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Gastric-Type Mixed Neoplastic and Non-Neoplastic Lesions in the Duodenal Bulb: A Case Supporting the Metaplasia–Neoplasia Sequence
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Gastric-Type Mixed Neoplastic and Non-Neoplastic Lesions in the Duodenal Bulb: A Case Supporting the Metaplasia–Neoplasia Sequence
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Gastric-Type Mixed Neoplastic and Non-Neoplastic Lesions in the Duodenal Bulb: A Case Supporting the Metaplasia–Neoplasia Sequence
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Journal Article
Gastric-Type Mixed Neoplastic and Non-Neoplastic Lesions in the Duodenal Bulb: A Case Supporting the Metaplasia–Neoplasia Sequence
2026
Overview
Gastric-type lesions in the duodenum, including pyloric gland adenoma and gastric foveolar metaplasia, have been increasingly recognized for their unique histogenesis and potential link through the metaplasia–neoplasia sequence. However, the coexistence of neoplastic and non-neoplastic gastric-type lesions within the same histological section has not been previously reported. Here, we present a case of a 73-year-old Japanese woman who underwent endoscopic submucosal dissection for a 34 × 20 mm elevated lesion in the duodenal bulb. Based on the preoperative biopsy results, pyloric gland adenoma was diagnosed; however, histopathological examination of the resected specimen revealed a far more complex picture. The main lesion consisted of two contiguous components: a hyperplastic polyp with gastric foveolar-type phenotype (Lesion I) and a pyloric gland adenoma mixed with gastric foveolar-type hyperplastic polyp (Lesion II). Importantly, the transitional zone between these components demonstrated histological continuity, with areas showing admixture of hyperplastic and adenomatous features within the same microscopic field. A separate hyperplastic polyp with gastric foveolar-type phenotype (Lesion III) was also identified, separated from Lesions I and II by intervening normal duodenal mucosa. All lesions shared a gastric-type mucin phenotype (MUC5AC-positive, CD10-negative), and extensive Brunner’s gland hyperplasia was observed throughout the specimen. This case provides compelling morphological evidence for a histogenetic link between non-neoplastic gastric-type hyperplasia and pyloric gland adenoma, supporting the concept of a metaplasia–neoplasia sequence in the duodenum. Furthermore, the presence of an additional separate lesion with the same phenotype suggests a field change in the development of gastric-type lesions.
