Key Word(s): 1. BRBNS; 2. severe anaemia; 3. angiodysplasia; 4. bleeding; Presenting Author: KAKA RENALDI Corresponding Author: KAKA RENALDI Affiliations: CiptoMangunkusumo Hospital Objective: Colonic diverticular bleeding is the most common cause of overt lower

gastrointestinal bleeding in adults. In most cases, the bleeding will stop spontaneously. However, if the bleeding persists, endoscopic, radiologic, or surgical intervention may be required. Here we demonstrate a case where the bleeding from colonic diverticulum can be manage with somatostatin and rebamipide. We thougt that the effect of somatostatin in decreasing the blood flow to the bowel and the effect of rebamipide in protecting the BGB324 solubility dmso colonic epithelial can overcome the bleeding. Methods: Case: A 65 year old woman, came with a syok, pale and hematoschezia. She had the history using asetyl salysilic

acid for 5 2 years for her chronic heart disease. From the gastroscopy there was no sign of active bleeding. At that time we could not perform Idasanutlin in vitro colonoscopy due to the condition. We gave blood transfusion, high dose PPI, somatostatin and rebamipde. After 3 days the bleeding resolve, but when the somatostatin was stoped, the bleeding appeared again. We continued to give somatostatin and after the bleeding stoped again we continued 3 days more. After 3 days without bleeding than we performed the colonoscopy. We saw many Diverticul selleck chemicals in colon, with sign of recent bleeding without any active bleeding. We than discharged the patient. Results: The use of Somatostatin and Rebamipide can stop colonic diverticular bleeding. Conclusion: Somatostatin and Rebamipide might be helpful in managing Colonic Diverticular Bleeding. Key Word(s): 1. diverticular; 2. bleeding; 3. somatostatin; 4. rebamipide; Presenting Author: SHAMALWALSAYED RAHIM SHAH Additional Authors: HUANGJIE AN Corresponding Author:

HUANGJIE AN Affiliations: guangxi medical university Objective: To review the peptic ulcer bleeding epidemiology, etiology, clinic, diagnosis and management by endoscopy. Methods: This article provided by the review of literature articles and the First Affiliated Hospital of Guangxi Medical University patients’ data bank. Results: Peptic ulcer bleeding is the most significant complication of ulcer disease, remaining the most important reason for upper gastrointestinal bleeding even in the era of Helicobacter pylori eradication. Endoscopic triage and management plays a vital role in the handling of these patients. Endoscopy is recommended within 24 h of presentation. Endoscopic therapy is indicated for patients with high-risk stigmata, in particular those with active bleeding and visible vessels. The role of endoscopic treatment for ulcers with adherent clots remains to be elucidated. Ablative or mechanical therapies are superior to epinephrine injection alone in terms of preventing of rebleeding.

In addition, it allows the detection of mixed H. pylori strains [34]. Besides molecular methods, essentially amplicon sequencing, the East Asian type cagA (D type) can also be detected by ELISA using a specific monoclonal antibody (sensitivity 88% and specificity 100%) [35] or by immunohistochemistry as was performed on a large number of strains (385) from Vietnam and Thailand.

The sensitivity and specificity of this ELISA versus sequencing were 96.7 and 97.9%, respectively [36]. Bernarde et al. used another approach: surface-enhanced laser desorption/ionisation time of flight (SELDI-TOF) mass spectrometry to detect proteins specific for strains involved in specific diseases. They found an overexpression of a 50S ribosomal protein L7/L12 (13.2 kDa) in gastric MALT lymphoma and of a urease subunit (23.6 kDa) in peptic ulcer disease KU-57788 order [37]. Many studies have evaluated UBT in different settings. In general, UBT had an excellent reliability provided patients receive pretreatment with citric acid, and the dose of 13C-urea administered was not lower than 75 mg. By contrast, lack of local validation, the elimination of the citric acid pretreatment, and the use of lower doses of 13C-urea seem to be associated with poor results. Along these lines,

Elitsur et al. [38] evaluated UBT in 176 American children undergoing endoscopy. Children this website received a 75- mg dose of 13C-urea plus citric acid and were tested before and 15 minutes after the urea administration. They found a sensitivity of 98% and a specificity of 96%. In addition, they reported that in children 2–5 years old, the urea hydrolysis rate, obtained by correcting the delta over baseline (DOB) values by the CO2 production rate, is more sensitive than, but equally specific to, the uncorrected DOB. Similarly, Vaira et al. [39] validated a new UBT consisting of two tablets each combining

citric acid with 37.5 mg of 13C-urea with breath sampling after 10 minutes and compared it to histology, urease test, and conventional UBT in 200 adult patients. They found that both the standard and the new UBT had a sensitivity and specificity >99% both before and after treatment. By contrast, Calvet et al. [40] compared commercially available UBT containing 100 mg of 13C-urea, but which did not include citric acid pretreatment, selleckchem to histology, urease test, and stool tests in 199 patients. They found an unexpectedly large number of false positive tests and an unacceptably low specificity (61%) for the UBT. The authors attributed the low specificity of the test to the absence of previous local validation. After recalculating the cutoff value, the sensitivity and specificity for the UBT improved but still remained lower than expected, around 90%. These suboptimal results were attributed to the lack of citric acid pretreatment. In addition, some studies dealt with special diagnostic situations. Adamopoulos et al.

The interactions of H. pylori VacA cytotoxin and ANTs were detected by yeast two-hybrid and co-immunoprecipitation assays. Results: Transfection of H. pylori VacA p37 increased the mRNA and protein expression of ANT1 and ANT3, but not ANT2. Moreover, VacA p37 up-regulated Bax expression of but down-regulated Bcl expression of -2 at both mRNA and protein levels in AGS cells. Yeast two-hybrid and

co-immunoprecipitation assays did not show any protein interaction between H. pylori VacA p37 and ANTs. Conclusion: H. pylori selleck VacA induces mitochondrion-mediated apoptosis of AGS cells in an ANT isoform-specific manner, and the Bcl-family is involved in this process. However, H. pylori VacA appears not to directly interact with ANTs to mediate mitochondrion-mediated apoptosis. Key Word(s): 1. Helicobacter pylori; 2. VacA cytotoxin; 3. ANTs; 4. Yeast two-hybrid; Presenting Author: FENGPING ZHENG Additional Authors: XIANYI LIN, LI TAO, YUNWEI GUO Corresponding Author: FENGPING ZHENG Affiliations: The Third Affiliated Hospital of Sun Yat-Sen University Objective: Increasing

resistance against H. pylori has resulted in reduced eradication rates. The efficacy and tolerability of a second-line furazolidone-containing triple regimen (PPI-amoxicillin-furazolidone) in the eradication of H. pylori was evaluated. Methods: 217 Patients with a diagnosis of HP-positive confirmed using endoscopy Pexidartinib or C13 urea breath testing were eligible for inclusion in this study. All patients underwent a washout period of 6 weeks from any prior antibiotic or PPI usage. Patients were randomized to either amoxicillin, furazolidone and esomeprazole therapy for 10 days, including amoxicillin 1000 mg twice daily with

meals, furazolidone 100 mg twice daily with meals, and esomeprazole 20 mg twice daily with meals, or esomeprazole, amoxicillin, and clarithromycin standard therapy for 10 days, which included esomeprazole 20 mg, amoxicillin 1 g with breakfast and dinner, and clarithromycin 500 mg with breakfast and dinner. HP eradication was confirmed selleck chemicals by C13 urea breath testing at least 4 weeks after cessation of therapy. Results: Intention-to-treat analysis revealed significant differences (P < 0.05) in the eradication rates of the amoxicillin, furazolidone, esomeprazole 10 days therapies were 82.9% (87/105) compared with those receiving standard treatment eradication rates were 73.2% (82/112). There were no differences in adverse effects between the groups. Conclusion: Amoxicillin, furazolidone and esomeprazole 10 days therapies were prior to standard treatment eradication. A large randomized controlled trial is warranted to further evaluate the efficacy of this regimen. Key Word(s): 1. Eradication; 2. Helicobacter Pylori; 3.

The interactions of H. pylori VacA cytotoxin and ANTs were detected by yeast two-hybrid and co-immunoprecipitation assays. Results: Transfection of H. pylori VacA p37 increased the mRNA and protein expression of ANT1 and ANT3, but not ANT2. Moreover, VacA p37 up-regulated Bax expression of but down-regulated Bcl expression of -2 at both mRNA and protein levels in AGS cells. Yeast two-hybrid and

co-immunoprecipitation assays did not show any protein interaction between H. pylori VacA p37 and ANTs. Conclusion: H. pylori selleck products VacA induces mitochondrion-mediated apoptosis of AGS cells in an ANT isoform-specific manner, and the Bcl-family is involved in this process. However, H. pylori VacA appears not to directly interact with ANTs to mediate mitochondrion-mediated apoptosis. Key Word(s): 1. Helicobacter pylori; 2. VacA cytotoxin; 3. ANTs; 4. Yeast two-hybrid; Presenting Author: FENGPING ZHENG Additional Authors: XIANYI LIN, LI TAO, YUNWEI GUO Corresponding Author: FENGPING ZHENG Affiliations: The Third Affiliated Hospital of Sun Yat-Sen University Objective: Increasing

resistance against H. pylori has resulted in reduced eradication rates. The efficacy and tolerability of a second-line furazolidone-containing triple regimen (PPI-amoxicillin-furazolidone) in the eradication of H. pylori was evaluated. Methods: 217 Patients with a diagnosis of HP-positive confirmed using endoscopy Belnacasan research buy or C13 urea breath testing were eligible for inclusion in this study. All patients underwent a washout period of 6 weeks from any prior antibiotic or PPI usage. Patients were randomized to either amoxicillin, furazolidone and esomeprazole therapy for 10 days, including amoxicillin 1000 mg twice daily with

meals, furazolidone 100 mg twice daily with meals, and esomeprazole 20 mg twice daily with meals, or esomeprazole, amoxicillin, and clarithromycin standard therapy for 10 days, which included esomeprazole 20 mg, amoxicillin 1 g with breakfast and dinner, and clarithromycin 500 mg with breakfast and dinner. HP eradication was confirmed selleck chemicals by C13 urea breath testing at least 4 weeks after cessation of therapy. Results: Intention-to-treat analysis revealed significant differences (P < 0.05) in the eradication rates of the amoxicillin, furazolidone, esomeprazole 10 days therapies were 82.9% (87/105) compared with those receiving standard treatment eradication rates were 73.2% (82/112). There were no differences in adverse effects between the groups. Conclusion: Amoxicillin, furazolidone and esomeprazole 10 days therapies were prior to standard treatment eradication. A large randomized controlled trial is warranted to further evaluate the efficacy of this regimen. Key Word(s): 1. Eradication; 2. Helicobacter Pylori; 3.

Only a subset of HDV carriers is reported to benefit from interferon-α (including peginterferon) treatment, the only approved anti-HDV therapy. Currently, there are no drugs in use to directly target HDV, and a number of anti-HBV drugs do not block HDV infection.1, 2, 5-8 In Europe, HDV-induced disease is frequent among immigrants from regions of higher HDV endemicity. HDV remains a serious problem in Vietnam, Iran, Pakistan, India, Tajikistan, Mongolia, Tunisia, Brazil, and other South American countries.1, 6, 9 Despite reports suggesting that chronic carriers of HBV/HDV have a 3-fold increased risk of HCC, and develop HCC ≈14 years earlier than

carriers of HBV only, there is no consensus opinion on the relationship between HDV infection and liver cancer. The molecular Opaganib solubility dmso basis of HDV pathogenesis is poorly understood and the role of HDV in HCC induction/development has yet to be elucidated.1, 5, 6, 10-13 To advance our understanding of the mechanism of HDV infection and its relation to liver Navitoclax concentration carcinogenesis, we determined whether HDV could infect in vivo the cells of hepadnavirus-induced HCCs. To accomplish this goal, we used woodchucks (Marmota monax) chronically infected with woodchuck hepatitis virus (WHV), a hepadnavirus that is closely related to HBV. The WHV carrier woodchucks are

a very valuable surrogate animal model to study HBV infection, hepadnavirus-induced HCC, and to test anti-HBV and anti-HCC drugs. Although chronic HBV carrier chimpanzees and wildtype HBV full genome selleck transgenic mice do not develop HCCs, 100% of chronic WHV carrier woodchucks develop HCCs usually within 12-36 months postinfection.4, 14 Furthermore, in the laboratory HDV can be coated with WHV envelope proteins, because the HDV-binding site is conserved within the orthohepadnavirus subfamily. Therefore, numerous in vivo studies on HDV infection were conducted using WHV carrier woodchucks superinfected with HDV.1, 2, 7 For HDV, a putative entry receptor

(the receptors for WHV and HBV are currently not identified) and the host range are defined by the origin of the hepadnavirus (i.e., HBV or WHV) envelope proteins forming the virion’s coat. For this reason, HDV is often used as a tool to study the mechanism of hepadnavirus attachment and entry.1, 2 Unlike previous studies, we for the first time have superinfected WHV carriers with WHV-enveloped HDV (wHDV) during the late stage of chronic WHV infection, when WHV-induced HCCs were already developed. Three out of three HDV-negative WHV carriers with formed HCCs were successfully superinfected with wHDV. All HCCs harvested upon the completion of the experiment were infected with wHDV.

Magnetic resonance imaging (MRI) with its excellent soft-tissue contrast, can accurately evaluate the early changes and the less advanced joint damage seen in patients receiving prophylactic therapy. MRI is the imaging PD0332991 method of choice for detecting the abnormalities of HA, staging their severity, and following the effects of treatment. “
“Most patients with hemophilia treated with nonvirally inactivated clotting factor concentrates have been infected with the hepatitis C virus (HCV). Viral inactivation introduced in 1985 virtually eliminated transmission. Spontaneous clearance occurred

in 15–20% in the first 6 months after infection. Chronic HCV may lead to cirrhosis, liver failure, and hepatocellular carcinoma (HCC) in the decades after infection. Independent risk factors for advanced liver disease included human immunodeficiency virus (HIV) coinfection, older age, alcohol abuse, and infection with HCV genotype 1. Death RG-7388 ic50 from liver failure in HCV-positive individuals is among the commonest causes of death in patients with inherited bleeding disorders. Current anti-HCV therapies are able to eliminate the virus in 50–80% of infected individuals depending on the treatment given and HCV genotype involved. The indications for liver transplantation in persons with hemophilia are the same as nonhemophilic individuals but the procedure has the major advantage of producing a phenotypic cure

of the hemophilia as a result of factor VIII production

by the transplanted liver. “
“Summary.  Carriers of haemophilia face difficult choices regarding prenatal diagnosis, but little is known about the determinants that influence their decisions. The aim of this study was to assess the incidence of prenatal diagnosis and potential determinants affecting the choice for prenatal diagnosis. A nationwide survey was performed among all women who underwent carriership testing for haemophilia in the Netherlands between 1992 and 2004. Prenatal diagnosis was assessed in 207 carriers of haemophilia A or B who had been pregnant. Prenatal diagnosis was categorized into early first trimester (Y-PCR testing or chorionic villus sampling) often intended to prevent the birth of a child with haemophilia, and selleck into late prenatal diagnosis (amniocentesis or ultrasound assessment) aimed at obstetrical management. Of 207 carriers 112 (54%) underwent prenatal diagnosis. Forty-eight women underwent early prenatal diagnosis and 64 women underwent late prenatal diagnosis. In 26 pregnancies early prenatal diagnosis was positive for haemophilia, and in 18 of these pregnancies termination was opted for. The choice for early prenatal diagnosis was associated with a liberal view towards termination of pregnancy (relative risk (RR) 12.5; 95% confidence interval (CI) 3.1–51.2), severe haemophilia in the family (RR 20.2; CI 2.7–153.6), absence of a religion (RR 1.9; CI 1.1–3.1) and older age (RR 2.0; CI 1.0–3.9).

Identification of clinical, radiological, and laboratory variables as well as new biomarkers independently associated with cognitive outcome remains an important challenge for further work involving severe TBI patients. With an incidence rate of 150–300 per 100,000 per year of hospitalized click here and fatal traumatic brain injuries (TBIs) in Europe – and higher in other parts of the world – head trauma

is likely to be the most probable aetiology of cognitive disorders due to a general medical condition (Bales, Wagner, Kline, & Dixon, 2009; Markowitsch & Staniloiu, 2012). TBI patients frequently suffer from long-term sequelae, which have personal, family, and social impact (Diaz et al., 2012; Marsh & Kersel, 2006). These sequelae are highly heterogeneous, comprising cognitive deficits, psychiatric disorders, motor and sensory impairments, epilepsy, and others (Diaz et al., 2012; Ietswaart, Milders, Crawford, Currie, & Scott, 2008; Schwarzbold et al., 2010). Cognitive deficits, however, stand out due to its elevated prevalence and impact in daily life (Larson, Perlstein, Demery, & Stigge-Kaufman, 2006).

Studies on moderate and severe TBI have found a significant impairment of cognition in up to 50% of patients (Kersel, Marsh, Havill, & Sleigh, 2001; Vakil, 2005). Studies on mild TBI have revealed selleck kinase inhibitor more variable results, with cognitive changes affecting less than 1%–20% of patients (Arciniegas, Anderson, Topkoff, & McAllister, 2005; Carroll et al., 2004). TBI can affect several domains of cognition, in particular attention, working, and long-term memory, processing speed, and executive functions (Mathias & Wheaton, 2007). Although patients tend to experience some improvement with time, cognitive selleck chemicals deficits frequently have a chronic evolution particularly after severe TBI, being present many years after trauma (Hoofien, Gilboa, Vakil, & Donovick, 2001; Ruttan, Martin, Liu, Colella, & Green, 2008). Moreover, cognitive deficits have been associated with poor psychosocial function, as well as behavioural and emotional problems (Chamelian & Feinstein, 2006; Mazaux et al.,

1997). Despite its importance, the mechanisms and determinants of cognitive impairment following TBI are poorly understood. From a neuroanatomical point of view, it is reasonable to consider that damage in a specific brain region may impair its function with regard to cognition. For example, damage to the dorsolateral prefrontal is likely to affect executive function and orbitofrontal damage seems to affect decision making (Bechara, Damasio, & Damasio, 2000). Temporal lesions may affect declarative memory (Markowitsch & Staniloiu, 2012). However, such neuroanatomical explanations are of limited value in the case of TBI, as TBI typically involves damage of a diffuse nature or in areas remote to the impact (Sidaros et al., 2008).

Identification of clinical, radiological, and laboratory variables as well as new biomarkers independently associated with cognitive outcome remains an important challenge for further work involving severe TBI patients. With an incidence rate of 150–300 per 100,000 per year of hospitalized PCI-32765 mw and fatal traumatic brain injuries (TBIs) in Europe – and higher in other parts of the world – head trauma

is likely to be the most probable aetiology of cognitive disorders due to a general medical condition (Bales, Wagner, Kline, & Dixon, 2009; Markowitsch & Staniloiu, 2012). TBI patients frequently suffer from long-term sequelae, which have personal, family, and social impact (Diaz et al., 2012; Marsh & Kersel, 2006). These sequelae are highly heterogeneous, comprising cognitive deficits, psychiatric disorders, motor and sensory impairments, epilepsy, and others (Diaz et al., 2012; Ietswaart, Milders, Crawford, Currie, & Scott, 2008; Schwarzbold et al., 2010). Cognitive deficits, however, stand out due to its elevated prevalence and impact in daily life (Larson, Perlstein, Demery, & Stigge-Kaufman, 2006).

Studies on moderate and severe TBI have found a significant impairment of cognition in up to 50% of patients (Kersel, Marsh, Havill, & Sleigh, 2001; Vakil, 2005). Studies on mild TBI have revealed Acalabrutinib datasheet more variable results, with cognitive changes affecting less than 1%–20% of patients (Arciniegas, Anderson, Topkoff, & McAllister, 2005; Carroll et al., 2004). TBI can affect several domains of cognition, in particular attention, working, and long-term memory, processing speed, and executive functions (Mathias & Wheaton, 2007). Although patients tend to experience some improvement with time, cognitive selleck chemicals deficits frequently have a chronic evolution particularly after severe TBI, being present many years after trauma (Hoofien, Gilboa, Vakil, & Donovick, 2001; Ruttan, Martin, Liu, Colella, & Green, 2008). Moreover, cognitive deficits have been associated with poor psychosocial function, as well as behavioural and emotional problems (Chamelian & Feinstein, 2006; Mazaux et al.,

1997). Despite its importance, the mechanisms and determinants of cognitive impairment following TBI are poorly understood. From a neuroanatomical point of view, it is reasonable to consider that damage in a specific brain region may impair its function with regard to cognition. For example, damage to the dorsolateral prefrontal is likely to affect executive function and orbitofrontal damage seems to affect decision making (Bechara, Damasio, & Damasio, 2000). Temporal lesions may affect declarative memory (Markowitsch & Staniloiu, 2012). However, such neuroanatomical explanations are of limited value in the case of TBI, as TBI typically involves damage of a diffuse nature or in areas remote to the impact (Sidaros et al., 2008).

In all CR patients after eradication treatment, the TLA finding had disappeared (100%); XL184 chemical structure however, in the non-CR patients, TLA remained the same as before the eradication therapy (p = 0.002). Conclusion: These results suggest that NBI magnifying endoscopy may be useful not only in the diagnosis but also in the evaluation of response to eradication therapy of MALT lymphoma of the stomach. Key Word(s): 1. NBI; 2. malt Presenting Author: KOUICHI NONAKA Additional Authors: KEN OHATA, MAIKO TAKITA, YASUSHI MATSUYAMA, TOMOAKI TASHIMA, YOHEI MINATO, NOBUYUKI MATSUHASHI Corresponding Author: KOUICHI NONAKA Affiliations: Ntt Medical Center Tokyo, Ntt Medical Center

Tokyo, Ntt Medical Center Tokyo, Ntt Medical Center Tokyo, Ntt Medical Center Tokyo, Ntt Medical Center Tokyo Objective: Probe-based confocal laser endomicroscopy (pCLE) is a new imaging modality that enables the in vivo histological RXDX-106 solubility dmso evaluation of gastrointestinal mucosa during ongoing endoscopy. As confocal imaging is possible by fluorescein of the tissue, fluorescein contrast is necessary for pCLE. Fluorescein is intravenously administered. The side effects of fluorescein include yellow-colored urine, nausea, and exanthema. However, these symptoms resolve over time. Other severe adverse effects are extremely rare. However, some studies indicated that the intravenous administration of fluorescein caused shock or arterial ischaemia. To promote the widespread application of pCLE,

an alternative method in which pCLE can be more safely performed compared

to the intravenous administration of fluorescein should be developed. We successfully obtained selleck compound an image quality similar to that on intravenous administration by dripping fluorescein in the duodenal mucosa, and not by intravenous administration, and reported it as a first in the world (Digestive Endoscopy, 2014). Methods: In 3 subjects, crystal violet, indigo carmine, Lugol’s iodine, and 10% fluorescein were dripped on the upper gastrointestinal mucosa (esophagus, gastric body, and duodenum) in this order. Finally, 2.5 mL of 10% fluorescein was intravenously injected, and the image with this was used as a control. Results: In the stomach and duodenum, images could be acquired only with the dripping and intravenous injection of fluorescein in all subjects, and the images were favorable for histological evaluation. In the esophagus, images could also be acquired only with the dripping and intravenous injection of fluorescein, but the images were insufficient to evaluate the histology. Conclusion: Confocal laser endomicroscopy was suggested to be inappropriate for histological evaluation of the esophageal mucosa. For the stomach and duodenum, it was suggested that dripping a very small amount of fluorescein is an alternative to intravenous administration, being a clue to promoting the widespread of confocal laser endomicroscopy. We also report on the preparation and skills for the fluorescein dripping method. Key Word(s): 1.

However, both LEA and HEA increased the level of S-SCF in 8 weeks compared with DM group. Conclusion: LEA and HEA at ST36 promoted the contraction of gastric antrum involved the SCF/c-kit pathway in diabetic rats. Key Word(s): 1. EA; 2. ICC; 3. contraction; 4. SCF/c-kit pathway; Presenting Author: KUILIANG LIU Additional Authors: JING WU, XIANGCHUN LIN, GUOJUN JIANG, HUI SU, HUI GE Corresponding Author: JING WU Affiliations: Beijing Shijitan Hospital Objective: To determine the high-resolution manometry (HRM) characteristics of esophageal motion in GERD patients which remains unknown. Methods: Analyze retrospectively the clinical data

Palbociclib price of patients underwent HRM using Manoscan™ (Given Imaging, Los Angeles, CA) between Nov. 2011 check details and Apr. 2013 in our institution. Identify the GERD patients without gastrointestinal neoplasm or surgery. Results: A total of 95 patients, including 36 males and 59 females, were included, the average age was 56.3 ± 11.8 years old. The average LES resting pressure was 13.37 ± 6.52 mmHg, LES residual pressure was 8.89 ± 4.94 mmHg, contractile front velocity (CFV) 4.13 ± 2.01 cm/s, intra bolus pressure (IBP) 3.90 ± 3.30 mmHg, distal Latency (DL) 6.50 ± 1.63 s, distal contraction integral

(DCI) was 1365.80 ± 1296.68 mmHg-s-cm. Compared to patients with DCI over 450 mmHg-s-cm, 23 patients (24.2%) with DCI no more than 450 had more extraesophageal symptoms (43.5% vs 21.0%, p = 0.013) and esophageal mucosa damage (47.8% vs 40.3%, p > 0.05). see more According to Chicago criteria of 2012,

in 948 evaluable swallows, 101 (10.7%) were failed peristalsis, 15 (1.5%) were weak contraction with large break, 94 (9.9%) were weak contraction with small break, 11 were panesophageal pressurization, 35 (3.7%) were premature contraction, 22 were rapid contraction (2.3%),1 was hypercontractile. Besides, 9 patients (9.5%) had motility disorder, including 2 of absent peristalsis, 6 of distal esophageal spasm, 1 of hypercontractile esophagus; 24 patients (25.3%) had peristaltic abnormalities, including 7 of frequent failed peristalsis, 2 of weak peristalsis with large breaks, 13 of weak peristalsis with small breaks (1 had accompanied rapid contraction); 3 of rapid contractions with normal latency; 6 patients (6.3%) had EGJ outflow obstruction. In patients with distal esophageal spasm, 2 (33.3%) had additional retrosternal pain and mild dysphagia respectively; in patients with rapid contractions with normal latency, 1 (33.3%) had additional mild dysphagia; in patients with EGJ outflow obstruction, 2 (33.3%) had additional retrosternal pain and mild dysphagia respectively. Conclusion: Decreased esophageal peristalsis is common in GERD patients and might be associated with extraesophageal symptoms; the significance of occasionally enhanced motion as well as IBP remains to be explored. Key Word(s): 1. esophageal motion; 2. GERD; 3.