Search

This review provides an overview of the treatment options available for gastric varices (GV) with a focus on endoscopic methods. Various minimally invasive techniques, including endoscopic band ligation, endoscopic cyanoacrylate injection, and transjugular intrahepatic portosystemic shunt, can be applied to the treatment of GV. Endoscopic cyanoacrylate injection is now recognized as a first‐line treatment for GV. Endoscopic ultrasound‐guided cyanoacrylate injection combined with coils has shown good security and effectiveness. Thrombin injection therapy is a promising treatment, with a similar hemostasis rate to cyanoacrylate injection but with fewer serious complications. With the deepening understanding of the hemodynamics of the GV system, various treatment methods and their combination are gradually evaluated to provide patients with safer and more effective treatment options. [ABSTRACT FROM AUTHOR]

Direct percutaneous endoscopic jejunostomy (DPEJ) is a useful method for the establishment of enteral nutrition (EN) pathway. However, the identification of stomal puncture points for DPEJ is difficult. Here we present a case treated with an improved technique for DPEJ puncture-point localization, which was named DPEJ with balloon-assisted ultrasonic localization (DPEJ-BAUL). There were four steps after insertion of an endoscope into the jejunum: (1) a balloon dilatation catheter was inserted through the endoscope working channel; (2) the balloon was fully filled with water; (3) the site of puncture was selected with an ultrasonic probe percutaneously locating the water-filled balloon; and (4) a jejunostomy tube was placed by introducer technique. Rapid localization of a puncture site was possible with BAUL and the DPEJ procedure was successful. The patient's nutritional status was improved with EN and no postoperative complications were observed. DPEJ-BAUL is a feasible and effective technique to increase the technical success rate of DPEJ in patients with negative transillumination test results., Author(s): Zhi-Yong Yang [sup.1] , Jing-Jing Wei [sup.1] , Ze-Hao Zhuang [sup.1] , Jun Zhang [sup.1] , Ya-Ting Xu [sup.1] , Xiao-Hua Huang [sup.2] Author Affiliations: (1) Department of Endoscopy, [...]

Background/aims: The aim of the present study was to investigate the effects of the combination treatment of pentasa and probiotics on the microflora composition and prognosis in patients with inflammatory bowel disease (IBD)., Materials and Methods: A total of 40 patients with IBD (19 control group and 21 observation group) were randomized. Patients in the control group were given pentasa, and patients in the observation group were given probiotics along with pentasa. The microflora composition, biochemical indices, inflammatory markers, and activity scores of the two groups were analyzed., Results: After treatment, the number of enterobacteria, enterococci, saccharomyces, and bacteroides; the levels of fecal lactoferrin, 1-antitrypsin, β2-microglobulin, high-sensitivity C-reactive protein, and interleukin (IL)-6; activity scores; and recurrence rate in the observation group were significantly lower than those in the control group. Bifidobacterium and lactobacillus counts and IL-4 levels were significantly higher in the observation group than in the control group., Conclusion: The combination of probiotics and pentasa can improve microflora composition in patients with IBD and reduce the level of inflammatory cytokines; therefore, it is worthy of further clinical validation.

Objective: To determine the frequency of duodenal ulcer (DU), as well as other clinical characteristics occurring after endoscopic variceal ligation (EVL) of the esophagus., Study Design: Descriptive study., Place and Duration of Study: The First Affiliated Hospital of Fujian Medical University, Fuzhou, China, from April 2012 to April 2013., Methodology: A total of 47 patients with esophageal varices (EVr) who had also undergone EVL and gastroscopic follow-up within 3 months of the procedure was retrospectively analyzed. The status of Helicobacter pylori(Hp) infection, Child-Pugh classification, and the grades of portal hypertensive gastropathy (PHG) were collected. Sixty EVr patients without EVL treatment, but with clinical data available, served as the control group., Results: The frequency of DU in the EVL group (29.8%, 14/47) was higher than the control group (6.7%, 4/60) (p=0.02). Hp infection rate in EVLgroup was 19.15% (9/47), while in control group was 21.67% (13/60) (p=0.813). Hp positive rate (12.5%, 1/8) in patients exhibited new DUs after EVL was comparable to the patients without DU in the EVL group (12.1%, 4/33) (p=1.00). Patients with DU after EVL received 18.79 ±8.48 of ligating bands, while in those who did not exhibit DUs received 13.85 ±6.47 (z = -2.042, p = 0.041). Logistic regression analysis showed that the occurrence of DU was not associated with age, gender, Child-Pugh classification, or the grade of PHG (p > 0.05)., Conclusion: Esophageal EVL is associated with a higher frequency of developing DU, which is related to a larger number of applied bands but is not correlated with Hp infection status or other variables.

Background: It is now clear that there are two histological types (type 1 and type 2) of autoimmune pancreatitis (AI P). The histological substance of type 1 AI P is known as lymphoplasmacytic sclerosing pancreatitis (LPSP) or traditional AIP, and type 2 AIP is characterized by distinct histology called idiopathic duct centric pancreatitis (IDCP). Serum IgG4 increase is considered as a marker for type 1 AI P. Far less is known about type 2 and it lacks predicting markers, so it easily leads to missed diagnosis and misdiagnosis., The Aim of This Study: The aim of this study was to describe multi-gene mutations in patients with type 2 AI P and its clinical features., Material and Methods: Three unrelated patients with type 2 AI P, 10 cases with type 1 AIP, 15 cases with other chronic pancreatitis and 120 healthy individuals were studied. The mutations and polymorphisms of 6 genes involved in chronic pancreatitis or pancreatic cancer - PRSS1, SPINK1, CFTR, MEN1, PKHD1, and mitochondrial DNA - were sequenced. Information of clinical data was collected by personal interview using a structured questionnaire., Results: Novel mutations were found in the genes encoding for MEN1 (p.546 Ala > The) and PKHD1 (c. 233586 A > G and c. 316713 C > T) from patients with type 2 AIP. What is more, the serum TCR (T cell receptor) level is relatively higher in patients with type 2 AIP than in patients with type 1 AIP and other chronic pancreatitis or normal controls. Weight loss was the major manifestation and no patients had extrapancreatic involvement in type 2 AIP., Conclusions: Type 2 AIP may occur with multi-gene mutations. For screening purposes, it is more reasonable to evaluate TCR levels in serum.

Background/aims: Chronic inflammatory processes and gastric contents related esophageal mucosal injury are two major characteristics of reflux esophagitis RE). This study was aimed to establish a rat model fitting RE major characteristics and to investigate the effects of mosapride, one of the 5-hydroxy tryptamine (5-HT)4 receptor agonists, on mucosal inflammation in RE., Methodology: Rat RE model was established by pyloric clip and section ligation-induced chronic acid reflux esophagitis. Animal body weight and survival was monitored. Animals were treated with 0.1 mg/kg/d, 0.5 mg/kg/d, or 2.5 mg/kg/d mosapride by gavage. Gastric emptying was examined. After two weeks, pathological changes of the esophagus were determined and endothelin-1 (ED-1) expression in esophageal tissues was evaluated by immunohistochemistry., Results: No significant differences were observed in the gastric emptying of RE rats after different doses of mosapride treatment (P > 0.05). Gross examination and pathological evaluation revealed that either 0.5 mg/kg/d or 2.5 mg/kg/d mosapride treatment attenuated the mucosal inflammation of RE, but a lower mosapride dose (0.1 mg/kg/d) had limited esophagoprotective effects (P > 0.05). Mosapride treatment greatly decreased the number of ED-1 positive monocytes in the esophagus compared with sham-operated controls (P < 0.05). 5-HT4 receptor and acetylcholine (Ach) receptor antagonists effectively reversed the protective effects of mosapride (P < 0.05)., Conclusions: Our results demonstrated that mosapride attenuated the mucosal inflammation of RE, suggesting that mosapride might provide esophagoprotective effects in addition to its well-known prokinetic actions.

Genetic risk factors of chronic pancreatitis (CP) have been identified and a number of studies have found that CP can lead to pancreatic cancer. Therefore, the detection of pancreatitis-associated gene mutations can aid the pancreatic cancer diagnostic process. Mutations in three genes, the cationic trypsinogen (PRSS1) gene, the cystic fibrosis transmembrane conductance regulator (CFTR) gene and the pancreatic secretory trypsin inhibitor (SPINK1) gene, have been identified as risk factors for CP. The aim of this study was to describe specific novel mutations in the intron of the PRSS1 gene in patients with pancreatic cancer and CP. A total of 65 unrelated patients with pancreatic cancer and 29 with CP were reviewed. Mutations and polymorphisms of the PRSS1 gene were analyzed by direct sequencing. Information regarding clinical data and smoking exposure was collected by personal interviews using a structured questionnaire. IVS 3+36 A>G mutation in the PRSS1 gene was found in 2 cases with pancreatic cancer, and these 2 patients were classified as never-smokers. IVS 3+127 T>A and IVS 3+157 G>C double mutations were identified in one patient with CP. All patients were found to have serum trypsin levels lower than that of the normal controls. Therefore, the PRSS1 gene mutation may be a special common cause of pancreatic cancer and CP.

Objective: To evaluated the efficacy of 9-day moxifloxacin-based triple therapy as first- or second-line treatment to eradicate Helicobacter pylori (H. pylori)., Methods: Three hundred and thirteen H. pylori-positive patients without previous treatment (Group A), 51 Hp-positive patients with once-failed treatment (Group B) and 32 with twice-failed treatment (Group C) were recruited to receive moxifloxacin, esomeprazole and tinidazole (MET) for 9 days.H. pylori status was re-assessed 4 weeks after the end of therapy by urea breath test. The eradication rate and its 95% confidence interval (95%CI) were calculated in intention-to-treat (ITT) and per-protocol (PP) analyses respectively., Results: In ITT analysis, the Hp-eradication rate was 89.8% (95%CI: 86.7% - 93.0%) in Group A, 81.2% (75.3% - 90.9%) in Group B and 81.2% (66.1% - 92.6%) in Group C, among which no significant difference was observed (chi(2) = 4.339, P > 0.05). However, in PP analysis there was a significant difference among them [93.9% (90.9% - 96.4%) in Group A, 84.8% (79.1% - 93.6%) in Group B and 81.2% (66.1% - 92.6%) in Group C (chi(2) = 9.294, P < 0.01)]. The rates were significantly lower respectively in Group B (chi(2) = 4.885, P < 0.05) and in Group C (chi(2) = 7.023, P < 0.01) than that observed in Group A according to PP analysis. But there was no significant difference between the patients with first-treated active ulceration and with first-treated gastritis (chi(2) = 1.670, P > 0.05 in ITT, or chi(2) = 0.030, P > 0.05 in PP analysis). Eradication rate in patients with 3rd-treated gastritis was lower than that in patients with first-treated gastritis according to PP analysis (chi(2) = 8.076, P < 0.01). The compliance rate was 95.99% in all patients., Conclusion: Nine-day moxifloxacin-based triple therapy provides an optimal eradication rate with a good compliance as first-line or second-line eradication of Hp.

Objective: This study updated the estimated prevalence of type 3c diabetes damage to the pancreas through different genotypes of PRSS1 and their clinical characteristics in the Han population., Subjects and Methods: Cross-sectional analysis was performed of the most recent (2003-2007) patients with pancreatitis from six hospitals of the Han population in South China (n = 253)., Results: There were 32 patients with pancreatitis carrying a PRSS1 gene abnormality within intron region among 253 cases of pancreatitis, including 27 patients carrying novel single nucleotide polymorphisms, namely, IVS 3 +75 A --> G conversion, and five patients with the mutation IVS3 + 10 T --> G. Among these patients, there were only three cases of patients with diabetes (9.37%). This was lower than the prevalence of abnormalities in the exons of the PRSS1 gene (51.92%): 12 patients with c.361 G --> A, eight patients with c.415 T --> A, and five patients with c.365G --> A. Among them were 12 persons with diabetes, including five requiring insulin to regulate blood sugar. What is more, among the 27 patients carrying PRSS1 gene polymorphism (c.486 C --> T, within the exon 4), there were 15 persons with diabetes symptoms. More than 40% of these patients required insulin to regulate blood sugar., Conclusions: An abnormality within the intron region of the PRSS1 gene represents one of the causes of pancreatitis in Chinese patients, but it is not related to pancreatic diabetes. However, the exon abnormality obviously raises the morbidity rate of type 3c diabetes, which relies on insulin.

Background & Objective: Local lymph node and blood metastasis could occur at early stage of esophageal squamous cell carcinoma (ESCC), which may be the key factors of its recurrence and poor prognosis. However, the mechanism of ESCC metastasis is unclear. This study was to analyze the genetic changes in primary lesion and lymph node metastases of ESCC, to screen for and locate ESCC metastasis-related genes., Methods: Genomic alterations in 15 pairs of primary lesions and matched metastatic lymph nodes of ESCC were analyzed by comparative genomic hybridization (CGH)., Results: In the 15 pairs of tissues, the most common chromosomal alterations were the gains of 3q, 8q, 6p, 20p, 5p, 18p, 2p, 2q and 1q, and the losses of 10p, 10q, 17p, 18q, 4p and 13q. Of these changes, the most significant finding was the gain of 6p with a frequency of 47% in metastatic lymph nodes and 13% in primary lesions, and the gain of 20p with a frequency of 73% in metastatic lymph nodes and 33% in primary lesions. The second interesting finding was the loss of 10p with a frequency of 53% in metastatic lymph nodes and 13% in primary lesions, and the loss of 10q with a frequency of 47% in metastatic lymph nodes and 13% in primary lesions., Conclusion: The gains of 6p and 20p and the losses of 10p and 10q are common genomic alterations in primary lesion and lymph node metastases of ESCC, which may code ESCC metastasis-related genes.

Aim: Microsatellites are the repeated DNA sequences scattered widely within the genomes and closely linked with many important genes. This study was designed to characterize the changes of microsatellite DNA loss of heterozygosity (LOH) in esophageal carcinogenesis., Methods: Allelic deletions in 32 cases of matched precancerous, cancerous and normal tissues were examined by syringe microdissection under an anatomic microscope and microsatellite polymorphism analysis using 15 polymorphic markers on chromosomes 3p, 5q, 6p, 9p, 13q, 17p, 17q and 18q., Results: Microsatellite DNA LOH was observed in precancerous and cancerous tissues, except D9S1752. The rate of LOH increased remarkably with the lesions progressed from basal cell hyperplasia (BCH) to squamous cell carcinoma (SCC) (P<0.05). Three markers, D9S171, D13S260 and TP53, showed the highest incidence of LOH (>60%). LOH loci were different in precancerous and cancerous tissues. LOH in D3S1234 and TP53 was the common event in different lesions from the same patients., Conclusion: Microsatellite DNA LOH occurs in early stage of human esophageal carcinogenesis, even in BCH. With the lesion progressed, gene instability increases, the accumulation of this change may be one of the important mechanisms driving precancerous lesions to cancer.

Objective: To characterize the profile of chromosomal imbalances of esophageal squamous cell carcinoma (SCC) in Linzhou, the high prevalence area of Henan province., Methods: Comparative genomic hybridization (CGH) was used to examine 52 cases of primary SCC of esophagus., Results: Gains in part or in whole of chromosome 3q, 8q, 5p, 1q, 6q, 18p, 20q and losses of 3p, 1p, 9q, 19p, 4p, 8p were detected frequently in SCC (> 20%). Gain of 3q, 5p, 1q, 11q13-14 and loss of 4pq, 13q were all significantly correlated with pathologic staging (P < 0.05). Gains of 8q, loss of 4p were linked to nodal metastasis (P < 0.05). Gains of 2p and loss of 4pq, 11q14-qter were associated with distant organ metastasis (P < 0.05)., Conclusion: These observations suggest that 3q, 8q, 5p, 1q, 6q, 18p, and 20q may contain SCC-related oncogenes; 3p, 1p, 9q, 19p, 4p and 8p may contain SCC-related tumor suppressor genes. It is likely that gain of 3q, 5p, 1q, 11q13-14 and loss of 4pq, 13q are the genetic aberrations critical for the development of esophageal carcinoma, whereas gains of 8q, 2p and loss of 4pq, 11q14-qter are considered later events associated with tumor progression and are thought to confer metastatic potential to esophageal carcinoma. Furthermore, nodal and distant organ metastases involve different genes.

Objective: To characterize the profiles of chromosome imbalance in esophageal squamous cell carcinoma (SCC) and gastric cardia adenocarcinoma (GCA) from the high incidence area in Henan., Methods: Chromosomal aberrations of 37 samples of SCC and 30 GCA were analyzed by comparative genomic hybridization comparative genomic hybridization (CGH)., Results: It was found that the most frequently detected gains were on chromosome arm 8q (78%), and followed by 3q, 5p, 6q and 7p. The most frequent loss was found on 3p (57%), and followed by 8p, 9q and 11q in SCC. For GCA, the most frequent gain was found on chromosome arm 20q (43%), and followed by 6q, 8q and 6p. The most frequent loss was on the chromosome 17p (57%), and followed by 19p, 1p and 4p., Conclusion: The present findings demonstrate that gains of 8q, 3q and 5p, and losses of 3p, 8p, and 9q are characteristic profile of chromosome imbalance in SCC, and the gains of 20q, 6q and losses of 17p, 19p and 1p are characteristic profile of chromosome imbalance in GCA, which provide important theoretic information for identifying and cloning novel SCC/GCA-related genes.

Aim: To characterize the protein files in blood from same patients with esophageal squamous cell carcinoma (ESCC) before and after operation at the high-incidence area for ESCC in Henan Province, China., Methods: Two-dimensional electrophoresis, silver staining and ImageMaster 2-DE analysis software were applied to the determination of protein files in the blood obtained from normal controls and ESCC patients before and after operation., Results: A total of 655, 662 and 677 protein spots were identified, respectively, from the normal controls and ESCC patients before and after operation. No significant difference in the number of protein spots was observed between the normal group and ESCC patients. A total of seven protein spots were identified with a dramatic difference among the samples before and after operation. Six protein spots were up-regulated and one protein spot was down-regulated in the group after operation compared with those in normal and before operation. Three protein spots were further characterized by matrix-assisted laser desorption/ionization time of flying mass spectrometry (MALDI-TOF-MS). The proteins from these three spots were identified as serum amyloid A (SAA), amyloid related serum protein and haptoglobin., Conclusion: Serum amyloid A, amyloid related serum protein and haptoglobin may be related with ESCC and/or surgery. The significance of these proteins needs to be further characterized. The present study provides informative data for the establishment of serum protein profiles related with ESCC.

Objective: To study the relationship between COX-2 expression in esophageal cancer cell (EC/CUHK-1) and mitomycin C (MMC) treatment., Methods: 2 mg/L of MMC was added to the well-grown EC/CUHK-1 cells cultured in RPMI-1640 including 10% FCS, and the medium was totally changed after 0.5, 1, 2, 4 and 8 h treatment, respectively. Cells were collected after another 24 h culture. Protein expression of COX-2, Bcl-2, Rb, p53 were examined by Western blot, and RT-PCR method was used to confirm the COX-2 expression in mRNA level. Cell cycle analysis for cells collected at 0, 0.5, 2, 4 and 8 h was performed on an EPICS profile analyzer., Results: The cell cycle analysis showed that the percentage of apoptosis cells were (4.12 +/- 0.83)%, (1.00 +/- 0.11)%, (4.32 +/- 0.99)%, (9.46 +/- 2.11)% and (31.10 +/- 3.57)%, respectively. COX-2 mRNA expression were 2.60, 1.70, and 0.08 times, COX-2 protein expression were 2.0, 3.1 and 2.8 times, Bcl-2 protein were 3.6, 14.0 and 12.0 times, p53 protein were 1.8, 0.5 and 0.2 times, hyperphosphorylated form Rb were 8.2, 8.4 and 6.2 times, underphosphorylated form Rb were 1.8, 0.5 and 0.2 times in 0.5, 2 and 4 h after MMC treatment, respectively, as compared with the control group., Conclusions: The COX-2 expression showed coincidence up-regulation according to the MMC-induced anti-apoptosis function activation in esophageal cancer cells, and the process was at least partly associated with Rb phosphorylation and p53 accumulation. It is implied that COX-2 may be a protecting factor in MMC induced esophageal cancer cell apoptosis, and the use of COX-2 inhibitor as an enhancer for esophageal cancer chemotherapy may be reasonable.

Aim: To further characterize the possible relationship between the molecular changes and prognosis of ESC and to elucidate the possible mechanisms involved., Methods: 114 specimens of ESC were collected from Linzhou city, and all patients were followed up for more than 5 years after resection. Histopathological analysis and immunohistochemical staining (ABC) were employed to detect the alteration of MUC1., Results: The positive immunostaining rate for MUC1 was 79 % (90/114), and the high-expression rate was 63 % (72/114). The mean survival periods (months) of those with high- and low-expression rates of MUC1 were 41 (95 % CI: 35, 47) and 52 (95 % CI: 45, 59), respectively. Patients in the low-expression group obviously survived longer than those in high-expression group, and the difference was significant (P<0.05). The expression of MUC1 protein in the esophageal carcinoma specimens with metastasis was stronger than those without metastasis, the difference was also significant (P<0.05). The stepwise multivariate analysis showed that "differentiation", "expression of MUC1" and "TNM staging" were the most important factors affecting the prognosis of esophageal carcinoma patients (P<0.05)., Conclusion: A good correlation between the alteration of MUC1 and the regional lymph node metastasis was observed. Furthermore, high-expression of MUC1 was associated with poor prognosis for esophageal cancer patients. These results indicated that MUC1 is a promising biomarker for predicting lymph node metastasis and prognosis in esophageal cancer.