A case of intraductal papillary mucinous neoplasm with high serum pepsinogen II level.

We report the case of a 65-year-old woman who had a high level of serum pepsinogen II. Several months earlier, she had found a mass on the right side of her upper abdomen. Esophagogastroduodenoscopy did not reveal atrophic or inflammatory findings. She had not taken proton pump inhibitors, and there was no indication of renal dysfunction. Imaging tests showed a mass of approximately 80mm in the pancreatic head. We performed pancreatoduodenectomy, and the histopathological examination revealed an intraductal papillary mucinous neoplasm (IPMN) of gastric type. Serum pepsinogen II levels substantially lowered after surgery. To the best of our knowledge, this is the first report on a relationship between IPMN and serum pepsinogen II.

Marked decrease in serum pepsinogen II levels resulting from endoscopic resection of a large duodenal tumor.

Studies have indicated that serum pepsinogen (PG) levels are not only markers for chronic atrophic gastritis but also predictive risk factors for gastric cancer. However, serum PG levels can change because of pathological conditions other than gastritis. We report the first case in which abnormally high serum PG II levels (168.8 ng/mL) led to the discovery of a large tumor covering a wide area in the duodenum, and after resection of the tumor, the serum PG II levels markedly decreased. Because endoscopic and histopathological examinations showed no indications of atrophic changes, inflammation of the gastric mucosa, or Helicobacter pylori infection, the serum PG II levels eventually returned to normal (10.1 ng/mL). The preoperative abnormally high PG II levels were probably caused by the large duodenal tumor that prevented PG II (which is produced by the duodenal Brunner's glands) from being secreted into the lumen, a condition that increased the amount transferred to the bloodstream. No previous reports have investigated serum PG II levels before and after resection of a large duodenal tumor. We believe this case provides valuable insight regarding the dynamics of PG II in the body and has important diagnostic implications.

[Primary adenosquamous carcinoma of the liver presenting with hematochezia due to tumor invasion of the colon].

A 69-year-old female was referred to our hospital with hematochezia. Dynamic computed tomography demonstrated a large tumor with rim enhancement and central necrosis that invaded into the transverse colon. The tumor was resected, and histopathological examination revealed mixed adenocarcinoma and squamous cell carcinoma with partial abscess formation. On the basis of a literature review and the findings from the present case, rim enhancement with central necrosis on imaging appears to be characteristic of this disease.

Scirrhous colonic metastasis from lobular carcinoma of breast.

A 68-year-old woman presented complaining of 2 months vague abdominal fullness and constipation. She had a history of surgery 5 years ago for invasive lobular carcinoma of the left breast. She had good appetite without any severe symptoms such as vomiting, diarrhea, or hematochezia. No abnormal subcutaneous lymph nodes were detected, and blood tests showed no abnormalities including serum tumor markers. Whole-body computed tomography and bone scintigraphy revealed no tumor recurrences. However, endoscopic findings demonstrated a smooth stenotic lesion with submucosal thickening in the transverse colon, but the colonic mucous membrane was grossly normal. The 3-cm-long stenotic lesion was confirmed by colon imaging using water-soluble contrast medium. A biopsy specimen revealed diffuse infiltration of noncohesive malignant cells with round, atypical nuclei from lamina propria to subserosa. Taken together with immunohistochemistry, a diagnosis of metastatic lobular carcinoma from the breast was made, and transverse segmentectomy was done. Colonic metastasis of breast cancer should be included as a differential diagnosis of any abdominal symptoms, even though mild, when patients have a present or previous history of breast cancer.

Usefulness of endoscopic treatment for duodenal adenoma.

In recent years, due to the increasing prevalence of upper gastrointestinal endoscopy, there have been an increasing number of reports on duodenal adenoma and early stage cancer. However, endoscopic techniques for the resection of duodenal adenomas are difficult, due to the anatomical features of the duodenum, and the long distance to the lesion. There have only been a few reports on the use of endoscopic techniques for duodenal adenomas compared to those focused on the stomach and large intestine. For duodenal adenomas, we used a conventional endoscope for lesions proximal to the major duodenal papilla, and a short-type double balloon endoscope for lesions distal to the papilla. The en-bloc resection rate was 93.8%. There was only one case of microperforation. Endoscopic manipulation is considered difficult in the deep areas of the duodenum, but double balloon endoscopy enabled stable manipulation and successful resection of the tumor in the majority of cases.

Molecular analysis of single isolated glands in gastric cancers and their surrounding gastric intestinal metaplastic mucosa.

The biological properties and underlying genetics of gastric cancer and gastric intestinal metaplasia evolve with neoplastic progression from the genetics of the original gland cell. PCR assay with crypt isolation was used in tumors from 20 patients to examine microsatellite alterations (allelic imbalance at 17p, 5q, 18q, 3p, 4p, and 9p, and microsatellite instability) in glands from each tumor and from intestinal metaplastic lesions. Tumor specimens were processed as either pooled-gland samples or single-gland samples. Pooled gland sample was composed of 10-20 tumor glands, intestinal metaplastic glands, or nonmetaplastic glands. Single gland sample was 10 tumor glands from tumor and single gland sample was 5 gastric intestinal metaplastic and 5 nonmetaplastic glands from its surrounding metaplastic mucosa. Multiple genetic alterations were found in individual tumor glands, with various subclonal expansions seen within the same tumor. Although microsatellite instability was found in 2 of 20 tumor single-gland samples, none was detected in metaplastic single-gland samples. Most cancers appear to have a heterogeneous composition. On the other hand, microsatellite alterations were also detected within the nonmetaplastic as well as intestinal metaplastic single-gland samples. In conclusion, the present data on tumor and corresponding intestinal metaplastic and nonmetaplastic glands suggest that genetic alterations already occur within the surrounding of the noncancerous mucosa.