from 8 cats diagnosed with pyloric or duodenal adenomas were examined by histopathology and immunohistochemistry. Normal pyloric and duodenal tissues of cats were assessed for comparison. All cases showed a papillary growth of cuboidal to columnar cells with eosinophilic, ground-glass cytoplasm. Mucin in tumor cells was positive for periodic acid–Schiff and paradoxical concanavalin-A staining, but was negative for Alcian blue. Immunohistochemically, tumor cells were positive for cytokeratin (CK) 19 in 8/8 cases and for CK20 in 5/8 cases, and weakly positive for CD10 in 4/8 cases, CK7 in 3/8 cases, and β-catenin in 2/8 cases. Nuclear accumulation of p53 was not detected in any case. DNA sequencing analysis identified no KRAS or GNAS mutations in the 4/8 cases and 5/8 cases for which the KRAS and GNAS genes could be amplified. The histological and immunohistochemical features of tumor cells were similar to those of mucous neck cells and the pyloric gland of normal feline tissue. The morphology of feline pyloric and duodenal adenomas was consistent with that of pyloric gland adenoma in humans; however, its molecular pathogenesis may differ given the lack of KRAS and GNAS mutations in the feline tumors.