28 Interestingly, considering only noninvasive parameters, the AUC of the model that includes vitamin D levels to predict severe fibrosis remains good. This suggests the potential use of serum 25(OH)D levels as a noninvasive marker

of liver fibrosis, a use that needs to be tested and validated in large prospective cohort studies in patients with CHC of all genotypes, and in chronic liver disease of other origins. It is conceivable that a reduced 25(OH)D level might by itself favor progression of fibrosis. Different experimental models showed that vitamin D, Protease Inhibitor Library via interaction with vitamin D receptor, protects against oxidative stress production,29 can influence the migration, proliferation, and gene expression of fibroblasts,30, 31 and reduces the inflammatory

and fibrogenic activity of liver stellate cells.32, 33 However further prospective cohort studies will Ku-0059436 cost be needed to determine the causal association between vitamin D deficiency and fibrosis in patients with CHC. Another interesting finding of this study is the evidence that lower 25(OH)D serum levels were an independent negative risk factor for SVR. Again, this observation will require further validation in different, large cohorts of patients, but is supported by experimental data that suggest a role of vitamin D in the modulation of the immune response,32, 33 and by recent clinical data36 reporting higher early virological response rate in CHC treated with standard of care plus vitamin D, compared with those treated with standard of care only. Finally, in line with data from the literature, we found that steatosis35 and lower cholesterol levels, a known surrogate marker of fibrosis severity,26 were independently associated with lower SVR rate. We did not find any association 上海皓元医药股份有限公司 between IR and SVR, in keeping the conflicting data reported in the literature on the role of IR as a predictor of SVR.36 The main limitation of this study lies in its cross-sectional nature and its inability to dissect the temporal relation between 25(OH)D and fibrosis. A further methodological drawback is the potentially limited external validity of the results for different

populations and settings. Another limitation of this study is the lack of data on the potential confounders that may influence the levels of vitamin D, such as exposure to sunshine, dietary intake, and the prevalence of osteoporosis. However, all of the subjects involved in this study lived in Sicily, where sunshine is abundant, even if we cannot rule out differences in sun exposure between healthy controls and CHC patients. However, data on the prevalence of osteoporosis were not available, nor was the dietary intake of vitamin D, which, however, remains a rather crude measure of vitamin D status because of recall bias. The lack of these data in both cases and controls makes a systematic error very unlikely. Also, data on osteoporosis were not available in both groups.

[20] Although clinical neurophysiological studies indicate that widespread changes in brain excitability occur preceding headache,[21] a specific role for the hypothalamus has been hypothesized

based on the symptoms involving changes in mood, appetite, and energy, all of which could be attributed to this selleck brain region. Recent imaging studies have begun to provide additional support for a significant role for the hypothalamus in migraine. A positron emission tomography (PET) study by Denuelle and colleagues showed increased blood flow in the hypothalamus during a migraine attack.[22] Recent studies specifically examining the premonitory phase of headache have exploited the fact that the migraine trigger nitroglycerin (NTG) may evoke not only migraine headache but premonitory symptoms as well.[23] Sprenger and colleagues have recently examined changes in brain activity during premonitory symptoms evoked by NTG using H2O PET. Preliminary reports of their findings

click here indicate that indeed, there are increases in hypothalamic blood flow that are correlated with migraine premonitory symptoms.[24] The exciting implication of these findings is that there may be specific hypothalamic mechanisms that are novel targets for therapies that could be administered before a headache takes hold. In addition to the multiple neurotransmitters and neuromodulators that regulate hypothalamic function, specific hypothalamic peptides may represent important new therapeutic targets. A good example is orexins, which show promise in animal models as potential mediators of migraine and targets for treatment.[25] The consistent occurrence of a premonitory phase raises multiple important questions. Given that the premonitory symptoms may be subtle, hard to quantify, and in some cases amplifications of sensations or behaviors that occur throughout the course of a normal non-migrainous day, at what point are these symptoms pathological and indicative of an impending 上海皓元 headache? Are there specific symptoms that are more reliable than

others at identifying the onset of a migraine attack? What occurs during the transition from the premonitory phase to the headache phase? At what stage is therapeutic intervention appropriate? Further quantitative study of the premonitory phase with prospective clinical studies, imaging, electrophysiological, and pharmacological approaches will yield key information regarding these important questions. Several recent studies have focused on the migraine aura and its relationship to the remainder of the attack. As with the premonitory phase, the migraine aura has traditionally been viewed as a distinct phase of the attack that precedes the headache and other symptoms associated with the headache phase.

[20] Although clinical neurophysiological studies indicate that widespread changes in brain excitability occur preceding headache,[21] a specific role for the hypothalamus has been hypothesized

based on the symptoms involving changes in mood, appetite, and energy, all of which could be attributed to this Selleckchem ABT-263 brain region. Recent imaging studies have begun to provide additional support for a significant role for the hypothalamus in migraine. A positron emission tomography (PET) study by Denuelle and colleagues showed increased blood flow in the hypothalamus during a migraine attack.[22] Recent studies specifically examining the premonitory phase of headache have exploited the fact that the migraine trigger nitroglycerin (NTG) may evoke not only migraine headache but premonitory symptoms as well.[23] Sprenger and colleagues have recently examined changes in brain activity during premonitory symptoms evoked by NTG using H2O PET. Preliminary reports of their findings

Transferase inhibitor indicate that indeed, there are increases in hypothalamic blood flow that are correlated with migraine premonitory symptoms.[24] The exciting implication of these findings is that there may be specific hypothalamic mechanisms that are novel targets for therapies that could be administered before a headache takes hold. In addition to the multiple neurotransmitters and neuromodulators that regulate hypothalamic function, specific hypothalamic peptides may represent important new therapeutic targets. A good example is orexins, which show promise in animal models as potential mediators of migraine and targets for treatment.[25] The consistent occurrence of a premonitory phase raises multiple important questions. Given that the premonitory symptoms may be subtle, hard to quantify, and in some cases amplifications of sensations or behaviors that occur throughout the course of a normal non-migrainous day, at what point are these symptoms pathological and indicative of an impending MCE headache? Are there specific symptoms that are more reliable than

others at identifying the onset of a migraine attack? What occurs during the transition from the premonitory phase to the headache phase? At what stage is therapeutic intervention appropriate? Further quantitative study of the premonitory phase with prospective clinical studies, imaging, electrophysiological, and pharmacological approaches will yield key information regarding these important questions. Several recent studies have focused on the migraine aura and its relationship to the remainder of the attack. As with the premonitory phase, the migraine aura has traditionally been viewed as a distinct phase of the attack that precedes the headache and other symptoms associated with the headache phase.

Davis et al Cytoskeletal Signaling inhibitor compared ketorolac 60 mg IM with promethazine 25 mg IM plus meperidine 75 mg IM and found that there was no difference between the 2 groups in percentage pain free at 30 minutes (promethazine/meperidine 20.8% vs ketorolac 22.3%).7 Harden et al found no difference in headache relief between ketorolac 60 mg IM (44.4%), meperidine 50 mg plus promethazine 25 mg IM (60%), or placebo/NS IM (54.5%).9 Duarte et al found no difference in pain reduction (VAS) for

ketorolac 60 mg IM compared with meperidine 100 mg IM plus hydroxyzine 50 mg IM (−33.5 vs −33.7, P = .76); the percentage complaining of nausea and drowsiness was not significantly less for ketorolac (28% vs 48%, P = .15).8 Larkin and Prescott compared ketorolac 30 mg IM with meperidine 75 mg IM; the percentage pain free at 1 hour was greater for meperidine (30% vs 6%, P < .05), as was sustained pain freedom at 24 hours (44% vs 13%, P < .02), and no adverse events were reported in either group.11 Klapper and Stanton found that ketorolac 60 mg IM was less effective in treating migraine than DHE 1 mg IV plus metoclopramide 5 mg IV; headache relief (4-PPS) at 1 hour was greater for DHE/metoclopramide (78% vs 33%, P = .031).22 Bigal et al compared metamizole (MMZ, also called dipyrone and not available in the USA) 1000 mg IV with placebo/NS buy IWR-1 IV.23 For migraineurs without aura, pain reduction (11-PPS) with

MMZ was more effective than placebo at 30 and 60 minutes (−4.0 vs −1.2, P < .01 and −6.0 vs −3.0, P < .01). For patients with aura, the reduction was also significantly greater with MMZ at 30 and 60 minutes (−4.9 vs −0.9, P < 0.01 and −6.4 vs −1.9, P < .01). Krymchantowski et al then compared MMZ 1000 mg IV with lysine clonixinate (LC, an NSAID not available in the USA) 200 mg IV, delivered as a 25 mL infusion over 5 minutes.24 The percentage pain free at 60 and 90 minutes was greater with LC (60 minutes: 33% vs 13%, P < .001; 90 minutes: 86.7% vs 73%, P < .001). There was no follow-up post-discharge. Patients receiving

LC had more injection-site pain than those receiving MMZ (13/15 vs 3/15, P < .0001). Engindeniz et al compared diclofenac sodium 75 mg IM with tramadol 100 mg IM. Headache relief at 2 hours was the same for both groups (80%).16 Ellis et al 上海皓元 compared ibuprofen 600 mg oral (PO) with metoclopramide 10 mg IV and placebo; pain reduction (VAS) was similar for metoclopramide and metoclopramide/ibuprofen (−75 vs −50) but was greater in both these groups (P < .01) than in the ibuprofen or placebo groups, which were the same (−25).25 Table 2 summarizes the studies involving ketorolac, diclofenac, ibuprofen, LC, and MMZ (the last not an NSAID). The rate of headache recurrence within 24-72 hours following discharge from the ED can exceed 50%, and corticosteroids typically are used in the ED in an attempt to reduce the frequency of such recurrence.

Davis et al Dabrafenib cost compared ketorolac 60 mg IM with promethazine 25 mg IM plus meperidine 75 mg IM and found that there was no difference between the 2 groups in percentage pain free at 30 minutes (promethazine/meperidine 20.8% vs ketorolac 22.3%).7 Harden et al found no difference in headache relief between ketorolac 60 mg IM (44.4%), meperidine 50 mg plus promethazine 25 mg IM (60%), or placebo/NS IM (54.5%).9 Duarte et al found no difference in pain reduction (VAS) for

ketorolac 60 mg IM compared with meperidine 100 mg IM plus hydroxyzine 50 mg IM (−33.5 vs −33.7, P = .76); the percentage complaining of nausea and drowsiness was not significantly less for ketorolac (28% vs 48%, P = .15).8 Larkin and Prescott compared ketorolac 30 mg IM with meperidine 75 mg IM; the percentage pain free at 1 hour was greater for meperidine (30% vs 6%, P < .05), as was sustained pain freedom at 24 hours (44% vs 13%, P < .02), and no adverse events were reported in either group.11 Klapper and Stanton found that ketorolac 60 mg IM was less effective in treating migraine than DHE 1 mg IV plus metoclopramide 5 mg IV; headache relief (4-PPS) at 1 hour was greater for DHE/metoclopramide (78% vs 33%, P = .031).22 Bigal et al compared metamizole (MMZ, also called dipyrone and not available in the USA) 1000 mg IV with placebo/NS PD-0332991 ic50 IV.23 For migraineurs without aura, pain reduction (11-PPS) with

MMZ was more effective than placebo at 30 and 60 minutes (−4.0 vs −1.2, P < .01 and −6.0 vs −3.0, P < .01). For patients with aura, the reduction was also significantly greater with MMZ at 30 and 60 minutes (−4.9 vs −0.9, P < 0.01 and −6.4 vs −1.9, P < .01). Krymchantowski et al then compared MMZ 1000 mg IV with lysine clonixinate (LC, an NSAID not available in the USA) 200 mg IV, delivered as a 25 mL infusion over 5 minutes.24 The percentage pain free at 60 and 90 minutes was greater with LC (60 minutes: 33% vs 13%, P < .001; 90 minutes: 86.7% vs 73%, P < .001). There was no follow-up post-discharge. Patients receiving

LC had more injection-site pain than those receiving MMZ (13/15 vs 3/15, P < .0001). Engindeniz et al compared diclofenac sodium 75 mg IM with tramadol 100 mg IM. Headache relief at 2 hours was the same for both groups (80%).16 Ellis et al MCE compared ibuprofen 600 mg oral (PO) with metoclopramide 10 mg IV and placebo; pain reduction (VAS) was similar for metoclopramide and metoclopramide/ibuprofen (−75 vs −50) but was greater in both these groups (P < .01) than in the ibuprofen or placebo groups, which were the same (−25).25 Table 2 summarizes the studies involving ketorolac, diclofenac, ibuprofen, LC, and MMZ (the last not an NSAID). The rate of headache recurrence within 24-72 hours following discharge from the ED can exceed 50%, and corticosteroids typically are used in the ED in an attempt to reduce the frequency of such recurrence.

1).16 They were differentiated in vitro to hepatocyte-like cells at passages 4 to 10 (Fig. 1A), according to a well-established multistep protocol.15, 16 Quality of differentiation was proven by an increased gene expression of cytochrome P450 3A4 (CYP3A4; P = 0.016), hepatocyte nuclear factor 4-α (HNF4α; P = 0.031), and albumin (P = 0.016), and the exhibition of functions typical of mature hepatocytes,

such as CYP3A4 activity (P = 0.031; Fig. 1B,C). Variability in differentiation selleck screening library quality among different donors is shown in Supporting Fig. 1E. To study the effect of differentiation state on HBV-cell interactions, we first assessed viral attachment to the cell membranes. At a temperature below 18°C, endocytosis is inhibited (Supporting Fig. 4A), whereas binding of viral particles to membrane receptors remains active.26 We incubated PHHs, UD-UCMSCs, and D-UCMSCs with HBV at an MOI of 1.0 ± buy PLX3397 0.8 × 105, for 2 hours at 4°C. Under these conditions, endocytosis was totally inhibited while cellular viability was not affected (Supporting Fig. 4B,C). After extensive washing (Supporting Fig. 4D), the amount of membrane-bound HBV DNA was similar for PHHs and D-UCMSCs, but lower for UD-UCMSCs (P = 0.052; Fig. 2A). To prove that binding of viral particles on cell membrane was receptor-mediated, after incubation with HBV at 4°C and extensive washing, cells were treated

with trypsin before DNA extraction. Protease detached 95% of the viral particles, without any difference between cell types (Fig. 2B), indicating that proteinaceous structures were involved in HBV binding. To assess whether viral particles attached to membrane receptors could be internalized, after the 2-hour incubation at 4°C and extensive washing cells were moved to a 37°C environment. They were cultured under standard conditions and DNA was extracted after 1, 4, and 上海皓元 24 hours. To make sure to extract only intracellular DNA,

trypsin was applied before DNA extraction, in order to detach all particles still bound to the cell membrane. After 1 hour at 37°C, PHHs, UD-UCMSCs, and D-UCMSCs were able to internalize 4.9 ± 0.7%, 6.3 ± 1.5%, and 5.5 ± 1.3% of membrane-bound HBV, respectively (P = ns; Fig. 2C). The proportion of viral uptake increased at 4 and 24 hours for PHHs (P = ns) and D-UCMSCs (P = 0.016), but remained stable for UD-UCMSCs. HBV uptake after 24 hours was significantly greater in D-UCMSCs than in UD-UCMSCs (P = 0.004). The amount of virus taken up by D-UCMSCs at 24 hours increased with the increase of MOI (Fig. 2D). Little increase was seen for MOI >103, suggesting saturation of the receptor(s). Viral entry after 24 hours at 37°C was confirmed by immunofluorescence. Both PHHs and D-UCMSCs, but not UD-UCMSCs, showed a positive staining for intracellular HBcAg (Fig. 2E).

Furthermore, a WGC is not a perfect method for the prevention of post-ERCP pancreatitis. A WGC might this website be just safer than a conventional biliary cannulation with

multiple contrast injection into the PD.1 Thus, a WGC by trainees might be the next learning step in achieving a successful biliary cannulation and preventing post-ERCP pancreatitis after the completion of learning on a conventional biliary cannulation with an accurate direction of bile duct. The effectiveness of an ERCP depends on high success rates and low complication rates. Competency in ERCP can improve its effectiveness. Evidence for the variable performance of an ERCP indicates that patient outcomes can be improved by a constructive process of continuous quality improvement that educates endoscopists about optimal ERCP techniques that reduce complications.15 Thus, continuous quality improvement is an integral part of any ERCP program.15 Because successful cannulation and complication rates are major quality indicators for ERCP,15 WGC can directly affect the outcome of ERCP. The next step on quality indicators for ERCP is the development of an expert consensus for a standardized C646 technique for WGC. A multicenter, prospective learning curve of WGC with a standardized technique and trainee involvement would also be very welcome in our attempts to improve this important procedure. “
“We recently read

an interesting article on sarcopenia in liver cirrhosis (LC) by Hayashi et al. in Hepatology Research.[1] They evaluated sarcopenia based on skeletal muscle mass (SMM) using impedance analysis and measurement of handgrip strength, and reported that sarcopenia in LC patients

was associated with physical inactivity and insufficient medchemexpress dietary intake.[1] Sarcopenia has received attention as an important predictor of prognosis in LC.[2-4] Evaluation of sarcopenia has included anthropometry of upper arm circumference, dual-energy X-ray absorption, and measurement of SMM using trunk computed tomography.[2-4] Impedance analysis has been used more recently as a convenient modality that does not involve radiation exposure.[5] Hayashi et al. used SMM / height2 as an index.[1] Multifrequency impedance analysis enables separate calculation of SMM at different sites, such as the arms, trunk and legs. The influence of edema of the lower extremities in LC can thus be eliminated. We therefore evaluated the usefulness of measuring SMM at different sites in LC, and also examined the influence on prognosis of sarcopenia. Participants in our study comprised 137 patients with LC (80 men, 57 women; mean age, 66 ± 9 years; mean Child–Pugh score, 6.7 ± 3.0). SMM was measured at different sites using a body composition analyzer (InBody 720; Biospace, Seoul, Korea) and compared with SMM in 554 patients with type 2 diabetes mellitus (DM) (323 men, 231 women; mean age, 65 ± 9 years).

In addition, the striking inverse correlations in the NASH CRN sample of the NAFLD-increasing allele with features of metabolic syndrome risk factors further rule out an indirect effect on NAFLD via metabolic syndrome risk factors. Indeed, this inverse association may be due to the ascertainment on NAFLD: individuals with the high-risk allele of rs738409 may accumulate enough steatosis and subsequent damage to their liver to develop NAFLD at lower levels of metabolic disease than individuals who do not carry this allele. Taken together, these results suggest that risk for metabolic disease can be www.selleckchem.com/products/GDC-0980-RG7422.html dissociated from fatty liver disease risk conferred

by rs738409 and that some mechanisms by which fat is deposited in liver may be related to the presence of obesity, dyslipidemia, glucose intolerance and hypertension whereas others Akt molecular weight may be more reflective of endogenous genetic predispositions to fat accumulation in the liver. Thus, through a genetic analysis we may be able to dissociate otherwise epidemiologically related traits, and such distinctions may eventually help us to predict which treatments aimed at which pathways might be most effective for different but related metabolic diseases. We extend

previous work by showing that the G allele of rs738409 in PNPLA3 is associated with histologic steatosis as well as NASH, fibrosis and cirrhosis. Particularly striking is the association of the G allele of medchemexpress rs738409 with decreased likelihood of having a zone 3 centered distribution

of steatosis. Zone 3 centered steatosis is more often observed in early stages of NAFLD and is less likely to be associated with ballooned hepatocytes, Mallory-Denk bodies or advanced fibrosis than panacinar or azonal distributions of steatosis.23 Zone 3 hepatocytes are characterized by higher levels of glycolysis, liponeogenesis and ketogenesis than periportal zone 1 hepatocytes which in turn have a higher level of gluconeogenesis, urea synthesis, and bile acid and cholesterol synthesis.24-27 Although zone 3 hepatocytes may be metabolically well-suited for lipogenesis in the normal liver, in advanced disease the ability of this zone to buffer the energy overload may be overwhelmed and fat deposition throughout the liver may predominate. When the normal mechanisms that protect hepatocytes from fatty acid damage get overwhelmed, lipotoxicity, cell death and triggering of stellate cell activation ensue.28 These processes can lead to the recruitment of inflammatory cells to the liver and to the deposition of extracellular matrix, resulting in fibrosis and cirrhosis.28 Consistent with this hypothesis, the G allele of rs738409 in PNPLA3 is associated more frequently with diffuse fat deposition (not just limited to zone 3) it may promote NASH, fibrosis and cirrhosis throughout the liver.

In addition, the striking inverse correlations in the NASH CRN sample of the NAFLD-increasing allele with features of metabolic syndrome risk factors further rule out an indirect effect on NAFLD via metabolic syndrome risk factors. Indeed, this inverse association may be due to the ascertainment on NAFLD: individuals with the high-risk allele of rs738409 may accumulate enough steatosis and subsequent damage to their liver to develop NAFLD at lower levels of metabolic disease than individuals who do not carry this allele. Taken together, these results suggest that risk for metabolic disease can be selleck chemical dissociated from fatty liver disease risk conferred

by rs738409 and that some mechanisms by which fat is deposited in liver may be related to the presence of obesity, dyslipidemia, glucose intolerance and hypertension whereas others BGB324 datasheet may be more reflective of endogenous genetic predispositions to fat accumulation in the liver. Thus, through a genetic analysis we may be able to dissociate otherwise epidemiologically related traits, and such distinctions may eventually help us to predict which treatments aimed at which pathways might be most effective for different but related metabolic diseases. We extend

previous work by showing that the G allele of rs738409 in PNPLA3 is associated with histologic steatosis as well as NASH, fibrosis and cirrhosis. Particularly striking is the association of the G allele of MCE rs738409 with decreased likelihood of having a zone 3 centered distribution

of steatosis. Zone 3 centered steatosis is more often observed in early stages of NAFLD and is less likely to be associated with ballooned hepatocytes, Mallory-Denk bodies or advanced fibrosis than panacinar or azonal distributions of steatosis.23 Zone 3 hepatocytes are characterized by higher levels of glycolysis, liponeogenesis and ketogenesis than periportal zone 1 hepatocytes which in turn have a higher level of gluconeogenesis, urea synthesis, and bile acid and cholesterol synthesis.24-27 Although zone 3 hepatocytes may be metabolically well-suited for lipogenesis in the normal liver, in advanced disease the ability of this zone to buffer the energy overload may be overwhelmed and fat deposition throughout the liver may predominate. When the normal mechanisms that protect hepatocytes from fatty acid damage get overwhelmed, lipotoxicity, cell death and triggering of stellate cell activation ensue.28 These processes can lead to the recruitment of inflammatory cells to the liver and to the deposition of extracellular matrix, resulting in fibrosis and cirrhosis.28 Consistent with this hypothesis, the G allele of rs738409 in PNPLA3 is associated more frequently with diffuse fat deposition (not just limited to zone 3) it may promote NASH, fibrosis and cirrhosis throughout the liver.

Therefore, our aim is to compare the efficiency and safety between hybrid POEM and conventional POEM. Methods: Thirty-five consecutive patients underwent

POEM by one fixed expert endoscopist (more than 30 POEMs before)between January 2012 and August 2012, 6 patients for hybrid POEM and 29 for conventional POEM. The procedures of conventional POEM were: submucosal injection, transverse mucosal incision, tunnel built-up, myotomy and mucosal entry closure. Procedures of hybrid POEM were performed mainly with one hybrid knife. Duration of different procedures and complication incidence were recorded prospectively. Results: Hybrid POEM was performed in 6 patients successfully (male : female (1 : 5), mean age 36 years, range 21–59). Clincal success (Eckardt score buy BVD-523 ≤3) was achieved in all the 6 patients at 3 month follow-up Sorafenib cost (Eckardt score, pre-treatment vs post-treatment: 8.2 vs 1.0, P < 0.05). Compared with conventional POEM, it took much less time in the process of the whole operation, tunnel built-up

and myotomy in hybrid knife group ((52.3 ± 8.0)min vs (63.0 ± 12.9)min P = 0.020, (28.8 ± 3.9)min vs (35.4 ± 7.5)min P = 0.001, (7.5 ± 1.2)min vs (10.0 ± 3.0)min P = 0.005). No complications were encountered in hybrid knife group. However, 5 Patients developed complications in the conventional group (5/29, 17.2%), 2 for mucosa perforation, 1 for subcutaneous emphysema, 1 for emphysema in both neck, mediastinum and abdominal cavity, 1 for Pneumothorax combined with subcutaneous emphysema. Conclusion: It preliminary showed that Hybrid knife, could not only finish POEM successfully, but also decrease operation time and reduce complication incidence obviously. Key Word(s): 1. Hybrid knife; 2. POEM; Presenting Author: ENQIANG LINGHU Additional Authors: YAQI

ZHAI, HUIKAI LI, ZHICHU QIN, LIHUA PENG, XIAOLIN SHI, XIAOYU QIU, YONGWEI ZHAO Corresponding Author: ENQIANG LINGHU Affiliations: Department of Gastroenterology and Hepatology, The PLA General Hospital; Department of Gastroenterology and Hepatology, The Chinese PLA General MCE Hospital Objective: Peroral endoscopic myotomy (POEM), with building submucosal tunnel, has opened up a new promising prospect for endoscopic therapy. Meantime, infection is potential to follow due to non-sterile operation and open esophagus. Presently, it still remains controversial whether preoperative antibiotics is necessary. Our aim was to evaluate the effects of preoperative antibiotics to prevent infection before the procedure. Methods: This is a prospective randomized controlled trial. Fifty-six consecutive patients who underwent POEM by one fixed expert endoscopist (more than 30 POEMs before)between January 2012 and December 2012 were enrolled. Four patients were excluded for getting a fever or recent usage of antibiotics. Patients in preoperative antibiotics group (n = 26)were administered intravenous ceftriaxone sodium (2.0 g) 30–60 min before operation, and the control group (n = 26)for equivalent normal saline.