A case of retrograde intussusception (acute type) of efferent limb into Braun side-to-side jejuno-jejunal anastomosis is presented. Intussusception, though infrequent, is well recognized complication after gastric surgery. Patient was 50 year old man who was admitted with epigastric pain and abdominal mass for 6 hours. Patient had a history of total gastrectomy 2 years before admission due to stage II gastric cancer. Seven hours after admission, hematemesis developed. Emergency fiberopticgastroscopy revealed type 4 jejunogastric intussusception. Segmental resection with end-to-end reanastomosis was performed.
Humans ; Intussusception/*etiology/pathology/surgery ; Jejunal Diseases/*etiology/pathology/surgery ; Male ; Middle Aged ; Postoperative Complications/*pathology ; Stomach/*surgery

No abstract available.
Aged ; Biopsy ; Endoscopy, Digestive System ; Female ; Humans ; Hypertension, Portal/*complications ; Polyps/*etiology/pathology ; Stomach Diseases/*etiology/pathology

Behcet's disease (BD) has been recognized as multi-systemic chronic vasculitic disorder of recurrent inflammation, characterized by the involvement of multiple organs and resulting in orogenital ulcers, uveitis, and skin lesions. Involvement of the central nervous system, vessels, and intestines in BD often leads to a poor prognosis. Digestive manifestations in BD have been reported in up to 1-60% of cases, although the rate varies in different countries. The most frequent extra-oral sites of gastrointestinal involvement are the ileocecal region and the colon. Gastric or esophageal involvement is reported to be very rare. Moreover, there have been no reports on the simultaneous involvement of the esophagus, stomach, ileum, and colon. Here, we present a 55-year-old Korean man with intestinal BD and multiple ileal and colonic ulcerations complicated by perforation, gastric ulcer with bleeding followed by perforation, and esophageal ulcers with bleeding.
Behcet Syndrome/complications/*diagnosis/pathology ; Cecal Diseases/complications/pathology ; Diagnosis, Differential ; Endoscopy, Digestive System ; Gastrointestinal Diseases/complications/*diagnosis ; Gastrointestinal Hemorrhage ; Humans ; Intestinal Perforation/*diagnosis/etiology/pathology ; Male ; Middle Aged ; Peptic Ulcer Perforation/pathology ; Stomach Ulcer/complications/pathology

OBJECTIVESTo study the role of cyclooxygenase 2 (COX 2) and prostaglandin I2 (PGI2) in the development of portal hypertensive gastropathy (PHG).

METHODSForty Wistar rats were divided into surgery group (32) and control group (8). Partial portal vein ligation method was used to narrow the sectional area of portal vein to establish the experimental model of PHG in surgery group rats. Then they were divided into four groups (8 rats in each). The free pressure of portal vein was determined at the 1st, 2nd, 3rd, 4th weeks after the operation, and 8 rats were killed to observe the pathological change of gastric mucosa. The levels of 6-keto-PGF1 alpha, a stable metabolite of PGI2, were determined by radioimmunoassay in gastric mucosa homogenate and the blood of portal vein. The expression of COX 2 in gastric mucosa was determined by immunohistochemistry.

RESULTSThe free pressure of portal vein increased rapidly after partial portal vein ligation and maintained a high stable level after 1 week. They were (2.40+/-0.15) kPa, (2.38+/-0.17) kPa, (2.52+/-0.21) kPa, and (2.46+/-0.17) kPa at the 1st, 2nd, 3rd, and 4th weeks after partial portal vein ligation, while it was (0.90+/-0.16) kPa in control group (t>or=17.356, P<0.05). The gastric mucosa appeared pale, edema, hyperaemia, surface erosion, punctate hemorrhage and these lesions were more apparent with the time after the operation. The pathological examination showed that the gastric mucosa and submucosa thickened. The vessels of gastric mucosa and submucosa expanded and increased. There were lymphocytes and neutrophils infiltration around the vessels in the gastric mucosa and submucosa. The 6-keto-PGF1 alpha levels in gastric mucosa and the blood of portal vein increased rapidly and maintained a high level after partial portal vein ligation,which were higher than those in control group (104.52pg/ml+/-25.11pg/ml vs 73.62pg/ml+/- 20.33pg/ml, t=2.710, P<0.05; 180.21pg /ml+/-37.56pg /ml vs 142.11pg /ml+/-31.51pg /ml, t=2.198, P<0.05). The results of immunohistochemistry showed that the intensity and degree of the COX 2 staining in gastric tissue increased at the 1st, 2nd, 3rd, 4th weeks after partial portal vein ligation, while the COX 2 in control group rats was negative.

CONCLUSIONSThe expression of COX 2 and PGI2 in gastric tissue increased in portal hypertension. PGI2 as an inflammatory medium, damages the gastric mucosa by expanding vessels and other mechanisms in portal hypertension. It may be one of the important factors contributing to the development of PHG.

Animals ; Cyclooxygenase 2 ; Disease Models, Animal ; Epoprostenol ; physiology ; Hypertension, Portal ; complications ; pathology ; Isoenzymes ; physiology ; Male ; Prostaglandin-Endoperoxide Synthases ; physiology ; Rats ; Rats, Wistar ; Stomach Diseases ; etiology ; pathology

BACKGROUND/AIMS: Anisakiasis is a well known parasitosis resulted from eating raw seafoods and there were many reports of cases. However, its endoscopic and clinical characteristics have not been reviewed well. The aim of this study was to clarify the gastric mucosal changes and influencing factors of upper gastrointestinal (UGI) anisakiasis. METHODS: We analyzed retrospectively the endoscopic and clinical characteristics of 141 cases with UGI anisakiasis diagnosed during UGI endoscopy, based on the review of medical records. The patients' data were collected consecutively from October 1999 through September 2006. RESULTS: In the 141 patients with UGI anisakiasis, the peak age was the 40s (44.7%). The female to male ratio was 1.82:1. The most prevailed season was winter (41.1%). The most frequent symptom was acute epigastric pain and 76.6% of the patients developed symptoms within 12 hours after the ingestion of raw seafoods. The greater curvature of body was the most preferred site of anisakid larvae. The median time from meal to symptom onset was shortest in esophageal location and longest in fundus location (3 vs. 18.7 hours). The various mucosal changes were observed and the most frequent mucosal change was edema (90.8%). Submucosal tumor was also found in 31.9% of the patients. The severity of mucosal change was related inversely with the time interval from meal to endoscopy (p=0.048). CONCLUSIONS: Anisakiasis presented various mucosal changes depending on the time interval from ingestion of raw seafood to endoscopy. Delayed endoscopy may lead chronic mucosal change and cause difficulty in the detection of anisakiasis. Therefore, the prompt endoscopic examination is required for the patients presenting acute gastrointestinal symptoms after taking raw fish.
Adult ; Aged ; Animals ; Anisakiasis/*diagnosis/parasitology ; Edema/etiology ; Esophageal Diseases/*parasitology/pathology ; Female ; Gastric Mucosa/parasitology/*pathology ; Gastroscopy ; Humans ; Male ; Medical Records ; Middle Aged ; Retrospective Studies ; Seafood ; Stomach Diseases/*parasitology/pathology ; Time Factors ; Upper Gastrointestinal Tract/parasitology/*pathology

OBJECTIVETo determine serum pepsinogen levels in patients with liver cirrhosis and investigate the functions of the gastric mucosa in these patients with concurrent portal hypertensive gastropathy (PHG).

METHODSFifty-one patients with liver cirrhosis and 22 healthy controls were studied by gastroscopy. The hepatic function of the patients with or without PHG were evaluated with Child-Pugh grade. Helicobacter pylori infection was detected using rapid urease test or exhalation of carbon 13. The serum pepsinogen I and II levels were tested by latex-enhanced immunoturbidimetry to calculate the PGI/PGII ratio (PGR).

RESULTSIn cirrhotic patients, the levels of serum PGI and PGR were lower than those in the healthy controls. The patients without PHG had a serum PGI level of 49.48+23.86 µg/L, significantly lower than that in PHG patients (74.85+30.27 µg/L, P=0.000). The levels of serum PG II in patients with H.pylori infection was significantly higher that in patients free of H.pylori infection (P=0.003).

CONCLUSIONThe serum level of PGI decreases obviously in patients with hepatic cirrhosis and PHG, who can have damages of the gastric mucosa lamina propria and reduced secretory function of the gastric mucosa. H.pylori infection may affect the level of PGII. There is no significant correlation between serum PG level and liver function, but to a certain extent, serum PG level especially PGI can reflect the function of gastric mucosa in patients of liver cirrhosis.

Adult ; Case-Control Studies ; Female ; Gastric Mucosa ; pathology ; Helicobacter Infections ; Humans ; Hypertension, Portal ; complications ; Liver Cirrhosis ; complications ; Male ; Middle Aged ; Pepsinogen A ; blood ; Stomach Diseases ; blood ; etiology ; microbiology

Animals ; Diagnosis, Differential ; Disease Models, Animal ; Gastric Antral Vascular Ectasia ; diagnosis ; pathology ; Gastric Mucosa ; pathology ; Gastrointestinal Hemorrhage ; etiology ; pathology ; therapy ; Gastroscopy ; Humans ; Hypertension, Portal ; complications ; epidemiology ; pathology ; Intestinal Mucosa ; pathology ; Liver Cirrhosis ; complications ; pathology ; Liver Cirrhosis, Experimental ; complications ; pathology ; Rats ; Stomach Diseases ; epidemiology ; etiology ; pathology ; therapy

Intestinal metaplasia (IM) has been regarded as a premalignant condition. However, the pathogenesis of IM is not fully understood. The aim of this study was to evaluate the role of CDX1 and CDX2 in the formation of IM and the progression to dysplasia and gastric cancer (GC). A total of 270 subjects included 90 with GC, dysplasia and age- and sex-matched controls. Real-time PCR (RT-PCR) was performed with body specimens for CDX1 and CDX2. The expression of CDX2 was significantly higher in H. pylori positive group than H. pylori negative group (P = 0.045). CDX1 and CDX2 expression increased proportional to the IM grade of the body (P < 0.001). CDX2 expression was significantly higher in incomplete type of IM than in complete type (P = 0.045). The expression of CDX1 in dysplasia group was significantly higher than in the control group (P = 0.001); in addition, CDX1 and CDX2 in cancer group was significantly higher than control group (P < 0.001, and P < 0.001, respectively). Aberrant expression of CDX1 and CDX2 correlated with H. pylori infection and grade of IM in the body. Furthermore, the results suggest that CDX1 and CDX2 play a role in the progression to GC and dysplasia.
Aged ; Female ; Helicobacter Infections/complications/microbiology ; Helicobacter pylori/isolation & purification ; Homeodomain Proteins/*genetics/metabolism ; Humans ; Intestinal Diseases/*genetics/microbiology/pathology ; Male ; Metaplasia/pathology ; Middle Aged ; Polymerase Chain Reaction ; Precancerous Conditions/metabolism/pathology ; Stomach Neoplasms/etiology/*genetics/microbiology

Helicobacter pylori can cause variety of upper gastrointestinal disorders such as peptic ulcer, mucosa associated lymphoid tissue (MALT)-lymphoma, and gastric cancer. The prevalence of H. pylori infection has significantly decreased in Korea since 1998 owing to active eradication of H. pylori. Along with its decrease, the prevalence of peptic ulcer has also decreased. However, the mean age of gastric ulcer increased and this is considered to be due to increase in NSAID prescription. Gastric cancer is one of the leading causes of cancer deaths in Korea and Japan, and IARC/WHO has classified H. pylori as class one carcinogen of gastric cancer. Despite the decreasing prevalence of H. pylori infection, the total number of gastric cancer in Korea has continuously increased from 2006 to 2011. Nevertheless, the 5 year survival rate of gastric cancer patients significantly increased from 42.8% in 1993 to 67% in 2010. This increase in survival rate seems to be mainly due to early detection of gastric cancer and endoscopic mucosal dissection treatment. Based on these findings, the prevalence of peptic ulcer is expected to decrease even more with H. pylori eradication therapy and NSAID will become the main cause of peptic ulcer. Although the prevalence of gastric cancer has not changed along with decreased the prevalence of H. pylori, gastric cancer is expected to decrease in the long run with the help of eradication therapy and endoscopic treatment of precancerous lesions.
Anti-Bacterial Agents/therapeutic use ; Anti-Inflammatory Agents, Non-Steroidal/adverse effects ; Gastrointestinal Diseases/complications/*epidemiology ; Helicobacter Infections/complications/drug therapy/epidemiology ; Humans ; Lymphoma, B-Cell, Marginal Zone/epidemiology ; Peptic Ulcer/epidemiology/etiology ; Prevalence ; Stomach Neoplasms/etiology/mortality/pathology

A 63-year-old man with a history of hepatitis-B-related hepatocellular carcinoma (HCC) in the left lateral portion of the liver received repeated transcatheter arterial chemoembolization (TACE) and salvage radiotherapy. Two months after completing radiotherapy, he presented with dysphagia, epigastric pain, and a protruding abdominal mass. Computed tomography showed that the bulging mass was directly invading the adjacent stomach. Endoscopy revealed a fistula from the HCC invading the stomach. Although the size of the mass had decreased with the drainage through the fistula, and his symptoms had gradually improved, he died of cancer-related bleeding and hepatic failure. This represents a case in which an HCC invaded the stomach and caused a hepatogastric fistula after repeated TACE and salvage radiotherapy.
Carcinoma, Hepatocellular/complications/radiography/*therapy ; *Chemoembolization, Therapeutic ; Drainage ; Gastric Fistula/*etiology ; Gastroscopy ; Hepatitis B/diagnosis ; Humans ; Liver Diseases/*etiology ; Liver Neoplasms/complications/radiography/*therapy ; Male ; Middle Aged ; Neoplasm Invasiveness ; Stomach/pathology ; Tomography, X-Ray Computed