Hemorrhagic duodenal lipoma managed by endoscopic resection.

The patient, an 81-year-old woman, was admitted to our hospital for a detailed examination; the chief complaint being melena. An upper gastrointestinal roentgenologic study revealed a submucosal tumor with a smooth surface and a stalk measuring 50 mm at the third part of the duodenum. Endoscopy depicted it as a yellowish submucosal tumor. Based on computed tomography and fluoroscopy of the small intestine, a diagnosis of duodenal lipoma was made. The esophagus, stomach, and the small and large intestines were free of lesions so the duodenal lipoma was judged to be the hemorrhagic source. The tumor was endoscopically polypectomized using a 2-channel scope. The excised specimen, measuring 50 x 20 x 20 mm, was covered by a normal duodenal mucosa with small ulcers in part. Photomicrographic findings included a tumor that was composed of mature adipose tissue in the submucosa, which coincided with a diagnosis of lipoma. Small ulcers had formed in part, exposing vessels, thus indicating the cause for hemorrhage. Lipoma is a benign tumor; and if the lesion is found to be pedunculated and an endoscope can reach it for treatment, minimally invasive endoscopic procedures should be selected.

Splenic large B-cell lymphoma in patients with hepatitis C virus infection.

Hepatitis virus infection, especially type C (hepatitis C virus [HCV]), has been suggested to be one of the important pathogenetic factors for low- and high-grade B-cell lymphoma, including splenic marginal zone lymphoma (SMZL), in southern Europe. Here, we analyzed the incidences of HCV and hepatitis B virus (HBV) infections, and the clinicopathologic features in 29 cases of splenic diffuse large B-cell lymphoma (DLBCL), 10 SMZL, 3 splenic mantle cell lymphoma, 1 hairy cell leukemia, 13 B-chronic lymphocytic leukemia, and 12 hepatosplenic T-cell and natural killer cell lymphoma. Fifteen (51.7%) splenic DLBCL cases were HCV antibody-positive, and another 6 (20.7%) had the HBsAg. The incidence of each was significantly (P < .01) higher than those of HCV (9.3%) and HBV (1.9%) infections in 54 node-based DLBCL cases. Four examined HCV-positive DLBCL cases showed no type II cryoglobulinemia. HCV RNA was detected in fresh tumor tissues from 6 of 7 examined DLBCL cases, and HBV DNA was present in another 2, as evaluated by real-time polymerase chain reaction. Immunohistologically, tumor cells in 5 of 7 examined DLBCL cases showed intracytoplasmic reactions for HCV NS3 and E2 proteins and the viral receptor CD81. Of 6 cases, 2 showed an intranuclear reaction for the HBV surface protein. By Southern blot analysis, no rearrangement of the Bcl2 gene was detected in the tumor tissue of 7 HCV-positive DLBCL cases. For the other types of malignant lymphoma, 1 case each of SMZL (10%) and hepatosplenic T-cell and natural killer cell lymphoma (8.3%) showed HCV infection. In conclusion, persistent human hepatitis virus infections, especially HCV, may play an important role in the tumorigenesis of splenic DLBCL in Japan.