Prevalence rate and clinical characteristics of esophageal ectopic sebaceous glands in asymptomatic health screen examinees.

Ectopic sebaceous glands in the esophagus have rarely been reported and, thus, represent an obscure medical condition. The aim of this study is to identify the prevalence rate and clinical characteristics of this lesion in an asymptomatic population. We prospectively enrolled health screen examinees who underwent esophagogastroduodenoscopy for gastric cancer screening. An esophageal biopsy was performed in the cases in which esophageal ectopic sebaceous glands were suspected. The general characteristics of the examinees were analyzed based on their medical records. A total of 9989 examinees were enrolled, and five examinees were diagnosed with esophageal ectopic sebaceous glands between December 2012 and June 2014. The endoscopic findings of the esophageal ectopic sebaceous glands indicated multiple yellowish patches or papules, which varied in size. The histopathological findings indicated several lobulated sebaceous glands in the squamous epithelium with inflammatory infiltration. The follow-up endoscopic findings indicated that there was no grossly discernible change. In conclusion, esophageal ectopic sebaceous glands are present in 0.05% of asymptomatic subjects. This lesion is thought to be benign and is not related to clinical symptoms. Therefore, esophageal ectopic sebaceous glands do not require further treatment or follow-up, which makes endoscopists free from active efforts for differential diagnosis with other malignant diseases.

Capsule Endoscopy with Retention of the Capsule in a Duodenal Diverticulum: A Case Report.

Capsule endoscopy is being increasingly recognized as a gold standard for diagnosing small bowel disease, but along with the increased usage, capsule retention is being reported more frequently. We report a case of capsule endoscopy retention in a diverticulum of the duodenal proximal third portion, which we treated by esophagogastroduodenoscopy. A 69-year-old male visited hospital with hematochezia. He had hypertension and dyslipidemia for several years, and was taking aspirin to prevent heart disease. CT and colonoscopy revealed a diverticulum in the third portion of the duodenum, rectal polyps, and internal hemorrhoids. Capsule endoscopy was performed but capsule impaction occurred. The capsule was later detected by CT in the diverticulum. Endoscopy was performed a day later and the capsule was removed using a net. A small bowel series was conducted after capsule removal, and no stenosis was found. The patient fully recovered and no recurrence of hematochezia was observed at his one month exam. This is the first case in Korea of capsule retention in a duodenal diverticulum, with successful removal by endoscopy.

[A case of liver metastasis of gastric hepatoid adenocarcinoma].

We report herein a case of hepatoid adenocarcinoma of the stomach with liver metastasis. Gastric carcinoma generally presents as adenocarcinoma and rarely shows a hepatoid pattern, which can produce alpha-fetoprotein (AFP). The stomach is one of the common sites at which hepatoid adenocarcinoma has been detected. A 75-year-old female patient was admitted to the hospital with a symptom of epigastric discomfort. Gastrofibroscopy revealed a large tumor occupying the greater curvature of the stomach body. The level of serum AFP was markedly increased. Abdominal computed tomography revealed multiple liver masses. Biopsy samples of the gastric lesion and liver masses finally confirmed her case as hepatoid adenocarcinoma in the stomach with liver metastasis. The AFP-producing gastric carcinoma needs special attention because it often presents with early liver metastasis and has a poor prognosis.

Detection of aberrant p16INK4A methylation in sera of patients with liver cirrhosis and hepatocellular carcinoma.

Hepatocellular carcinomas (HCCs) show genomic alterations, including DNA rearrangements associated with HBV DNA integration, loss of heterozygosity, and chromosomal amplification. The genes most frequently involved are those encoding tumor suppressors. The p16INK4A tumor suppressor gene frequently displays genetic alteration in HCC tissues. The present study was performed to examine the incidence of methylated p16INK4A in the sera of liver cirrhosis (LC) and HCC patients, and to evaluate its role as a tumor marker of HCC. The sera of 23 LC patients and 46 HCC patients were examined in this study. The methylation status of p16INK4A was evaluated by methylation-specific PCR of serum samples. Methylated p16INK4A was detected in 17.4% (4/23) of LC patients and in 47.8% (22/46) of HCC patients. No association was demonstrated between p16INK4A methylation and serum AFP level. As the status of p16INK4A methylation was not associated with serum AFP level, it may have a role as a tumor marker of HCC.

NF-kappa B binding activity and cyclooxygenase-2 expression in persistent CCl(4)-treated rat liver injury.

The involvement of NF-kappa B binding activity is known to be important in the mechanism of acute liver injury and in the induction of cyclooxygenase (COX-2). This study was performed to evaluate NF-kappa B binding activity and the expression of COX-2 in chronic liver injury induced by carbon tetrachloride (CCl(4)). Liver tissues from Sprague-Dawley rats were collected at 1, 3, 5, and 7th week after intraperitoneal injection of 0.1 mL of CCl(4)/100 g body weight twice a week. Reactive oxy-gen species (ROS) were measured in the postmitochondrial fraction by dichlorofluorescein formation with a fluorescent probe. An electrophoretic mobility shift assay was performed for NF-kappa B binding activity. Western blot was performed to measure the level of COX-1, COX-2, p65, p50, and I B proteins. ROS and NF-kappa B activity increased during the CCl4-induced chronic liver injury. The expression of nuclear p65 protein and p50 protein increased compared with that of the control, while the cytoplasmic I B protein decreased as the inflammation persisted. The expression of COX-2 in CCl(4)-treated rat liver increased compared with that of the control. It could be suggested that ROS produced by CCl(4) treatment increased NF-kappa B binding activity and thereby COX-2 expression, and these might be implicated in the progress of chronic liver damage.