Endoscopic submucosal dissection to relieve a flexure of the gastric conduit after esophagectomy.

Background and study aims A 70-year-old-man underwent an esophagectomy and posterior mediastinal reconstruction for esophageal cancer that was curatively resected. Although the patient was allowed to eat after surgery, he repeatedly vomited after drinking water or eating meals and required continuous hospitalization. An upper gastrointestinal series and endoscopic examination revealed an obstruction due to the flexure of the gastric conduit, which was repeatedly treated with endoscopic balloon dilation. Endoscopic balloon dilation was completely ineffective, however, because the obstruction was not due to a small lumen diameter, but rather to severe flexure. We hypothesized that the power of contraction provided by ulcer scar formation after mucosal resection could straighten the flexure, and thus removed a piece of the mucosa 8 cm in diameter on the oral side of the flexure by endoscopic submucosal dissection (ESD) 4 months after the esophagectomy. Endoscopic examination on post-ESD Day 10 revealed that the gastric conduit flexure was straightened due to ulcer scarring, and obstruction at the flexure opened over time. Meals were restarted and the patient could eat without vomiting. He was discharged from the hospital 5 weeks after ESD. This is the first case report of obstruction due to flexure of the gastric conduit after esophagectomy that was successfully treated with mucosectomy using ESD. Mucosectomy using ESD may be an effective treatment option for obstruction due to flexure of the gastric conduit after esophagectomy.

A well-differentiated early gastric cancer in a patient confirmed negative for Helicobacter pylori.

A woman in her 70s was an outpatient at our hospital. Esophagogastroduodenoscopy revealed a slightly elevated lesion with erosion, 10mm in diameter, located at the greater curvature of the antrum. Helicobacter pylori testing yielded negative results, and there was no atrophy of the gastric mucosa. Biopsy revealed a well-differentiated tubular adenocarcinoma. Complete en bloc resection was performed via endoscopic submucosal dissection, in accordance with the current Japanese guidelines. The gastric adenocarcinoma of the fundic gland type and coexisting with a hyperplastic or fundic gland polyp was negative according to the histological examination.

An early gastric cancer concurrent with a hyperplastic polyp in a patient confirmed negative for Helicobacter pylori.

A 58-year-old man was suspected of having a gastric polyp based on an upper gastrointestinal series. Esophagogastroduodenoscopy showed a gastric polyp, approximately 7mm in diameter, located at the greater curvature of the upper gastric body. Helicobacter pylori testing yielded negative results, and there was no atrophy of the gastric mucosa. Biopsy revealed a well differentiated tubular adenocarcinoma (Group 5). Endoscopic submucosal biopsies were performed, and histopathology revealed a well differentiated tubular adenocarcinoma coexisting with a hyperplastic polyp. Complete en bloc resection was performed, in accordance with the current Japanese guidelines.

[Resected Focal Nodular Hyperplasia That Was Difficult to Differentiate from Hepatocellular Carcinoma--A Case Report].

We report a case of a 62-year-old woman with a growing liver tumor that was difficult to differentiate from hepatocellular carcinoma (HCC). Abdominal CT revealed a hypervascular tumor (36 mm in diameter) in segment 3 of the liver that showed early enhancement and which had grown from 30 mm to 36 mm over the previous year. A fatty liver and gallstones were also detected. Magnetic resonance imaging (MRI) showed high intensity staining of the tumor on both T1- and T2-weighted images, and EOB-MRI revealed a mass that showed high signal intensity in the hepatobiliary phase. The imaging findings were not typical for HCC; however, the possibility of malignancy could not be ruled out due to the enlargement of the mass. Therefore, in February 2015, we performed a laparoscopic left lateral segmentectomy with cholecystectomy. After a good postoperative course, the patient was discharged from the hospital 11 days after surgery. Histological assessment revealed the tumor was focal nodular hyperplasia (FNH).

Cimetidine reduces impairment of cellular immunity after transcatheter arterial embolization in patients with hepatocellular carcinoma.

BACKGROUND/AIMS: Natural killer cells have an intrinsic ability to recognize and attack some tumor cells and infected cells. Natural killer cell cytotoxicity is depressed in patients with hepatocellular carcinoma. In particular, cell-mediated immunity is impaired after transcatheter arterial embolization, which is an effective therapy for hepatocellular carcinoma. There have been reports that cimetidine can activate cellular immunity and increase the survival time in patients with some cancers. Therefore, we investigated whether cimetidine could improve cellular immunity after transcatheter arterial embolization, especially in relation to natural killer activity. METHODOLOGY: Thirty-four patients with hepatocellular carcinoma and cirrhosis who underwent transcatheter arterial embolization at our hospital were studied prospectively after giving informed consent. The patients were divided into three groups. In group A, 14 patients were administered 800 mg of cimetidine a day. In group-B, 13 patients were administered 40 mg of famotidine or 300 mg of nizatidine a day. In group-C 7 patients did not receive histamine 2 receptor antagonists. Natural killer cell activity in peripheral blood was measured before transcatheter arterial embolization and on days 1 and 7. RESULTS: The % natural killer cell activity on day 1 was 74 in group A, 52 in group B, and 52 in group. The % activity on day 7 was 98 in group A, 71 in group B, and 82 in group C. Cimetidine group showed the significant higher % natural killer cell activity on day 1 (p = 0.032). CONCLUSIONS: Our study raises the possibility that cimetidine has the effect to preserve cell-mediated immune response during transcatheter arterial embolization.