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Rationale: The small intestine (SI) does not commonly harbor cancer but is occasionally involved by metastatic cancer from other organs. To manage SI cancer appropriately, surveillance for primary origin outside the SI is essential. Patient concerns: This study presents a 54-year-old Thai man diagnosed with SI obstruction which required laparoscopy- assisted partial ileal resection. Diagnoses: On the basis of the expression pattern of cytokeratins (CKs) and mucins (MUCs) in the resected SI adenocarcinoma, we suspected this was metastasized from the pancreatobiliary tract. Imaging studies revealed a hepatic segmental atrophy with an occlusion of the posterior segmental blanch of the portal vein without any contrast-enhanced lesions in the liver. Pathology of the liver biopsy revealed intrahepatic cholangiocarcinoma (ICC) with the same expression pattern of CKs and MUCs as the SI adenocarcinoma. Interventions: Systemic chemotherapy (gemcitabine and cisplatin) was initiated. Outcomes: Despite of the chemotherapy for 20 months, he died of ICC. Lessons: This is the first case of SI obstruction caused by the metastasis of ICC. We demonstrate that immunohistochemical staining of CKs and MUCs discriminate between primary and metastatic SI cancer and predict its primary origin outside the SI. This case also suggests that a hepatic segmental atrophy with portal vein occlusion would be an atypical but important finding to diagnose ICC.

A 46-year-old woman underwent upper endoscopy for evaluation of anemia, which revealed whitish granules at the duodenal papilla, diagnosed as duodenal follicular lymphoma (DFL) by biopsy. Computed tomography and abdominal ultrasonography revealed that follicular lymphoma was confined to the duodenum. Seven years after the diagnosis, fluorine-18 fluorodeoxyglucose positron emission tomography scanning revealed multiple lesions including in bone marrow and lymph nodes. Bone marrow biopsy of the right iliac bone revealed diffuse large B-cell lymphoma, indicating systemic dissemination and histologic transformation of the DFL. The patient responded to chemotherapy and has been progression-free for 2.5 years. Although DFL is usually indolent even without any treatment, systemic dissemination with histologic transformation can occur. This case suggests that the life-time follow-up that is usually done for patients with nodal follicular lymphoma should be provided to patients with DFL.

Mucinous adenocarcinoma (MC) is a unique pathological type of colorectal cancer (CRC). The development of MC is often associated with intestinal inflammation and/or microsatellite instability (MSI). Moreover, MC has clinicopathological characteristics that render making the correct diagnosis difficult such as extramural progression. Meanwhile, intestinal spirochetosis (IS) is a condition in which colonic epithelial cells are colonized and/or infected by spirochetes. Intestinal inflammation due to IS occurs by the destruction of colonic microvilli and induces chronic diarrhea. Recently, it was reported that the prevalence of IS tended to be high in patients with sessile serrated adenomas/polyps, the precursor of MSI-high CRC including MC. This study presents a case of MC in the setting of intestinal inflammation due to IS and tries to clarify the cause of MC development by performing immunohistochemical stain of resected specimen for DNA mismatch repair (MMR) proteins. This patient is a 63-year-old man with no symptoms who had a positive fecal occult blood test. Subsequent endoscopic findings and biopsy results revealed intestinal stricture of the transverse colon and chronic infective colitis associated with IS. Metronidazole therapy was initiated but was not effective. Although follow-up colonoscopy was performed repeatedly, intestinal perforation occurred 20 months later. Subtotal colectomy and ileostomy were performed. Pathological examination of resected specimens revealed MC with normal expression of MMR proteins, including MLH1, MSH2, MSH6, and PMS2. The histopathological classification was Union for International Cancer Control (UICC) IIIB and adjuvant chemotherapy was initiated. This is an interesting case of MC developing in the setting of chronic colitis associated with IS. It seemed that the cause of MC development was not MSI but intestinal inflammation. Besides, endoscopic diagnosis of MC in this case was difficult because of the extramural progression and lack of obvious atypical colonic glands in biopsy specimens. This report provides evidence for an association between neoplasm and IS-induced intestinal inflammation. Moreover, we suggest that making the diagnosis of MC could be difficult because of its unique clinicopathological characteristics.