Treatment with anti-interleukin-6 receptor antibody ameliorates intestinal polyposis in Apc(Min/+) mice under high-fat diet conditions.

The prevalence of colorectal malignancies is increasing in the world. The parallel increase of metabolic syndrome gives a speculation between these two conditions, although the precise mechanism is still unclear. Interleukin-6 (IL-6) is a cytokine known to correlate with obesity and serve as a proinflammatory adipokine. In the present study, we investigated the effect of IL-6 signaling blockade on intestinal polyp formation in obesity using a mouse model of adenomatous polyposis coli (Apc). Male C57BL/6J-Apc(Min/+) mice were fed a high-fat diet from 5 weeks of age, and the overweight mice thus obtained were given a weekly intraperitoneal injection of anti-mouse IL-6 receptor antibody (MR16-1) from 6 to 15 weeks of age, while control mice received IgG or phosphate-buffered saline (PBS). The total number of intestinal polyps was significantly decreased in the MR16-1-injected group (53.1 ± 6.8) relative to the control groups (PBS-injected, 81.3 ± 6.1; rat IgG-injected, 74.7 ± 4.8, p = 0.01), and in particular the number of polyps larger than 2 mm in diameter was markedly decreased. In addition, the mean diameter of polyps in the MR16-1-injected group was significantly smaller than that in the control groups. On the other hand, no significant differences in body weight, epididymal fat pad mass, or the plasma levels of glucose, insulin and triglyceride were observed among the three groups. Thus, treatment with anti-IL-6 receptor antibody suppressed polyp growth in obese Apc(Min/+) mice fed the high-fat diet. We suggest that IL-6 signaling may be responsible for the obesity-associated colorectal tumorigenesis.

Esophageal carcinoid tumor treated by endoscopic resection.

The present report describes a rare case of esophageal carcinoid tumor that was treated by endoscopic resection. A 43-year-old woman underwent esophagogastroduodenoscopy at her family clinic for screening of the upper digestive tract and a small lesion resembling a submucosal tumor was detected in the lower esophagus. A biopsy sample from the lesion was diagnosed as esophageal carcinoid tumor and the patient visited our hospital for detailed examination. The tumor was approximately 3 mm in diameter and its surface appeared to be covered with normal squamous epithelium. The tumor had a shiny reddish surface without ulceration or erosion. Magnifying endoscopy with narrow-band imaging showed structures resembling reticular vessels under the epithelium. Endoscopic ultrasonography depicted the tumor as a low-echoic mass within the lamina propria. Computed tomography did not detect the tumor and no metastatic lesions were evident in other organs. With the patient's informed consent, the tumor was resected using endoscopic submucosal dissection, with a sufficient free margin in both the vertical and horizontal directions. Magnifying endoscopic examination showed the resected tumor to have abundant reticular vessels. Finally, the tumor was diagnosed immunopathologically as an esophageal carcinoid tumor (neuroendocrine cell tumor, grade 1), without lymphatic or vascular invasion.

[Characteristics of group A patients according to the ABC classification for gastric cancer risk screening].

In the ABC classification for gastric cancer risk screening, group A (Helicobacter pylori infection-negative, pepsinogen [PG]-negative) patients are assumed to be at low risk, but some patients do have atrophic gastritis and H. pylori infection. This study aimed to identify the characteristics of group A patients. Healthy adults in Yamagata City who underwent barium radiography and ABC classification participated in the survey. Patient radiographs were randomly interspersed and reviewed by two gastroenterologists who were blinded to the H. pylori and PG statuses. Group A patients (n=1462) was subclassified as follows: atrophic gastritis group, 21.5%; intermediate group, 15.7%; and no atrophic gastritis group, 62.8%. Elderly subjects and those with H. pylori antibody titers of 3.0-9.9U/ml should be carefully evaluated while interpreting the results of the ABC classification for gastric cancer risk screening.

[A case of metastatic colorectal cancer with hyperammonemic encephalopathy induced by 5-FU in a patient continuously treated with XELOX therapy].

We report a rare case of a patient with metastatic colorectal cancer who experienced hyperammonemic encephalopathy induced by 5 -fluorouracil(5-FU)and was continuously treated with capecitabine plus oxaliplatin(XELOX)therapy. A 60 years man with anorexia and weight loss was diagnosed with Stage IV rectal cancer, and chemotherapy with XELOX was initiated. When the second course of XELOX therapy was administered, the patient found it difficult to take oral capecitabine. Subsequently, modified FOLFOX6 was administered. Complications such as nausea and vomiting were observed on day 2, with confusion and cognitive disturbances on day 3 . Laboratory examination revealed hyperammonemia, and therefore, branched-chain amino acid solutions were administered as treatment. The patient's symptoms disappeared entirely on day 4. He is currently receiving XELOX therapy.

[Chylothorax in a patient with advanced gastric cancer and mediastinal lymph node metastasis causing thoracic duct obstruction].

We report the case of a 61-year-old female with advanced gastric cancer and mediastinal lymph node metastasis who developed chylothorax. The patient presented with cough, dyspnea and pain in the left lower limb, back, and hips. Her lower limb symptoms were attributed to cellulitis. Computed tomography revealed right-sided pleural effusion, multiple lymph node swelling, and thickening of the gastric wall. Following pleural aspiration, the effusion was identified to be chyle. Cytopathologically, numerous adenocarcinoma cells were detected in clumps, and subsequent esophagogastroduodenoscopy revealed type 3 gastric cancer. We diagnosed multiple lymph node metastases with pleural dissemination. Chemotherapy was administered; however, she eventually succumbed to disease progression. We suspected that the chylothorax resulted from the mediastinal lymph node metastasis that caused thoracic duct obstruction.

[Successful management with partial splenic embolization (PSE) of splenomegaly and thrombocytopenia caused by oxaliplatin-based chemotherapy for advanced colorectal cancer].

We report here two cases of advanced colorectal cancer which received chemotherapy, in which partial splenic embolization (PSE) had been effective for controlling splenomegaly and thrombocytopenia. Case 1: A 50-year-old man presented with bloody urine and bloody stool. Computed tomography (CT) showed rectosigmoid cancer with urinary bladder invasion. He underwent colostomy and received chemotherapy. After 3 courses of FOLFOX and 6 courses of bevacizumab/FOLFOX, he suffered from thrombocytopenia with splenomegaly, which led to discontinuation of the therapy. PSE improved thrombocyte counts and enabled him to resume therapy. Case 2: A 72-year-old man presented with bloody stool. Endoscopy and CT showed an advanced rectosigmoid cancer with multiple liver metastases. He underwent low anterior resection and received chemotherapy with FOLFOX and FOLFIRI, together with bevacizumab. After 13 courses of chemotherapy, he also suffered from splenomegaly and thrombocytopenia. PSE produced an increase in thrombocyte count and allowed for a restart of chemotherapy. Oxaliplatin-based chemotherapy may possibly produce hepatic sinusoidal dilation and induce splenomegaly owing to portal hypertension. PSE seemed to be useful for treating thrombocytopenia with splenomagaly, and allowed continuation of the chemotherapy.

[An autopsy case of retroperitoneal paraganglioma that had presented with pheochromocytoma multisystem crisis].

A 40's woman was seen at the emergency room because of severe back pain and vomiting. Abdominal CT scan revealed a tumor about 7cm in diameter located on the retroperitoneum. For 6 hours after admission, her body temperature was 39°C and respiratory failure occurred. After 30 hours, the patient died because of a complication in circulatory failure. From the abnormally high level of catecholamines in the blood and autopsy results, we determined that pheochromocytoma multisystem crisis had been caused by the retroperitoneal paraganglioma.

[Endoscopic pancreatic stenting was effective in a case of pancreatic duct disruption and leakage due to pancreatic cancer].

A 79-year-old man was admitted on the suspicion of acute pancreatitis. Computed tomography showed acute fluid collection but not typical acute pancreatitis; it formed pseudocysts gradually around the pancreas. Endoscopic retrograde pancreatography (ERP) revealed pancreatic disruption and leakage. Endoscopic nasopancreatic drainage (ENPD) and endoscopic pancreatic stenting (EPS) resulted in collapse of pseudocysts, improvement of symptoms and laboratory data, and a mass in the pancreatic body became distinct. The specimens obtained with endoscopic ultrasound-guided fine-needle aspiration biopsy (EUS-FNA) showed pancreatic cancer. In conclusion, ENPD and EPS are effective for pancreatic leakage with disruption of the pancreatic duct, and we should take into consideration the possibility of pancreatic cancer when we see patients with pancreatic disruption.

Effect of Cellulose Acetate Beads on the Release of Transforming Growth Factor-ß.

Transforming growth factor-ß (TGF-ß) is released by activated platelets and induces the differentiation of T-helper 17 from naïve T cells. Contact between blood and cellulose acetate (CA) beads induces cytokine release, although their inflammatory effects on TGF-ß release are unclear. We aimed to clarify the effect of CA beads on the release of TGF-ß in vitro. We incubated peripheral blood with and without CA beads and measured platelets and TGF-ß. Compared with blood samples incubated without beads, the platelet count and amount of TGF-ß significantly decreased in blood samples incubated with CA beads. In conclusion, CA beads inhibited the release of TGF-ß from adsorbed platelets. The biological effects of this reduction of TGF-ß release during platelet adsorption to CA beads need further clarification.

Characteristics of Small Bowel Polyps Detected in Cowden Syndrome by Capsule Endoscopy.

Cowden syndrome is an uncommon, autosomal dominant disease characterized by multiple hamartomas and hyperplastic lesions in the skin, mucous membrane, brain, breast, thyroid, and gastrointestinal tract. About 30% of Cowden syndrome cases are reportedly complicated by malignant diseases. Hamartomatous polyps occur throughout the gastrointestinal tract, the most common sites being the stomach, colon, esophagus, and duodenum. Small bowel polyps can occur in Cowden syndrome; however, they are difficult to detect by conventional examination, including double-contrast X-ray study. Here, we report three cases of Cowden syndrome with small bowel polyps, which were detected by capsule endoscopy. The small bowel polyps of Cowden syndrome frequently occur at the oral end of the small bowel, especially in the duodenum and jejunum, and their color is similar to that of the surrounding mucosa; additionally, the polyps are relatively small (2-5 mm). Capsule endoscopy is useful for detecting small bowel polyps in Cowden syndrome.