Overexpressions of RHOA, CSNK1A1, DVL2, FZD8, and LRP5 genes enhance gastric cancer development in the presence of Helicobacter pylori.

BACKGROUND AND STUDY AIMS: Intestinal metaplasia (IM), and Helicobacter pylori (HP) infection can be shown as risk factors in the development of gastric cancer (GC). WNT signaling pathway plays a critical role in carcinogenesis. However, the literature studies are limited on the significance of this pathway for the transition from IM to GC. PATIENTS AND METHODS: We aimed to investigate the importance of the genes of WNT signaling pathways diagnostic and prognostic markers in the presence and absence of HP in conversion from IM to GC. 104 patients, (GC group n = 35, IM group n = 45, control group n = 25) were included in this case-control study. Expression of genes in WNT signalling were searched in study groups with qRT-PCR array and qRT-PCR method. Data were analysed using PCR array data analysis software. RESULTS: Statistically significant overexpression of RHOA, CSNK1A1, DVL2, FZD8 and LRP5 genes was detected in the GC and IM groups compared to the control group (p < 0.05). Statistically significant overexpression of RHOA, CSNK1A1, DVL2, FZD8 and LRP5 genes was observed in patients with metastatic GC compared to patients with GC without metastasis (p < 0.05). It was found that the RHOA, CSNK1A1, DVL2, FZD8 and LRP5 genes were statistically significantly over-expressed in diffuse GC patients compared to non-diffuse GC patients (p < 0.05). Statistically significant overexpression of RHOA, CSNK1A1, DVL2, FZD8 and LRP5 genes was detected in HP positive IM patients compared to HP negative IM patients (p < 0.05). CONCLUSION: Overexpression of RHOA, CSNK1A1, DVL2, FZD8 and LRP5 genes in IM may suggest that these genes are important markers in the development of IM and inflammation with HP. In addition, these genes are linked to tumor burden in the GC group. Consequently, we can conclude that these genes are poor prognosis biomarkers for GC and have the potential to be used as markers for future treatment monitoring.

Steroid Resistance/Dependence Might Be an Alarming Feature for Cytomegalovirus Infection Among Ulcerative Colitis Patients With Increased Disease Activity.

Background/Aims This study aimed to determine the prevalence of cytomegalovirus (CMV) infection among patients with moderate to severe active ulcerative colitis (UC) and to determine the risk factors for CMV infection according to the demographic features of these patients. Patients/Methods A total of 183 patients with severe or moderate active UC were enrolled in the study after retrospective analysis. The disease severity of UC was determined according to the Mayo Score. CMV infection was investigated by real-time quantitative polymerase chain reaction (PCR) and the immunohistochemical (IHC) staining method in colonic mucosal biopsies. Results CMV infection was diagnosed in 33.9% of patients with UC. UC patients diagnosed with CMV infection had significantly higher Mayo Score levels (9.68 vs 8.56 and p=0.001). The long-term presence of UC disease, steroid, azathioprine (AZA), and anti-tumor necrosis factor-alpha (anti-TNF-alpha) usage increased the risk of CMV infection (p=0.001 and odds ratio=1.168; p=0.001 and odds ratio=2.967; p=0.004 and odds ratio=2.953; p=0.003 and odds ratio=3.861, respectively). CMV infection increases the risk of developing steroid resistance or dependency (p=0.002 and odds ratio=3.147; p=0.002 and odds ratio=5.085, respectively). Post-treatment clinical remission and mucosal healing rates were higher in CMV-negative patients than in CMV-positive patients (99.2% vs 91.9%, p=0.018 and 86.8% vs 70.9%, p=0.015). A higher rate of need for colectomy had been found in patients with CMV infection (5 patients vs 1 patient; p=0.034 and odds ratio=10.526). Conclusions The presence of CMV infection increases the severity of the disease and worsens clinical outcomes, leading to adverse treatment outcomes. CMV infection increases the requirement for colectomy. The presence of steroids, immunosuppressives such as AZA, and anti-TNF-alpha usage increases the occurrence of CMV infection. CMV infection should be suspected in patients with moderate to severe UC activity.

Mean platelet volume can indicate dietary adherence and disease severity of celiac disease.

Objective: At present, there is no reliable indicator for dietary compliance and disease severity in patients with celiac disease (CD). The aim of this study is to evaluate mean platelet volume (MPV) level as a biomarker for detection of disease activation, dietary adherence, and assessment of disease severity. Methods: Eighty-one patients with CD and 50 healthy subjects were enrolled in this study. The diagnosis of CD was established by both positive antibodies against endomysium or gliadin and histopathological criteria (lymphocytic infiltration and total villous atrophy in duodenal biopsies). Results: MPV was observed to be significantly higher among CD patients when compared to healthy controls (8.14±0.26 fL vs. 7.82±0.29 fL and p=0.001). Overall dietary adherence rate was 72.8% (58/81 CD patients). After induction of a gluten-free diet, the MPV was significantly lower in the dietary adherent group than non-adherent patients (7.86±0.17 fL vs. 8.07±0.30 fL and p=0.001). The increase of MPV was correlated with Marsh classification (Marsh 3 active CD vs. Marsh 2 active CD vs. Marsh 1 active CD; 8.32±0.27 fL vs. 8.12±0.19 fL vs. 7.98±0.19 fL; p=0.004 and p=0.009). Conclusion: Based on these data, we believe that increased MPV can provide additional benefit to screening in patients with CD. It can indicate the activation of the disease and adherence to the diet.

Potential role of chromatin remodeling factor genes in atrophic gastritis/gastric cancer risk.

BACKGROUND/AIMS: Atrophic gastritis (AG), intestinal metaplasia (IM), and Helicobacter pylori (HP) are the risk factors for the development of gastric cancer (GC). Chromatin remodeling is one of the epigenetic mechanisms involved in the carcinogenesis of GC. The purpose of this study was to investigate the expression profiles of defined chromatin remodeling genes in gastric mucosal samples and their values as gastric carcinogenesis biomarkers. MATERIALS AND METHODS: In total, 95 patients were included in the study. Patients were divided into 3 groups as: GC group (n=34), AG group (n=36), and control group (n=25). AG group was further divided into subgroups based on the presence of HP and IM in gastric mucosa. Chromatin remodeling gene expressions were analyzed using real-time PCR (RT-PCR) array in all groups. Data were evaluated using the RT-qPCR primer assay data analysis software. RESULTS: EED, CBX3, and MTA1 were more overexpressed, whereas ARID1A, ING5, and CBX7 were more underexpressed in the AG and GC groups compared with the controls. No significant differences were observed between the AG and GC groups concerning the expression of these 6 genes, although the fold change levels of these genes in the GC group were well above than in the AG group. EED, CBX3, and MTA1 were significantly more overexpressed in HP- and IM-positive AG subgroup compared with the HP- or IM-negative AG subgroup. CONCLUSION: In conclusion, our results provide an evidence of epigenetic alterations in AG. Expressions of EED, CBX3, MTA1, ARID1A, ING5, and CBX7 may be considered as promising markers to be used in GC screening for patients with AG.

Expression profiles of histone modification genes in gastric cancer progression.

Gastric cancer (GC) development can be attributed to several risk factors including atrophic gastritis (AG), intestinal metaplasia (IM), and the presence of Helicobacter pylori (HP). Also, histone modification is an epigenetic mechanism that plays a pivotal role in GC carcinogenesis. In this preliminary study, we aimed to describe the expression profiles of histone modification in the AG, IM, and GC patient groups. A total of 80 patients with AG (n = 27), IM (n = 25), and GC (n = 28) with an additional 20 control subjects were included in the study. Expression profiles of three histone phosphorylation genes (PAK1, NEK6, and AURKA) and five histone deacetylation genes (HDACs 1, 2, 3, 5, and 7) were examined based on the results of Real Time qPCR method. It was observed that AURKA and HDAC2 genes were significantly overexpressed in all groups compared to the control (P < 0.05). In GC patients, overexpression of HDAC2 gene was detected in the absence of metastasis, and overexpression of AURKA, HDAC2, and NEK6 genes was detected in the presence of metastasis. When cancer involvements were compared, significant overexpression of the HDAC2 gene was noted in overall and corpus involvements (P < 0.05). In addition, overexpression of AURKA, NEK6, HDAC1, and HDAC2 genes and underexpression of HDAC5 gene were detected in the antrum involvement (P < 0.05). In conclusion, decreased expression of HDAC5 in GC is reported for the first time in this study, while supporting the existing literature in AURKA, NEK6, HDAC1, and HDAC2 up regulations during GC development.

Treatment of inflammatory bowel disease by leukocytapheresis.

Studies about leukocytapheresis have emerged with the need of search for alternatives to conventional treatment in inflammatory bowel diseases (IBD). Leukocytapheresis is a novel non-pharmacologic approach for active ulcerative colitis (UC) and Crohn's disease (CD), in which leukocytes are mechanically removed from the circulatory system. Patients with active IBD treated with leukocytapheresis using a Cellsorba E column between 2012 and 2015, were enrolled in Turkey. In our experience, the results of leukocytapheresis therapy in 6 patients with CD and 20 patients with active UC were overviewed. Leukocytapheresis (10 sessions for remission induction therapy, 6 sessions for maintenance therapy) was applied to the patients with their concomitant medications. Intensive leukocytapheresis (≥4 leukocytapheresis sessions within the first 2 weeks) was used in 30% patients with active severe UC. The overall clinical remission rate in patients with UC was 80%, and the mucosal healing rate was 65%. Patients were followed for an average of 24 months. It was observed that clinical remission has continued in 65% of patients with UC. Mild relapse was observed in 3 patients with UC during follow up period. In 5 patients with CD significant clinical remission was achieved except only one patient. Surgical needs were disappeared in 3 patients with obstructive type Crohn's disease. Adverse events were seen in only 4.3% of 416 sessions. Any concomitant medications did not increase the incidence of adverse events. Our results indicate that leukocytapheresis is efficacious in improving remission rates with excellent tolerability and safety in patients with IBD.

Alteration in Methylation Pattern of Retinoblastoma 1 Gene Promotor Region in Intestinal Metaplasia with or without Helicobacter pylori and Gastric Cancer Patients.

BACKGROUND: Helicobacter pylori, intestinal metaplasia (IM), and gene methylation play important roles in gastric carcinogenesis. However, the association among H. pylori infection, IM, gastric cancer (GC), and gene methylation is not fully understood. Cell cycle control involving retinoblastoma 1 (RB1) gene is one of the main regulatory pathways reported to be altered in gastric carcinogenesis. OBJECTIVES: The purpose of this research is to assess the methylation status of RB1 gene in GC and IM with or without H. pylori infection, and to discuss the possible role of H. pylori-induced RB1 gene methylation in the mechanism of gastric carcinogenesis. MATERIAL AND METHODS: The methylation profile of RB1 gene was analyzed by sodium bisulfite modification and methylation-specific PCR in GC (n = 24), IM patients with H. pylori positive (n = 20) and negative (n = 20), and control subjects (n = 20). RESULTS: According to methylation levels in RB1 gene; the high correlation values were detected between H. pylori positive-IM group and GC group, and between H. pylori positive-IM and H. pylori negative-IM groups (p < 0.05). No correlations between H. pylori negative-IM and GC groups and between GC and control groups were detected in methylation status of RB1 gene. CONCLUSIONS: High methylation levels in RB1 gene in H. pylori positive individuals may suggest an elevated risk of gastric cancer occurrence.

The potential role of the NEK6, AURKA, AURKB, and PAK1 genes in adenomatous colorectal polyps and colorectal adenocarcinoma.

Colorectal adenomatous polyp (CRAP) is a major risk factor for the development of sporadic colorectal cancer (CRC). Histone modifications are one of the epigenetic mechanisms that may have key roles in the carcinogenesis of CRC. The objective of the present study is to investigate the alternations in the defined histone modification gene expression profiles in patients with CRAP and CRC. Histone modification enzyme key gene expressions of the CRC, CRAP, and control groups were evaluated and compared using the reverse transcription PCR (RT-PCR) array method. Gene expression analysis was performed in the CRAP group after dividing the patients into subgroups according to the polyp diameter, pathological results, and morphological parameters which are risk factors for developing CRC in patients with CRAP. PAK1, NEK6, AURKA, AURKB, HDAC1, and HDAC7 were significantly more overexpressed in CRC subjects compared to the controls (p < 0.05). PAK1, NEK6, AURKA, AURKB, and HDAC1 were significantly more overexpressed in the CRAP group compared to the controls (p < 0.005). There were no significant differences between the CRAP and CRC groups with regards to PAK1, NEK6, AURKA, or AURKB gene overexpression. PAK1, NEK6, AURKA, and AURKB were significantly in correlation with the polyp diameter as they were more overexpressed in polyps with larger diameters. In conclusion, overexpressions of NEK6, AURKA, AURKB, and PAK1 genes can be used as predictive markers to decide the colonoscopic surveillance intervals after the polypectomy procedure especially in polyps with larger diameters.

Never in mitosis gene A-related kinase 6 and aurora kinase A: New gene biomarkers in the conversion from ulcerative colitis to colorectal cancer.

Ulcerative colitis (UC) is an important risk factor for colorectal cancer (CRC). Histone modifications are one of the epigenetic mechanisms that may have key roles in the carcinogenesis of CRC. At present, there are no studies comparing histone modification patterns of UC and CRC in the literature. Therefore the aim of the present study was to investigate whether genes, particularly those involved in histone modification, have value in patient monitoring with regards to CRC development in UC. Key gene expressions of the histone modification enzyme were assessed and compared in CRC, UC and control groups using the RT-PCR array technique. Patients were divided into subgroups based on the extent and duration of the disease and inflammatory burden, which are considered risk factors for CRC development in UC patients. In UC and CRC groups, a significantly higher overexpression of the NEK6 and AURKA genes compared to the control group was identified. In addition, there was a significantly higher overexpression of HDAC1 and PAK1 genes in the UC group, and of HDAC1, HDAC7, PAK1 and AURKB genes in the CRC group. NEK6, AURKA, HDAC1 and PAK1 were significantly overexpressed in patients with a longer UC duration. Overexpression of AURKA and NEK6 genes was significantly more pronounced in UC patients with more extensive colon involvement. HDAC1, HDAC7, PAK1, NEK6, AURKA and AURKB are important diagnostic and prognostic markers involved in the carcinogenesis of CRC. HDAC1, PAK1, NEK6 and AURKA may be considered as diagnostic markers to be used in CRC screening for UC patients.

Schizophrenia and gastroesophageal reflux symptoms.

BACKGROUND: Psychological factors and psychiatric disorders play a role in a variety of gastrointestinal illnesses, including esophageal diseases. AIM: The aim of the present study was to evaluate the frequency of gastroesophageal reflux disease symptoms in patients with schizophrenia in Turkey. PATIENTS AND METHODS: Ninety-eight patients with schizophrenia and one hundred control individuals were enrolled in the study, which was undertaken at the Manisa State Hospital for Mental Health and Neurological Disorders and Celal Bayar University Gastroenterology Department. Case and control subjects alike underwent 30-45 min oral interviews conducted by a designated study coordinator (E.K.). The coordinator gathered information about demographic characteristics, social habits, and a large variety of symptoms suggestive of reflux disease or other gastrointestinal conditions. RESULTS: In terms of reflux symptoms, cough was the only significant association in schizophrenic patients than controls. Heartburn and regurgitation were more frequent in schizophrenic patients who smoked than in controls who were smokers. However, the prevalence of reflux symptoms in cigarette smokers versus nonsmoker patients with schizophrenia was similar. Heartburn and/or regurgitation occurred more frequently in patients with schizophrenic than controls with alcohol use. CONCLUSIONS: Psychiatric disorders might indirectly affect esophageal physiology through increased consumption of alcohol and nicotine.

The association between insulin resistance and hepatic fibrosis in patients with chronic hepatitis C: an observational, multicenter study in Turkey.

BACKGROUND/AIMS: To evaluate the association between insulin resistance and hepatic fibrosis in patients with chronic hepatitis C. MATERIALS AND METHODS: A total of 104 chronic hepatitis C patients were included in this non-interventional, open-label, observational, multicenter, cross-sectional study conducted at 20 gastroenterology clinics in Turkey. The primary end point was the correlation between stage of hepatic fibrosis and insulin resistance evaluated via the homeostasis model of assessment-insulin resistance index. Confounders of hepatic fibrosis and insulin resistance were the secondary end points. RESULTS: The mean age of patients was 52.8 years; 65.4% were female. Type 2 diabetes was present in 6.8% and insulin resistance noted in 38.0% of patients. Further, 45.7% of the patients had mild (A0/A1) and the remaining had moderate/severe (A2/A3) hepatic necroinflammatory activity. Patient distribution according to Metavir fibrosis stage was as follows: F0/F1 (57.0%); F2 (6.5%); F3 (23.7%); and F4 (12.9%). A univariate analysis revealed significant positive correlations between Metavir fibrosis stage and insulin resistance (r=0.297; p=0.007). Logistic regression analysis showed that significant predictors of insulin resistance were high alanine transaminase levels (odds ratio, 0.97; 95% confidence interval, 0.944-0.997) and liver fibrosis stage (odds ratio, 0.114; 95% confidence interval, 0.021-0.607). CONCLUSION: Our findings revealed significant associations between insulin resistance and hepatic fibrosis.

Aurora kinase A (AURKA) and never in mitosis gene A-related kinase 6 (NEK6) genes are upregulated in erosive esophagitis and esophageal adenocarcinoma.

Gastroesophageal reflux disease is a risk factor for esophageal adenocarcinoma yet studies that have investigated the relationship between erosive esophagitis and esophageal adenocarcinoma have usually focused on symptom-related evidence or polymorphisms. There are no epigenetic gene expression studies on this topic. In this study, we aimed to evaluate the relationship between erosive esophagitis and esophageal adenocarcinoma to identify whether there is a genetic predisposition for esophageal adenocarcinoma. The Human Epigenetic Chromatin Modification Enzyme RT(2) Profiler(™) PCR array (PAHS-085A) was used to detect the expression of 84 key genes encoding enzymes. This was carried out prospectively for samples from 60 patients (20 patients as a control group, 20 patients with erosive esophagitis and 20 patients with esophageal adenocarcinoma). AURKA, AURKB, NEK6 were expressed at significantly higher levels in esophageal adenocarcinoma compared to the control group. MBD2 was expressed at significantly lower levels in the esophageal adenocarcinoma group compared to the control group. AURKA, AURKC, HDAC9 and NEK6 were expressed at significantly higher levels in erosive esophagitis compared to the control group. There was no difference in upregulated gene expression between the erosive esophagitis and esophageal adenocarcinoma. MBD2 was significantly downregulated in esophageal adenocarcinoma compared to erosive esophagitis. NEK6 and AURKA were significantly upregulated in esophageal adenocarcinoma and erosive esophagitis compared to the control group. This is a novel study on the genetic predisposition for erosive esophagitis and esophageal adenocarcinoma. AURKA and NEK6 are two promising genetic markers for erosive esophagitis and esophageal adenocarcinoma.

GSTP1 gene methylation profiles in Helicobacter pylori (+) and (-) antral intestinal metaplasia and distal gastric tumour patients in Turkish population.

BACKGROUND/AIMS: Gastric cancer (GC) is the second most common malignancy worldwide, with a high mortality rate. The incidence of GC has declined in the western countries during the last decades. The glutathione S-transferases comprise a group of enzymes that are critical in the detoxification of carcinogens. In this study we aimed at the relationship GSTP-1 methylation in patients with intestinal metaplasia with and without Helicobacter pylori infection, gastric cancer and controls. METHODOLOGY: The methylation status of GSTP1 gene was analyzed by methylation specific PCR after bisulfate modification in H. pylori (+) (n=25) and (-) (n=25) intestinal metaplasia (IM) patients, GC (n=25) and control subjects (n=15) between September 2009 to November 2011. RESULTS: During the study period 90 patients who underwent endoscopic examination were included in the study. When we considered the GSTP1 gene methylation profile in all of the groups; 26 (28%)patients had methylated GSTP1 gene, 31 (34%) patients had unmethylated GSTP1 gene and 33 (36%) patients had heterogeneously methylated GSTPI gene. CONCLUSIONS: GSTP1 gene methylation profile is not appropriate for early diagnosis of cases with gastric cancer.

Does Helicobacter pylori treatment improve the symptoms of globus hystericus?

BACKGROUND/AIMS: Globus hystericus is a feeling of tension in the throat, irrelevant of swallowing, persisting for at least 12 weeks. Since the cause of globus hystericus is not fully described, the treatment is controversial. We aimed in this study to determine the symptoms of gastroesophageal reflux disease, upper gastrointestinal endoscopic findings, prevalence of Helicobacter pylori,and post-treatment symptoms (symptoms of gastroesophageal reflux and/or Helicobacter pylori) in patients with a diagnosis of globus hystericus. MATERIALS AND METHODS: One hundred twenty three patients were recruited from the archives of the Department of Gastroenterology and Endoscopy at Celal Bayar University Medical School between January 2009 and August 2010. RESULTS: Helicobacter pylori was positive in 75 (60%) of 123 patients with globus hystericus. Helicobacter pylori (+) patients had significantly more heartburn, regurgitation, and inlet patch in upper esophagus than Helicobacter pylori (-) patients. Significantly more Helicobacter pylori (-) patients had normal endoscopy findings when compared to Helicobacter pylori (+) patients. While 27 (50%) of Helicobacter pylori-eradicated patients had regressing globus symptoms, 12 (17.3%) of them did not have any regression in globus symptoms. Improvement in symptoms showed a positive correlation with Helicobacter pylori eradication (p=0.001). CONCLUSIONS: Helicobacter pylori rate among cases with globus sensation was similar to values in the general population. Helicobacter pylori eradication was found to decrease globus symptoms.

Correlation among standard endoscopy, narrow band imaging, and histopathological findings in the diagnosis of nonerosive reflux disease.

BACKGROUND AND AIMS: Gastroesophageal reflux disease (GERD) is caused by the reflux of gastric contents into the esophagus. Narrow band imaging (NBI) facilitates mucosal surface evaluation and may improve the endoscopic diagnosis of GERD. The diagnosis of GERD is based on the combination of clinical symptoms, endoscopic findings, and histological changes. In this study we aimed to show the differences between standard white light endoscopy and the NBI technique in squamo-columnar junction evaluation. We also evaluated the patients with NERD, as determined by standard white light endoscopy, using the NBI technique and histopathological mucosa examination (inflammation or normal mucosa). METHODS: A total of 60 subjects were recruited prospectively: 40 with nonerosive reflux disease (NERD) and 20 with erosive reflux disease (ERD). Patients were subjected to esophagogastroduodenoscopy and, in all of them, two biopsies were taken 2 cm above the esophagogastric junction. RESULTS: NBI was more sensitive than standard white light endoscopy in distinguishing normal endoscopic findings. Histopathological findings were more prevalent than the mucosal changes diagnosed by the standard white light endoscopy and NBI. CONCLUSION: NBI is more sensitive than white light endoscopy in detecting inflammation in NERD patients. However, histopathological evaluation is the most sensitive, therefore taking a biopsy will remain useful.

The role of heme in hemolysis-induced acute pancreatitis.

BACKGROUND: The aim was to reveal the mechanism of hemolysis-induced acute pancreatitis and to evaluate the role of heme and heme oxygenase activity in inducing pancreatic inflammation in an experimental hemolysis model. MATERIAL/METHODS: Hemolytic anemia was induced in rats by intraperitoneal injection of 60 mg/kg acetylphenylhydrazine (APH). To evaluate the toxic effect of free heme after hemolysis, heme oxygenase inhibitor (HOI) was used to inhibit the enzyme which decreases the free heme concentration after hemolysis. One hundred and fifty rats were divided into two treatment and three control groups. Rats in the hemolysis group were given APH intraperitoneally. Rats in the HOI+hemolysis group were given Cr(III)mesoporphyrin IX chloride as HOI and then APH intraperitoneally. Serum amylase and lipase levels as well as pancreatic tissue cytokine content were determined and histological examination performed. RESULTS: No hemolysis or pancreatitis was seen in the control groups. Massive hemolysis was seen in 22 of the 30 rats of the hemolysis group and 20 of the 30 rats of the HOI+hemolysis group. The total pancreatitis rates were 60% and 76.6% in the hemolysis and HOI+hemolysis groups, respectively (p<0.05). Pancreatic cytokine levels were significantly higher in the HOI+hemolysis and hemolysis groups than in all control groups. The highest ICAM-1 and MCP-1 levels were in the HOI+hemolysis group. Histological signs of acute pancreatitis were also more severe in this group. CONCLUSIONS: Acute massive hemolysis can induce acute pancreatitis. Excess of free vascular heme seems to be an inducer of inflammation by modulating ICAM-1 and MCP-1.

Midazolam-induced sedation for upper gastrointestinal endoscopy: assessment of endoscopist and patient satisfaction.

Upper gastrointestinal endoscopy can be performed without intravenous sedation but the evidence suggests most patients and endoscopists prefer some form of premedication. Intravenous diazepam or midazolam are used by the majority of endoscopists in the United States, though it is not common practice in Turkey where this study was conducted. This study aimed to evaluate the efficacy and safety of midazolam in performing upper gastrointestinal endoscopy. A total of 352 patients undergoing upper gastrointestinal endoscopy were sedated with midazolam given as a bolus injection over 5 seconds. Ages of the patients ranged between 16 and 79 years (average: 41.6 +/- 12.7 years). The course of endoscopy, anterograde memory, degree of cooperation, degree of sedation, side effects, and acceptability of further intervention were evaluated by a questionnaire given to the patients and endoscopists.

Somatostatin infusion and hemodynamic changes in patients with non-variceal upper gastrointestinal bleeding: a pilot study.

BACKGROUND: Intravenous somatostatin decreases acid secretion, splanchnic blood flow, and portal pressure, but the evidence for its efficacy in the treatment of non-variceal upper gastrointestinal bleeding has been mixed. We aimed to evaluate the vasoactive effect and possible mechanisms of somatostatin infusion in the cessation of non-variceal upper gastrointestinal bleeding. MATERIAL/METHODS: Patients with non-variceal upper gastrointestinal bleeding without portal hypertension were enrolled in the study. They were given somatostatin infusion in a dose of 250 microgr/hour for 72 hours. Superior mesenteric arterial average flow velocity (SMA-V), SMA pulsatility index (SMA-PI), portal venous volume flow (PV-F), and renal artery resistance index (RA-RI) were measured two times for each patient by Doppler ultrasound; once on the first day of infusion therapy and again 6 hours or more after stopping the infusion. RESULTS: 21 patients (12 male, mean age 44.1 +/- 9.9) with bleeding peptic ulcer were enrolled. During somatostatin infusion, PV-F was 33.7 +/- 12.7 cm3/sec. After stopping infusion, it increased to 56.3 +/- 16.0 cm3/sec (p=0.001). SMA-V was 39.7 +/- 13.1 cm/sec and 64.4 +/- 15.1 cm/sec during somatostatin infusion and after cessation of somatostatin respectively (p=0.01). SMA-PI was 2.0 +/- 0.8 during somatostatin infusion but 2.8 +/- 0.8 without somatostatin infusion (p=0.02). However, RA-RI showed no difference between states with or without somatostatin infusion (p>0.05). CONCLUSIONS: Somatostatin infusion causes a decrease in arterial blood flow to the stomach and duodenum in patients with non-variceal upper gastrointestinal bleeding without portal hypertension. Somatostatin therapy also decreases portal blood flow while not altering renal blood.