Endoscopically proven case of rapid esophagogastric variceal progression and rupture as a result of portal hypertension with liver sarcoidosis.

Sarcoidosis is a multi-systemic disease of unknown etiology that results in the development of non-caseating epithelioid granulomas. The liver is the third most frequently involved organ after the lymph nodes and the lungs. Most cases of liver sarcoidosis do not present with symptoms and involve minimal liver dysfunction, but some cases display progression to portal hypertension and liver cirrhosis, and finally to liver failure. The mechanism and the risk of progression in liver sarcoidosis are still unknown because of the diagnostic difficulty associated with this condition, and because follow-up examinations can only be done in an invasive manner. Here, we present an informative case of liver sarcoidosis with rapid progression of esophagogastric varices. Four months prior to the definitive diagnosis, no signs of varices were observed on endoscopy, and developmentof esophagogastric varices, rapid progression, and eventual rupture occurred in a short period of time. A liver biopsy, carried out after endoscopic sclerotherapy, revealed that granulomas primarily affected the portal area without fibrotic and cirrhotic changes, which is considered a primary cause of portal hypertension and esophagogastric varices. Following the liver biopsy, the patient was given systemic steroids and is currently receiving outpatient care. Thus, we should consider the possibility that liver sarcoidosis, even in the absence of cirrhotic changes, can cause serious events such as esophagogastric variceal rupture following rapid progression as a result of portal hypertension.

Esophageal Adenocarcinoma Developing after Eradication of Helicobacter pylori.

A 75-year-old man underwent endoscopic hemostatic therapy for hemorrhagic gastric ulcer in September 2002. After healing of the gastric ulcer, he underwent Helicobacter pylori eradication therapy in February 2003. In August 2007, an irregular tumor was detected in the lower esophagus at annual checkup for gastric cancer screening using X-ray. Endoscopic examination showed that the lower margin of the tumor almost coincided with the esophagogastric junction and that a short segment of Barrett's epithelium existed near the tumor. Biopsies of the tumor showed moderately to poorly differentiated adenocarcinoma. Mild reflux esophagitis and minor hiatal hernia was also observed, and the previously treated gastric ulcer was not recurrent. Absence of H. pylori was confirmed by serum antibody and urea breath test. Surgical resection of the lower esophagus and proximal stomach was performed. The tumor invaded into the muscularis propria of the esophageal wall but had no evidence of lymph node metastasis. Based on macroscopic and pathological findings, the tumor was recognized as esophageal adenocarcinoma. Previous endoscopic examination did not detect any apparent signs of tumor in the esophagogastric junction. As far as we know, this is the first report documenting a newly developed esophageal adenocarcinoma after the successful eradication of H. pylori.

[A case of gastrointestinal stromal tumor of the stomach arising from the muscularis mucosae].

A 75-year-old man, in whom upper gastrointestinal endoscopy revealed a submucosal tumor in the greater curvature of the gastric angle, was hospitalized for further investigations. Since the tumor was shown to be located in the submucosal layer by endoscopic ultrasonography, we performed endoscopic mucosal resection. Pathological studies of the resected specimen revealed a gastrointestinal stromal tumor of the stomach. It was also formed that the tumor was connected not to muscularis propria, but to the muscularis mucosae. There has been no previous report about a case of gastrointestinal stromal tumor of the stomach arising from the muscularis mucosae in Japan.

Solid cystic tumor of the pancreas: report of six cases and a review of the Japanese literature.

Although many cases of solid cystic tumor of the pancreas (SCT) have been reported, its nature and histogenesis remain controversial. We herein report six cases of SCT, including three cases of noncystic type. A review of 22 cases of noncystic type SCT, including our 3 cases, was carried out to compare their features with those of 173 cases of classic SCT reported in Japan. Noncystic type SCTs tend to occur in male patients and are smaller in size and less frequently symptomatic, although they show histological characteristics similar to those of classic SCTs. The developmental process might be a cause of cyst formation. The accumulation and analysis of many, at present, "atypical" cases for clarification of its nature, will, it is hoped, lead to a new nomenclature for this condition that adequately describes its biological origin.