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Case Reports
. 2025 Jun 1;64(11):1684-1690.
doi: 10.2169/internalmedicine.4004-24. Epub 2024 Nov 8.

Duodenal Adenocarcinoma with a Gastric Phenotype Demonstrating a Rapidly Progressive Course

Affiliations
Case Reports

Duodenal Adenocarcinoma with a Gastric Phenotype Demonstrating a Rapidly Progressive Course

Sho Matsuyama et al. Intern Med. .

Abstract

We herein report a rare case of duodenal adenocarcinoma with a rapidly progressive course. Esophagogastroduodenoscopy revealed Brunner's gland hyperplasia in the bulbs of the duodenum three years prior to this presentation. Two years earlier, gastric foveolar metaplasia had been observed in the bulbs. One year earlier, the lesion had increased slightly in size. At this time, the lesion had markedly increased in size, and the duodenum was circumferentially stenotic due to the mass. Pathologically, he was diagnosed with duodenal adenocarcinoma with a gastric-dominant immunophenotype and he died two months later. Although extremely rare, we should keep in mind that duodenal tumors with a gastric phenotype may sometimes progress rapidly within a short period of time.

Keywords: Brunner's glands; MUC5AC; MUC6; duodenal adenocarcinoma with a gastric phenotype; gastric foveolar metaplasia; gastric-type duodenal adenocarcinoma.

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Conflict of interest statement

The authors state that they have no Conflict of Interest (COI).

Figures

Figure 1.
Figure 1.
EGD images. Three years previously, multiple erythematous flat-elevated lesions were observed in the bulbs of the duodenum and were diagnosed as Brunner’s gland hyperplasia (a). Two years prior, EGD showed a 15 mm erythematous elevated lesion in the duodenal bulb (b). One year before, EGD showed that the lesion had slightly increased in size and that erythematous change had slightly increased (c).
Figure 2.
Figure 2.
Hematoxylin and Eosin (H&E) staining and immunostaining of Ki-67 for a biopsy specimen from the duodenal lesion (two years before). H&E staining revealed gastric foveolar metaplasia with a serrated pattern and mild disruption of cell polarity, which was considered to be reactive change [a, c (blue arrows)]. Ki-67 positive cells were not observed in the area of reactive change [b, d (blue arrows)].
Figure 3.
Figure 3.
CT image and EGD images. CT showing gastroduodenal obstruction due to a duodenal mass (a, yellow arrowheads). The duodenal mass is drastically enlarged and protrudes from the pyloric ring into the antral stomach (b). NBI showed expansion of the intervening part between the crypts and a gyrus-like surface pattern (c). The duodenum is circumferentially stenotic from the bulbs to the superior duodenal angle due to the mass (d, e).
Figure 4.
Figure 4.
Hematoxylin and Eosin staining of the biopsy specimen. Biopsy specimens revealed the tumor to be adenocarcinoma due to the proliferation of glandular structures with a papillary pattern and nuclear atypia in the deeper section (a, c), and that contiguous glandular structures with mucin were Brunner’s glands (b, d).
Figure 5.
Figure 5.
Immunostaining of the biopsy specimen. Immunostaining showed a high ratio of Ki-67 positive cells of the tumor cells. Immunostaining also showed positive staining for MUC5AC, MUC6, and CDX2, and negative staining for MUC2 and CD10 in the tumor cells.
Figure 6.
Figure 6.
PET-CT images. PET-CT revealed the accumulation of fluorodeoxyglucose in the duodenal mass (a), peritoneal dissemination (b, d), and left supraclavicular fossa lymph node metastasis (c).
Figure 7.
Figure 7.
The possible origin of duodenal adenocarcinoma with the gastric-dominant immunophenotype in our case.

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