2A] and a higher dying risk (adjusted HR = 1.37 for XPC-LG and adjusted HR = 1.51 for XPC-GG; Table 5), particularly under high AFB1 exposure conditions (Fig. 2B,C). Furthermore, some evidence of multiplicative interaction was found for XPC genotypes Dactolisib manufacturer and AFB1 exposure years (Pinteraction = 0.012; Table 5). Because our previous study showed that the XPD codon 751 polymorphism, another DNA repair

gene involved in NER, modifies HCC risk in the Guangxi population,7 we explored possible interactions between XPC and XPD in 618 cases and 712 controls who had been previously studied.7 Because of the small number of subjects with both the homozygotes of the XPD codon 751 Gln alleles (XPD-GG) and XPC-GG, the combination

of these two genes was divided into four strata (Table 6). We found that individuals with both XPC-LG/GG and genotypes of the XPD codon 751 Gln alleles (XPD-LG/GG), in comparison with those with both XPC-LL and homozygotes of the XPD codon 751 Lys alleles (XPD-LL), might face a higher HCC risk (adjusted OR = 2.02, 95% CI = 1.42-2.87). A likelihood ratio test showed that there were multiplicatively interactive effects of XPC and XPD on the HCC risk (Pinteraction = 0.019). The most common cause of HCC is AFB1 exposure via the consumption of corn and groundnuts, which are Selleckchem NVP-BGJ398 primary food types for the Guangxi population, and HCC is one of the major cancer types in the Guangxi Zhuang Autonomous Region of China.1 Our previous studies5-7, 25, 27 and this study also show that HCC patients have more AFB1 exposure years and higher AFB1 exposure levels; moreover, we found that HCC risk is associated with different AFB1 exposure statuses. AFB1 is an important chemical carcinogen that is mainly metabolized by

cytochrome P450 into the genotoxic metabolic AFB1 epoxide; this GBA3 can bind to DNA, cause the formation of AFB1 guanine adducts, and induce DNA damage, including base damage and oxidative DNA damage that can be repaired by the NER pathway.2-4 XPC is an important DNA damage recognition molecule involved in the detection of a variety of DNA adducts formed by exogenous carcinogens such as AFB1.8-10 Some recent studies have shown that defects in XPC are related to many types of malignant tumors.21, 29 For example, Takebayashi et al.21 analyzed the loss of heterozygosity of XPC in sporadic ovarian, colon, and lung carcinomas. Their results showed that a deficiency of XPC results in the carcinogenesis of human tumors. Transgenic mouse studies have also revealed a predisposition to many types of tumors in XPC gene knockout mice.30 Our data also imply that a deficiency of XPC function promotes the carcinogenesis of HCC induced by AFB1 exposure. These results suggest that the XPC gene plays an important role in the prevention of DNA damage–mediated malignant tumor occurrence.

“
“Summary.  Currently, patients with severe haemophilia can expect

to lead a relatively normal life including prevention of disabling arthropathy as a result of the development of factor replacement therapy and advances in the understanding of the use of such therapy given prophylactically. Unfortunately, a subset of patients develops neutralizing antibodies termed inhibitors rendering such therapy ineffective. These patients frequently develop recurrent joint bleeding resulting in arthropathy. Until recently, prophylactic PD0325901 purchase therapy was not considered for patients with inhibitors because of the perceived lack of an effective therapeutic agent. However, an accumulation of case reports and a recent prospective study have suggested that prophylaxis with the currently

available bypassing agents could be effective and appears to be safe in selected cases. This report will review the current data on prophylaxis with bypassing agents and suggest specific situations in which prophylaxis in inhibitor patients could be considered. “
“Summary.  For patients with haemophilia, gastrointestinal (GI) bleeding is a life-threatening complication and can be caused by the Helicobacter pylori infection. Among children with haemophilia who had visited with GI bleeding, the prevalence of H. pylori infection and the recurrence rate after H. pylori eradication was investigated. Seven children with haemophilia A with hematemesis (age: 5.3–17.0 years) were evaluated for the causes GDC-0449 mouse of GI bleeding and the detection of H. pylori. Gastroendoscopy was done to find the bleeding focus and for further evaluation including rapid

urease test and mucosal biopsy. Four patients had dyspepsia and abdominal pain for several weeks or months prior to hematemesis. Three patients Reverse transcriptase did not show any symptoms of bleeding. From gastroendoscopy, four patients were diagnosed as duodenal ulcer, one as H. pylori associated chronic gastritis and one as haemorrhagic gastritis. One patient showing a normal finding was diagnosed with adenoid haemorrhage after nasopharyngoscopy. Helicobacter pylori infection was found in four of six patients with GI bleeding (3, duodenal ulcer; 1, H. pylori associated chronic gastritis). The patients with H. pylori infection had an eradication treatment of triple therapy and no recurrence happened. In children with haemophilia, H. pylori should also be considered as an important cause of GI bleeding. The recurrence of the infection and GI bleeding can be prevented with eradication of H. pylori. Screening test for H. pylori would be needed in children with haemophilia in endemic area. “
“Effective healthcare delivery necessitates evaluation of the effect of interventions in the form of outcome assessment.

Patients negative for both inversions were analysed using Conformation Sensitive Gel Electrophoresis click here for mutations in all exons, promoter region and 3′-UTR. sHA causative mutations were identified in 49 patients. Intron-22 and -1 inversions were detected in 41% and 0% of patients respectively. Besides these two mutations, 25 different mutations were identified, including nine nonsense, four small deletions, two small insertions, four missense, three splicing mutations and three large deletions. Seven novel mutations were identified, including two nonsense mutations, two small deletions,

one small insertion, one missense mutation and one splicing mutation. Thirty one percent of the patients with identified mutations developed inhibitors against exogenous FVIII. This is the first report of F8 mutations in patients with sHA in Venezuela; the data from this study suggests that the spectrum of gene defects found in these patients is as heterogeneous as reported previously for other populations. “
“Summary.  To prevent bleeding related to adenoidectomy and tonsillectomy, coagulation screening tests were, until recently, performed routinely in the Czech

Republic for all paediatric patients. The aim of this study was to evaluate benefit of preoperative coagulation screening tests in children. We retrospectively analysed laboratory and clinical Pictilisib manufacturer data of children referred for abnormal preoperative coagulation test results (aPTT, PT) to the outpatient haematology clinic. A total of 274 paediatric patients were retrospectively evaluated due to abnormal preoperative coagulation tests results. In 140 of 274 patients (51.1%), coagulation tests were normal on repeated see more testing in a specialized haematology clinic. Ten patients had decreased factor XII. Five patients had a suspected bleeding disorder which was confirmed in two of them. One patient had low levels of von Willebrand factor, and one patient had mild factor VII deficiency. Both these patients had positive personal and/or family history of bleeding. Each case history was taken individually, without

use of standardized questionnaires. Bleeding complications were not observed, and coagulation factor replacement was not needed perioperatively in our cohort. The majority of abnormal findings in aPTT and PT appeared only transiently. All the bleeding disorders found in our cohort of patients were mild in nature. Our findings provide supportive evidence for the current national Czech recommendation: laboratory coagulation screening should be performed only in patients with positive family and/or personal bleeding history. “
“Little data exist, especially for adolescent and young adult (AYA) persons with haemophilia (PWH), about the relationship between adherence to prescribed treatment regimen and chronic pain.

There was no difference in the proportion of deficiencies between elderly who reported a dental visit in the preceding year or not having seen a dentist. A quarter of the prostheses required replacement. The findings from this and the NHANES studies demonstrate that an engaged and recognized prosthodontic dental school faculty continues to be as important now as it was a generation ago. “
“Purpose: The purpose of this study was to assess the performance of an intraoral dental colorimeter. Materials and Methods: In GDC-0449 concentration vivo repeatability of an intraoral colorimeter was assessed by performing color measurements of 30 individuals’ right maxillary central incisor.

Three consecutive measurements from each individual were made. In the in vitro part of the study, 25 metal-ceramic and 25 all-ceramic specimens were prepared. Five shades of metal-ceramic

and all-ceramic specimens were selected for color determination. A widely recognized in vitro colorimeter was used as the control group for the in vitro performance assessment of the in vivo colorimeter. The color differentiation capability of two colorimeters was compared with the readings obtained from ceramic specimens. ΔE values between shade groups of ceramic specimens were calculated and statistically analyzed with Student’s t-test. The repeatability of the intraoral instrument was evaluated statistically with Intraclass correlation coefficient. Results: The in vivo evaluation results showed that the overall repeatability coefficient values of L*, a*, and b* notations of the intraoral Belnacasan concentration colorimeter were “excellent.” The color differences (ΔE) calculated between the colorimeters were significant only between shades A1-B1 for metal-ceramic specimens (p= 0.002); however, from 5 of 10 shade couples of all-ceramic specimens, the color differences obtained from the readings of the in vivo colorimeter were significantly different from that of the in vitro

colorimeter (p < 0.001). For all specimens, the differences between Bumetanide ΔE values were within clinically acceptable limits (<3.5). Conclusions: Within the limitations of this study, the intraoral colorimeter exhibited successful in vivo repeatability; however, the color difference detection performance of the device varied depending on the translucency of the specimens. "
“When a screw fracture occurs on a cement-retained, implant-supported restoration, the abutment and restoration are completely separated from the implant’s internal connection. Traditionally, an access hole is drilled through the crown to retrieve the broken screw, and the restoration can be placed again as a screw-retained restoration. This clinical report documents a patient whose broken abutment screw was retrieved from the restoration by burning off the cement and separating from the abutment without drilling an access hole.

We measured see more costs, quality adjusted life years (QALYs), incremental cost-effectiveness ratios (ICERs) and clinical outcomes such as development of hepatocellular carcinoma (HCC). Results: Results: We estimated that there are 1.5 million CHB infected persons in Shanghai. The M&T strategy costs US$20,730 per patient and results in a gain of 0.10 discounted QALYs per patient, with an ICER of US$2,996 per QALY gained, compared to the current practice. If variables such as adherence to monitoring and treatment are increased the M&T strategy

would reduce HCC by 70% and CHB-related mortality by 83% (Table 1). Conclusion: Conclusion: Lifelong monitoring of inactive CHB carriers is cost-effective in Shanghai, but achieving substantial population-level health

gains depends on identifying more CHB-infected cases in the population, and increasing rates of treatment, monitoring and treatment adherence. Key Word(s): 1. chronic hepatitis B; 2. inactive hepatitis B; 3. monitoring; 4. cost-effectiveness; Table 1. Cost-effectiveness of monitoring inactive chronic hepatitis B carriers Program % HBV Ever Tested % of Follow-up Total cost per patient (US$) QALYs US$ per QALY gained (ICER) % HCC % Cirrhosis % CHB related deaths * values tested for the monitor & terat strategy, compared to the current practice Presenting Author: MARIA DI PACE Additional Authors: NELIA HERNANDEZ, GERMAN MESCIA, CRAMEN POLLIO, GABRIELA ROBAINA, LAURA QUINTANA, CARLA BIANCHI Corresponding Author: MARIA DI PACE Affiliations: Uruguayan Gastroenterology Society; ♣ Uruguayan Gastroenterology Society Objective: Background. Obeticholic Acid supplier Numerous clinical trials shows the effectiveness of antiviral therapy with pegylated interferon plus rivbavirina for chronic hepatitis C virus infection (54%–56%). However, the results of this treatment in usual

clinical practice are more uncertain. Objective. To evaluate the effectiveness of combined treatment with peginterferon and ribavirin for chronic hepatitis C in Uruguay, in daily clinical practice. Methods: Material and Methods. In this retrospective and multicentric study were reviewed the medical records of patients who received antiviral therapy (pegylated interferon alfa-2a plus ribavirin) between January selleck 2001 and January 2013. Patients who completed the treatment as well as those that ended it earlier were included in the analysis. Results: Results. One hundred and twenty three patients were enrolled (male gender represented 63%, average age was 44 years, genotype 1 meant 57% and 43% of patients had cirrhosis or advanced fibrosis). The global sustained virological response, according to intention-to-treat analysis, was 51%. Cirrhosis (or advanced fibrosis) was the only variable that influenced the response to treatment. The discontinuation rate was 17%, similar to observed in others clinical studies.

Cellular signaling responses that limit cell death and structural damage allow a cell to withstand insult from sepsis to prevent irreversible organ dysfunction. One such protective pathway to reduce hepatocellular injury is the up-regulation of heme oxygenase-1 (HO-1) signaling. HO-1 is up-regulated in the liver in response to multiple stressors, including sepsis and lipopolysaccharide (LPS), and has been shown to limit cell death. Another recently recognized rudimentary cellular response to injury is autophagy.

The aim of these investigations was to test the hypothesis that HO-1 protects against hepatocyte cell death in experimental sepsis in vivo or LPS in vitro via induction of autophagy. These data demonstrate that both HO-1 and autophagy are up-regulated find more in the liver after cecal ligation and puncture (CLP) in C57BL/6 mice or in primary mouse hepatocytes after treatment with LPS (100 ng/mL). CLP or LPS results in minimal RO4929097 mw hepatocyte cell death. Pharmacological inhibition of HO-1 activity

using tin protoporphyrin or knockdown of HO-1 prevents the induction of autophagic signaling in these models and results in increased hepatocellular injury, apoptosis, and death. Furthermore, inhibition of autophagy using 3-methyladenine or small interfering RNA specific to VPS34, a class III phosphoinositide 3-kinase that is an upstream regulator of autophagy,

resulted in hepatocyte apoptosis in vivo or in vitro. LPS induced phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK), in part, via HO-dependent signaling. Moreover, inhibition 4-Aminobutyrate aminotransferase of p38 MAPK prevented CLP- or LPS-induced autophagy. Conclusion: Sepsis or LPS-induced autophagy protects against hepatocellular death, in part via an HO-1 p38 MAPK-dependent signaling. Further investigations are needed to elucidate how autophagic signaling prevents apoptosis and cell death. (HEPATOLOGY 2011;) Sepsis is a systemic inflammatory response that occurs as a consequence of an infectious insult. It is a significant health problem, with a mortality rate of 30%-60%. The predominant cause of morbidity and mortality is the development of multiple system organ dysfunction with subsequent organ failure. The cause of early organ dysfunction in the setting of sepsis is secondary both to cellular activation by bacterial products, including lipopolysaccharide (LPS), elaborated inflammatory cytokines, as well as hemodynamic abnormalities, leading to decreased oxygen delivery. Interestingly, early organ dysfunction from sepsis usually is not associated with cell death. Several studies have illustrated that in response to infection and sepsis, cells will undergo a metabolic shutdown as an adaptive response to protect against tissue injury and long-term structural damage.

Together, these results indicate that blocking the LDLR with mAb MK-8669 mw C7 affects the ratio of several host cell lipids. To further investigate the role of the LDLR in HCV entry, we used sLDLR to determine its effect on HCV infectivity. sLDLR inhibited HCVcc infectivity in a dose-dependent manner (Fig. 4). There was no effect of sLDLR on SINV infectivity, a virus that is not dependent on LDLR for its entry, and sLDLR had minimal effect on HCVpp infectivity (Fig. 4).

Together, these results suggest that the LDLR can potentially interact with HCVcc. In the blood, lipoproteins are known to be processed by LPL, an enzyme that modifies triglyceride-rich lipoproteins and targets them to the liver. LPL hydrolyzes triglycerides in VLDL and mediates interactions with HSPGs, enabling lipoprotein clearance from the circulation.28 Because of the potential role of lipoproteins in HCV entry, LPL might potentially affect HCV entry. Indeed, LPL has been shown to increase serum-derived HCV binding to target cells and to inhibit virus infection,29 suggesting that LPL might promote HCV internalization

by the same mechanism as lipoprotein uptake, leading to nonproductive virus uptake. Furthermore, the modification of HCVcc-associated lipoproteins by LPL seems to account for the loss of infectivity.30 To further investigate the effect of LPL on HCV entry, HCVcc were preincubated with LPL at 4°C or 37°C in the presence PAK6 or absence of the LPL inhibitor, GSI-IX order THL, followed by viral infection at 4°C or 37°C, respectively. When HCVcc were incubated with LPL at 4°C, infectivity did not change, unless the THL inhibitor was present. In the latter condition, a 1 log10 increase in infectivity was observed (Fig. 5A). In contrast, when HCVcc were incubated with LPL at 37°C, infectivity was reduced by nearly 1 log10 in the absence of THL,

whereas the level of infectivity was similar as the treatment at 4°C when the THL was added (Fig. 5A). Similar experiments were performed in the HCVpp system. In contrast to the effects observed on HCVcc, treatment with LPL in the absence of THL at 37°C did not reduce HCVpp infectivity (Fig. 5B). Rather, a slight increase in virus entry was observed, suggesting that the enzymatic activity of LPL does not affect HCVpp infectivity. However, a stronger increase in HCVpp infectivity was observed in the presence of THL. This effect seems to be specific for the HCVpp, because a similar treatment of pseudoparticles containing vesicular stomatitis virus (VSV)-G envelope protein had no effect (Fig. 5C). One reason for this effect could be that THL stabilizes LPL in a conformation that is better in facilitating HCVpp entry. It is worth noting that LPL treatment strongly increased IDL binding to Huh-7 cells (Supporting Fig. 1). Furthermore, the majority of LPL-treated IDL were internalized after incubation for 1 hour at 37°C (data not shown).

At the end of treatment, we found a significant expansion of the total serum bile acid pool and marked UDCA and LCA enrichment in the UDCA-treated patients versus the placebo group when pretreatment levels were compared. Additionally, we found that the increases in serum bile acid levels seemed to correlate with worse outcomes because the subset of patients that reached the clinical endpoints of disease progression during UDCA therapy tended to have higher bile acid levels. The proposed UDCA mechanisms of action in hepatobiliary disorders include expansion of

the hydrophilic bile acid pool and hypercholeresis.16 Early studies in gallstone patients showed that UDCA administration Trametinib nmr could modify the composition of circulating bile acids and lead to UDCA predominance.17, 18 Multiple subsequent studies, most of them in patients with primary biliary cirrhosis, this website have verified this modification and have generally revealed an overall expansion

of the total bile acid pool.8, 9, 13, 14, 19-22 Rost et al.13 in a study of biliary bile acid composition in patients with PSC specifically indicated that UDCA enrichment was augmented (43.1% ± 0.3% to 58.6% ± 2.3% of total bile acids) parallel to an escalating dose of UDCA (10-13 to 22-25 mg/kg/day) and reached a plateau at the highest dose. This enrichment did not further increase beyond that dose.13 In our study, the mean changes in UDCA and total bile acid levels post-treatment were significantly higher in the UDCA group compared to the placebo group (P < 0.0001). The mean posttreatment UDCA percentage in the bile acid pool was 74%, far higher than that ever reported in any other study, and

this implies that enrichment is increased proportionally to the dose. Nonetheless, this high enrichment did not correspond to a better outcome. Therefore, further investigation of biliary enrichment has to be performed, especially with respect to clinical outcome. Changes in the levels of other bile acids under UDCA treatment have been generally considered to follow an inverse relationship between the increase in UDCA levels Avelestat (AZD9668) and the decrease in CA, CDCA, DCA, and LCA levels. Results, however, are not homogeneous, and the changes are not significant in the majority of cases.13, 21, 22 In PSC patients, one study has suggested that LCA levels are not increased, even after high-dose UDCA treatment.13 Nonetheless, the antibiotics administrated in that study during the endoscopic retrograde cholangiography procedure used to obtain samples for bile acid analysis might have interfered with the results. Nonsignificant changes between the two treatment groups for CDCA, CA, and DCA levels were observed in our study after treatment. Levels of CDCA, CA, and DCA were slightly decreased in the placebo group, whereas in the UDCA group, CA showed a tendency to decrease, and DCA and CDCA were slightly increased.

001).

Interestingly, greater hepatocyte proliferation in rAd.A20 versus rAd.βgal livers occurred despite significantly higher basal hepatic IL-6 levels in the latter (Fig. S5; n = 4-5; P < 0.001). Higher IL-6 in rAd.βgal-treated livers is caused by the inflammatory response to rAd. that is contained in rAd.A20-treated livers by the anti-inflammatory function of this protein. We evaluated SOCS3 expression in livers of A20 HT and WT mice before and 24 hours following EH. A20 KO mice die within 3-6 weeks of age, and hence cannot be used for these experiments.21 HT livers showed a tendency towards higher SOCS3 mRNA and protein (IHC) (Fig PD0325901 molecular weight 6A; n = 5-6) and lower miR203 levels than WT, 24 hours after EH (Fig. 6B; n = 5-6). Increased SOCS3 levels in HT livers associated with impaired hepatocyte proliferation and delayed LR, as evidenced by lower number of Ki67/HNF4α-positive hepatocytes in HT versus WT livers,

36 hours after EH (Fig. 6C; n = 2 (WT) and 5 (HT); P < 0.001). This also correlated with lower P-STAT3 levels in HT versus WT livers 4 hours following EH (Fig. 6D; n = 2), and with inadequate up-regulation of CCND1 (P < 0.05) and CCNA (P < 0.05) mRNA, 24 hours after EH (Fig. 6E,F; n = 5-6). IL-6/STAT3 signaling also triggers an acute inflammatory response in hepatocytes that, DNA Damage inhibitor if uncontrolled, causes liver damage and counterproductively stuns cell cycle progression.9 Accordingly, we measured mRNA levels of STAT3-dependent liver-derived acute phase response proteins serum amyloid A 1 (SAA1) and fibrinogen (FGG) in A20-overexpressing and knockdown livers, at baseline and following EH. Overexpression of A20 significantly decreased EH-induced up-regulation of FGG (Fig. 7A,B; n = 6; P < 0.01), and reduced baseline and EH-induced Cyclic nucleotide phosphodiesterase up-regulation of SAA1. Conversely, A20 HT livers expressed higher levels of SAA1 (Fig 7C; n = 5-6; P < 0.01) and FGG (Fig. 7D; n = 6) following EH. These findings suggest that A20 does not aggravate and may even moderately decrease IL-6-induced pro-inflammatory signals. A20, a newly identified player in LR, is induced in mice and humans as part of the hepatocyte's

regenerative response following hepatectomy.15, 20 Overexpression of A20 dramatically improves LR and survival in mouse models of extended (78%) and lethal (87%) hepatectomy in part through decreasing the expression of CDKI, p21.15 In contrast, A20 knockdown significantly impairs and delays LR (Studer et al., in prep.). We initiated this work to determine which A20 domain supports this function in hepatocytes. Our results showed that both Nter and 7Zn mutants independently promote hepatocyte proliferation, but neither recapitulates A20′s effect on p21. Akin to A20′s NF-κB inhibitory function, both domains were required to decrease p21. Inhibition of NF-κB by A20 has been ascribed to its sequential N-terminus-mediated deubiquitination of signaling mediators such as RIP and NEMO, followed by C-terminus-mediated degradative polyubiquitination of the same substrates.

The decreased effect of acid-suppressing, H+/K+-ATPase expression and its activity induced by nesfatin-1 were partly abolished by intraperitoneal injection of histamine. Conclusion: Our results showed that nesfatin-1 exert a central inhibitory effect on gastric acid secretion in conscious rats and this may because of the central suppression of nesfatin-1 on DMV neurons and subsequently suppression of histamine synthesis, So as to finally result in the suppression of the secretion

of gastric acid. Key Word(s): 1. Nesfatin-1; 2. acid secretion; 3. DMV; 4. histamine; Presenting Author: LIUQIN JIANG Additional Authors: KUNYAN HAO, LIN LIN Corresponding Author: LIUQIN JIANG, KUNYAN HAO Affiliations: The First Affiliated Hospital, Nanjing Medical University Objective: Negative association has been reported between presence of Helicobacter pylori and developing gastroesophageal reflux disease (GERD) and its complications. The aim of the study is to analyze clinical characteristics of GERD with helicobacter pylori infection, and evaluate the relationship between helicobacter pylori infection and GERD. Methods: We

collected the GERD patients (≥18 years old) in our out-patient clinic from 2007 to 2008, who underwent the endoscopy and rapid urease test and/or 13C breath test. All patients were divided into two groups, with helicobacter pylori infection group (A group) and without helicobacter pylori infection group (B group). According to Montreal definition and selleck antibody inhibitor classification of GERD, Rome III criteria, we made out the questionnaire, which included helicobacter pylori infection, the frequencies of esophagitis analyzed by the Los Angeles classification, GERD symptom scores, evaluation of quality

of life (SF-36). Results: 514 patients were included in the study. The frequency of helicobacter pylori infection positivity in all cases was 29.4 % (151). It was no difference between the two groups in the age and gender (P > 0.05). There were 37.7% (57/151) Galactosylceramidase patients with reflux esophatitis in A group, which was less than 49.9% (181/363) in B group (P < 0.05). In comparison with B group, esophagitis of LC and LD was decreased in A group patients (P < 0.05). There was no difference between the two groups in GERD symptom total scores and typical symptoms (heartburn and regurgitation) scores, morbidity of extra-esophageal symptoms (P > 0.05). Compared with B group, A group patients reported higher in scores of role physical and role emotional (P < 0.05), and it was no difference in other aspects in quality of life (P > 0.05). There was no difference in the two groups in the scores of anxiety and depression (P > 0.05).