Biomedical subjects

F K Chan

Publications and source records attributed to F K Chan.

At least 37 records · Page 2Linked to original sources

PubMed2001

Dysfunction of oesophageal motility in Helicobacter pylori-infected patients with reflux oesophagitis.

BACKGROUND: Helicobacter pylori infection has been suggested to be protective against gastro-oesophageal reflux disease. However, a significant proportion of patients with gastro-oesophageal reflux disease are infected by H. pylori. AIM: To study oesophageal motor function in H. pylori-infected patients with reflux oesophagitis. METHODS: Patients with erosive reflux oesophagitis were recruited prospectively for stationary oesophageal manometry and 24-h ambulatory oesophageal pH monitoring. H. pylori status was determined by biopsy urease test. Non-reflux volunteers were recruited as controls. RESULTS: Seventy-four patients with erosive oesophagitis (34 H. pylori-positive, 40 H. pylori-negative) and 48 non-reflux patient controls (22 H. pylori-positive, 26 H. pylori-negative) were recruited. There was no difference in severity of oesophagitis (median grade, 1; P=0.53) or oesophageal acid exposure (total percentage time oesophageal pH < 4, 7.6% vs. 6.8%; P=0.57) between H. pylori-positive and H. pylori-negative groups. Compared to H. pylori-negative patients, H. pylori-positive patients had significantly lower basal lower oesophageal sphincter pressure (12.2 mmHg vs. 15.3 mmHg; P=0.03) and amplitude of distal peristalsis (56.9 mmHg vs. 68.4 mmHg; P=0.03). Ineffective oesophageal motility (14% vs. 7%; P=0.02) and failed oesophageal peristalsis were also significantly more prevalent in H. pylori-positive patients. CONCLUSIONS: Among patients with a similar degree of reflux oesophagitis, H. pylori-infected patients have more severe oesophageal dysmotility and lower oesophageal sphincter dysfunction. Oesophageal motor dysfunction probably plays a dominant role in the development of gastro-oesophageal reflux disease in patients with H. pylori infection.

Adult↗

PubMed2001

Role of acid suppressants in prophylaxis of NSAID damage.

Gastric acid contributes to the pathogenesis of non-steroidal anti-inflammatory drug (NSAID)-induced ulceration via several mechanisms, including conversion of superficial to deeper injury, impairment of haemostasis, and interference with ulcer healing. The suppression of acid secretion has been shown to reduce the severity of NSAID-induced mucosal damage in experimental models and clinical studies. Current evidence indicates that proton pump inhibitors (PPIs) are the preferred treatment for the healing of gastric ulcers when NSAIDs cannot be discontinued. PPIs are superior to standard-dose H(2)-receptor antagonists and equivalent to low-dose misoprostol in preventing NSAID-induced gastric ulcers. Whether there is any significant advantage of PPIs over higher doses of H(2)-receptor antagonists or misoprostol is unknown. The efficacy of PPIs is enhanced in the presence of H. Pylori infection. Omeprazole has been shown to be effective for the secondary prevention of ulcer bleeding in H. pylori -infected NSAID users. The efficacy of PPIs for the prevention of ulcer complications in H. pylori-negative NSAID users remains uncertain.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2001

Is non-Helicobacter pylori, non-NSAID peptic ulcer a common cause of upper GI bleeding? A prospective study of 977 patients.

BACKGROUND: Non-Helicobacter pylori, non-NSAID ulcer is relatively common in Western countries. Whether it is a significant problem in the Orient is unclear. The aim of this study was to investigate the incidence of non-H pylori, non-NSAID ulcers presenting with GI bleeding. METHODS: A prospective study was done of 1675 consecutive patients presenting with upper GI bleeding over a period of 12 months. Upper endoscopy was performed with biopsy specimens taken from the antrum and body of the stomach for a biopsy urease test (BUT) and histology for detection of H pylori. Exposure to nonsteroidal anti-inflammatory drugs (NSAID) or aspirin within 4 weeks of hospitalization was carefully scrutinized. A 6-week course of treatment with an H2-receptor antagonist was prescribed for patients who did not use an NSAID and had a negative BUT result. Follow-up endoscopy was performed to confirm H pylori status with a BUT and histology. Positive histology at either initial or follow-up endoscopy was used as the standard for diagnosing H pylori infection. RESULTS: Among 977 patients who were found to have ulcer bleeding, 434 (44%) had exposure to aspirin or an NSAID. Of the 543 non-NSAID users, 431 (79.4%) had a positive BUT and 112 (20.6%) were BUT negative on initial endoscopy. Eighty-nine of 112 patients who were NSAID negative, BUT negative returned for follow-up endoscopy. Forty-nine of 89 (55.1%) were found to have a positive BUT and positive histology at follow-up endoscopy. Only 40 of 977 (4.1%) patients admitted with ulcer bleeding were confirmed to have non-H pylori, non-NSAID ulcers. CONCLUSIONS: Non-H pylori, non-NSAID bleeding ulcer is uncommon. A negative BUT is unreliable for exclusion of H pylori infection during the acute phase of ulcer bleeding.

Adolescent↗

PubMed2001

Incidence of gastroesophageal malignancy in patients with dyspepsia in Hong Kong: implications for screening strategies.

BACKGROUND: A "test-and-treat" strategy for H pylori infection has been recommended in Europe and North America as safe and cost-effective for management of patients with dyspepsia. The primary aim of this study was to determine the frequency of gastroesophageal cancer in 2 groups of patients with dyspepsia: those 45 years of age or younger without "alarm" symptoms (low-risk group) and patients over 45 years of age or any patient with "alarm" symptoms (high-risk group). A secondary aim was to determine the frequency of gastric cancer among patients in the low-risk group with or without a positive serology for H pylori. METHODS: Patients with persistent dyspepsia were recruited from 4 regional hospitals in Hong Kong. Those in the low-risk group were evaluated for H pylori by using a whole blood serology test; they underwent endoscopy within 1 week. Those in the high-risk group and those taking nonsteroidal anti-inflammatory drugs (NSAIDs) underwent endoscopy promptly. Alarm symptoms were as follows: weight loss (10 or more pounds over 8 weeks), recurrent vomiting, dysphagia, bleeding, or anemia. RESULTS: Of 2627 patients enrolled, 1017 were in the low-risk group and 1610 in the high-risk group. Twenty-three patients (0.9%) had gastroesophageal cancers (20 gastric, 3 esophageal). Four patients with cancer (17.4%) were in the low-risk group (3 gastric, 1 esophageal); all except the patient with esophageal cancer had a positive serology test. In the high-risk group, 19 patients had cancer (17 gastric, 2 esophageal). CONCLUSION: Gastric cancer is relatively frequent among young patients with dyspepsia who have no alarm features in Hong Kong. This finding raises concerns as to the safety of the "test-and-treat" strategy for the management of patients with dyspepsia in Asia.

Adult↗

PubMed2000

Effect of intravenous omeprazole on recurrent bleeding after endoscopic treatment of bleeding peptic ulcers.

BACKGROUND: After endoscopic treatment of bleeding peptic ulcers, bleeding recurs in 15 to 20 percent of patients. METHODS: We assessed whether the use of a high dose of a proton-pump inhibitor would reduce the frequency of recurrent bleeding after endoscopic treatment of bleeding peptic ulcers. Patients with actively bleeding ulcers or ulcers with nonbleeding visible vessels were treated with an epinephrine injection followed by thermocoagulation. After hemostasis had been achieved, they were randomly assigned in a double-blind fashion to receive omeprazole (given as a bolus intravenous injection of 80 mg followed by an infusion of 8 mg per hour for 72 hours) or placebo. After the infusion, all patients were given 20 mg of omeprazole orally per day for eight weeks. The primary end point was recurrent bleeding within 30 days after endoscopy. RESULTS: We enrolled 240 patients, 120 in each group. Bleeding recurred within 30 days in 8 patients (6.7 percent) in the omeprazole group, as compared with 27 (22.5 percent) in the placebo group (hazard ratio, 3.9; 95 percent confidence interval, 1.7 to 9.0). Most episodes of recurrent bleeding occurred during the first three days, which made up the infusion period (5 in the omeprazole group and 24 in the placebo group, P<0.001). Three patients in the omeprazole group and nine in the placebo group underwent surgery (P=0.14). Five patients (4.2 percent) in the omeprazole group and 12 (10 percent) in the placebo group died within 30 days after endoscopy (P=0.13). CONCLUSIONS: After endoscopic treatment of bleeding peptic ulcers, a high-dose infusion of omeprazole substantially reduces the risk of recurrent bleeding.

Aged↗

PubMed2000

A domain in TNF receptors that mediates ligand-independent receptor assembly and signaling.

A conserved domain in the extracellular region of the 60- and 80-kilodalton tumor necrosis factor receptors (TNFRs) was identified that mediates specific ligand-independent assembly of receptor trimers. This pre-ligand-binding assembly domain (PLAD) is physically distinct from the domain that forms the major contacts with ligand, but is necessary and sufficient for the assembly of TNFR complexes that bind TNF-alpha and mediate signaling. Other members of the TNFR superfamily, including TRAIL receptor 1 and CD40, show similar homotypic association. Thus, TNFRs and related receptors appear to function as preformed complexes rather than as individual receptor subunits that oligomerize after ligand binding.

Amino Acid Substitution↗

PubMed2000

Fas preassociation required for apoptosis signaling and dominant inhibition by pathogenic mutations.

Heterozygous mutations encoding abnormal forms of the death receptor Fas dominantly interfere with Fas-induced lymphocyte apoptosis in human autoimmune lymphoproliferative syndrome. This effect, rather than depending on ligand-induced receptor oligomerization, was found to stem from ligand- independent interaction of wild-type and mutant Fas receptors through a specific region in the extracellular domain. Preassociated Fas complexes were found in living cells by means of fluorescence resonance energy transfer between variants of green fluorescent protein. These results show that formation of preassociated receptor complexes is necessary for Fas signaling and dominant interference in human disease.

Animals↗

PubMed2000

Measurement of molecular interactions in living cells by fluorescence resonance energy transfer between variants of the green fluorescent protein.

Many signal transduction pathways operate through oligomerization of proteins into multi-subunit complexes. Although biochemical assays can identify potential protein-protein interactions, studying these interactions in living cells is more challenging. Fluorescence resonance energy transfer (FRET) has been used as a "spectroscopic ruler" to measure molecular proximity, but these methods have been limited by the need for chemical labeling of target proteins or labeled antibodies. We present methods for examining interactions between target proteins molecularly fused to cyan and yellow variants of the green fluorescent protein (GFP) by FRET in living cells. Flow cytometric and microscope-based methods are described that have been applied to a variety of interacting proteins.

Cell Line↗

PubMed2000

A crucial role for p80 TNF-R2 in amplifying p60 TNF-R1 apoptosis signals in T lymphocytes.

Tumor necrosis factor-alpha (TNF-alpha) can elicit many cellular responses including programmed cell death or apotosis. TNF-alpha-induced apoptosis has been largely attributed to the p60 TNF-R1 receptor. The role of p80 in TNF-alpha-mediated apoptosis is largely unknown. We now present evidence that signaling through p80 switches on the previously dormant apoptotic machinery associated with p60. This effect on p60-associated apoptosis involves the proximal activation of caspases and proceeds in the presence of strong NF-kappaB induction. We evaluated the role of TRAF2 in p80-assisted apoptosis and found that a decrease in TRAF2 protein occurs with p80 but not p60 stimulation. However, the decrease in TRAF2 protein can be dissociated from apoptosis in the presence of a caspase inhibitor. Hence, one means by which p80 TNF-R2 regulates apoptosis is through its ability to amplify internally apoptotic signal transduction from p60 TNF-R1.

Antigens, CD↗

PubMed2000

Cyclooxygenase-2 expression in Helicobacter pylori-associated premalignant and malignant gastric lesions.

Expression of cyclooxygenase-2 (COX-2) in various stages of the Helicobacter pylori-associated gastric carcinogenesis pathway has not been elucidated. We investigated the distribution and intensity of COX-2 expression in premalignant and malignant gastric lesions, and monitored the changes after H. pylori eradication. Gastric biopsies from H. pylori-infected patients with chronic active gastritis, gastric atrophy, intestinal metaplasia (IM), gastric adenocarcinoma, and noninfected controls were studied. Expression of COX-2 was evaluated by immunohistochemistry and in situ hybridization. Endoscopic biopsies were repeated 1 year after successful eradication of H. pylori in a group of IM patients for comparing COX-2 expression and progression of IM. In all H. pylori-infected patients, COX-2 expression was predominantly found in the foveolar and glandular epithelium and, to a lesser extent, in the lamina propria. In the noninfected group, only 35% of cases demonstrated weak COX-2 expression. Intensity of COX-2 was not significantly different between the chronic active gastritis, gastric atrophy, IM, and gastric adenocarcinoma groups. In 17 patients with IM, COX-2 expressions in the epithelial cells and stromal cells were reduced 1 year after H. pylori eradication. However, the changes in COX-2 expression did not correlate with progression/regression of IM. Both premalignant and malignant gastric lesions demonstrate strong COX-2 expression. Successful eradication of H. pylori leads to down-regulation of COX-2 expression but failed to reverse IM at 1 year.

Adenocarcinoma↗

PubMed2000

The multifaceted role of Fas signaling in immune cell homeostasis and autoimmunity.

Originally identified as a cell surface receptor that triggered the death of lymphocytes and tumor cells, it is now recognized that Fas (also known as CD95 or Apo-I) has distinct functions in the life and death of different cell types in the immune system. Fas signaling may also be involved in T cell costimulation and proliferation. Although Fas deficiency in humans and mice predisposes them towards systemic autoimmunity, Fas-FasL interactions can also facilitate organ-specific immunopathology. Proximal signaling by Fas and related receptors depends on subunit preassembly, which accounts for the dominant-negative effect of pathogenic receptor mutants and natural splice variants.

Animals↗

PubMed2000

Salvage therapies after failure of Helicobacter pylori eradication with ranitidine bismuth citrate-based therapies.

BACKGROUND: Salvage therapies after initial Helicobacter pylori eradication failure of ranitidine bismuth citrate (RBC)-based regimens remain undefined. AIM: To test the efficacy of 1-week omeprazole, amoxycillin and clarithromycin as a second-line treatment and 1-week quadruple therapy after repeated failures of RBC- and proton pump inhibitor-based regimens. METHOD: Patients were recruited from a recently published prospective randomized study if confirmed to have failed H. pylori eradication with RBC-based regimens. They were given omeprazole 20 mg, amoxycillin 1 g and clarithromycin 500 mg (OAC) b.d. for 1 week. 13C-urea breath test was performed 4 weeks after the conclusion of medication. Those who failed to respond to OAC were given 1-week quadruple therapy (bismuth subcitrate 120 mg, tetracycline 500 mg and metronidazole 400 mg q.d.s. plus omeprazole 20 mg b.d.). RESULTS: Among 398 patients receiving RBC-based therapies, 40 (10%) had failed eradication (RAC=7, RC-2=12, RMC=7, and RMT=14). OAC was prescribed to 31 patients (RAC=4, RC-2=9, RMC=6, and RMT=12) and 68% had successful eradication. Nine out of 10 patients with failed second treatment received quadruple therapy; successful eradication occurred in 83% (5 out of 6) after repeated failures of clarithromycin-based regimens. CONCLUSION: One-week OAC is not an optimal second-line therapy when RBC-clarithromycin combinations fail. Quadruple therapy appears to be effective despite repeated failures of clarithromycin-based RBC or proton pump inhibitor therapies.

Amoxicillin↗

PubMed2000

Helicobacter pylori infection is associated with milder gastro-oesophageal reflux disease.

BACKGROUND: We have previously demonstrated a negative relationship between the prevalence of Helicobacter pylori and gastro-oesophageal reflux disease (GERD). AIM: To study the effects of H. pylori infection on the severity of GERD. METHODS: Ethnic Chinese patients with frequent heartburn and/or endoscopic oesophagitis were studied. Endoscopic examination was performed to assess the severity of oesophagitis (modified Savary-Miller grading) and the presence of hiatus hernia. Biopsies were taken for rapid urease testing and confirmation of Barrett's oesophagus. Risk factors which may affect the severity of oesophagitis (age, sex, smoking, drinking, diabetes mellitus, hiatus hernia, H. pylori status and body mass index) were evaluated by a multiple regression model. The cagA status of H. pylori infected GERD and age-and-sex matched controls were determined by Western blot. Age-and-sex matched non-reflux patients were recruited as controls for comparison. RESULTS: Two hundred and twenty-five patients with GERD were studied, of whom 77 (34%) were infected with H. pylori. Oesophagitis and Barrett's oesophagus were found in 140 patients (62%) and six patients (3%), respectively. H. pylori infected patients had significantly less severe oesophagitis compared to the uninfected group (P=0.022). All patients with Barrett's oesophagus were uninfected. Factors that predicted severe oesophagitis included age over 60 years (P < 0.001) and hiatus hernia (P < 0.001). H. pylori infection was the only factor that showed a negative correlation with severe oesophagitis (P=0.011). The prevalence of the cagA positive strain in endoscopy-negative GERD, erosive oesophagitis and control subjects was 70, 76 and 78%, respectively (P=0.75). CONCLUSIONS: H. pylori infection is associated with milder GERD.

Adult↗

PubMed2000

Interaction of Helicobacter pylori eradication and non-steroidal anti-inflammatory drugs on gastric epithelial apoptosis and proliferation: implications on ulcerogenesis.

BACKGROUND: Apoptosis is associated with loss of gastric mucosal integrity and may play an important role in ulcer development. AIM: To examine how Helicobacter pylori and NSAIDs interact to effect apoptosis and proliferation of the gastric mucosa. METHODS: Patients presenting with musculoskeletal pain requiring NSAID treatment and without previous exposure to NSAID or pre-existing ulcers were recruited. Patients were divided into three groups: (A) H. pylori-infected; (B) H. pylori-eradicated; and (C) non-infected patients. They were given naproxen for 8 weeks. Patients with non-ulcer dyspepsia and H. pylori infection who were given anti-Helicobacter therapy were recruited as controls (D). Endoscopy was performed at baseline and 8-weeks after receiving naproxen. Gastric antral biopsies were obtained to assess apoptosis by terminal uridine deoxynucleotidyl nick end-labelling (TUNEL) and proliferation by Ki67 immunostaining. RESULTS: A total of 55 patients were studied. H. pylori-positive patients had a higher apoptosis and proliferation index at baseline than non-infected patients (P < 0.0001), and eradication of H. pylori resulted in a significant reduction in these parameters. The NSAID induced apoptosis in non-infected subjects (P=0.03) whilst apoptosis was reduced in H. pylori-positive patients receiving NSAID (P=0.02). After 8 weeks of NSAID, post-treatment apoptosis was significantly higher in patients with persistent H. pylori infection than in non-infected patients (P=0.01). CONCLUSIONS: Eradication of H. pylori prior to NSAID therapy significantly reduces the level of apoptosis in the gastric mucosa, which may contribute to maintaining mucosa integrity and preventing ulcer development.

Adult↗

PubMed2000

Non-steroidal anti-inflammatory drug toxicity in the upper gastrointestinal tract.

Non-steroidal anti-inflammatory drug (NSAID) toxicity in the upper gastrointestinal tract is the most common serious drug-induced toxicity reported to drug regulatory authorities. In the last two decades, the rediscovery of H. pylori, development of potent ulcer-healing drugs and specific Cox-II inhibitors have opened new horizons in the management of NSAID toxicity. A Working Party composed of gastroenterologists and rheumatologists in the Asia-Pacific region met in Cairns, Australia, in 1999 to review the literature and develop appropriate guidelines. Recommendations were made based on the latest existing evidence. The importance of clinical events as study endpoints was emphasized. While differences exist between NSAIDs and aspirin, most studies have shown that advanced age, history of peptic ulcer disease, serious concomitant illnesses and coprescription of NSAID/aspirin with anticoagulants and steroids are high risk factors. These patients should be considered for prophylactic anti-ulcer therapy. Helicobacter pylori infection may aggravate the toxicity of NSAIDs and, in selected cases, should be treated before NSAID/aspirin is prescribed. Proton pump inhibitors and misoprostol are the most promising agents in preventing gastric and duodenal ulcers. When NSAID/aspirin needs to be continued in patients who develop an NSAID-related ulcer, proton pump inhibitors offer the best healing effect. With the discovery of cyclo-oxygenase isoforms (Cox-I and Cox-II), preferential and specific Cox-II inhibitors have been developed. While early clinical data have suggested promising antiinflammatory effects and improved safety profile in the gastrointestinal tract, several key issues on long-term safety remain unresolved. The use of potent anti-ulcer therapy, treatment of H. pylori infection and the development of Cox-II inhibitor will change the scenario of NSAID/aspirin-related gastrointestinal toxicity in the next millennium.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2000

How does Helicobacter pylori infection interact with non-steroidal anti-inflammatory drugs?

There have been conflicting clinical data on whether Helicobacter pylori (H. pylori) contributes to the pathogenesis of ulcers induced by non-steroidal anti-inflammatory drugs (NSAIDs). The discrepant findings reflect the complex interaction between H. pylori and NSAIDs, which has generated divergent results under different clinical conditions. This chapter reviews the pathogenetic mechanisms in ulcer formation that are common to H. pylori and NSAIDs, and explains how a better understanding of these factors might resolve some of the controversies. Existing evidence indicates that the interaction between H. pylori and NSAIDs is not an 'all-or-none' relationship. Factors such as previous exposure to NSAIDs, a past history of ulcer complication, gastric acid output, neutrophil infiltration, concurrent acid suppressive therapy and the type of NSAID used (aspirin versus non-aspirin NSAIDs) would influence the role of H. pylori as a risk factor in NSAID users. Recommendations on H. pylori eradication for different subgroups of NSAID users are proposed.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2000

Aeromonas infection in acute suppurative cholangitis: review of 30 cases.

OBJECTIVES: Aeromonads, though not common pathogens in biliary sepsis, caused substantial mortality in patients with impaired hepatobiliary function. Our aim was to study the pathogenic role of Aeromonas in acute suppurative cholangitis. METHODS: Between 1996 and 1998, the medical records of patients with a diagnosis of biliary sepsis were reviewed. Those who fulfilled the diagnostic criteria for acute suppurative cholangitis and had positive bile or blood cultures for Aeromonas species were studied. RESULTS: One thousand and forty-five patients were confirmed to have acute suppurative cholangitis. Of these, 30 patients (2.9%) had Aeromonas species isolated from bile; four were complicated by aeromonas septicaemia with simultaneous recovery of the bacteria from blood. All except two isolates were A. hydrophila. Twenty-four patients (80%) had bile duct stones, four (13%) had cholangiocarcinoma and two (7%) pancreatic cancer. Twenty-five cases (83%) had previous exploration of the biliary tract. There was substantial resistance to piperacillin (58%), ceftazidime (30%) and imipenem (15%). Most patients improved after biliary decompression. Only three patients (10%) died, two had terminal malignancy and one had end-stage liver failure. No excess mortality was attributable to Aeromonas infection in biliary sepsis. CONCLUSIONS: Previous instrumentation facilitated ascending Aeromonas infection of the biliary tract from the gastrointestinal tract. Unlike early reports, our results showed that aeromonads did not adversely affect the clinical outcome of acute suppurative cholangitis with successful drainage of biliary obstruction.

Acute Disease↗

PubMed2000

EUS-guided injection of cyanoacrylate for bleeding gastric varices.

BACKGROUND: Bleeding gastric varices is a highly fatal condition. Recurrent bleeding after hemostasis achieved by endoscopic methods is common, and obliteration of gastric varices is difficult to assess. Our aim was to investigate the use of endosonography (EUS) in monitoring cyanoacrylate injection to obliterate gastric varices. METHODS: Patients who presented with bleeding gastric varices were treated with bolus injection(s) of cyanoacrylate (0.5 mL cyanoacrylate mixed with 0.7 mL Lipiodol) until bleeding was controlled; 47 patients received "on-demand" injection only in response to recurrent bleeding (on-demand group). Another group of 54 patients underwent biweekly EUS followed by repeated injection of cyanoacrylate (repeated-injection group) until all gastric varices were obliterated. The primary outcome was recurrent bleeding-free interval and survival rate. RESULTS: The two groups of patients were comparable demographically. Although the rates of early (</=48 hour) bleeding recurrence were similar with repeated or on-demand injection (7.4% versus 12.8%, p = 0.5), late recurrence of bleeding (>48 hour) was significantly reduced in the repeated-injection group (18.5% versus 44.7%, p = 0.0053, odds ratio 0.28 (95% CI [0.12, 0. 69]). Cumulative probability of recurrent bleeding-free interval was higher in the repeated-injection than the on-demand group (log-rank test, p = 0.0053). There was a numeric trend toward improved survival in the repeated-injection group. CONCLUSION: Gastric varices obliteration with cyanoacrylate under EUS monitoring reduces recurrent bleeding and may improve survival.

Adult↗