10 In order to explore whether serum adiponectin levels were functionally relevant for hepatic lipid metabolism, the authors demonstrated a correlation between hepatic adiponectin staining and AMPK and acetyl-CoA carboxylase 1 and 2 (ACC1/ACC2) phosphorylation. Notably, phosphorylation of ACC2, the main ACC isoform in human liver, inhibits this enzyme and reduces its product, malonylCoA,

a CPT1α inhibitor, therefore indirectly promoting FA oxidation.11 Previous studies in patients with NASH revealed that adipoRI expression was stable, while adipoRII was reduced concomitantly with reduced hepatic see more adiponectin expression.12 Given the specific roles of adipoRI and RII, their relative amounts in advanced NASH may be important to estimate the net response. Since adipoRI remains stable and regulates AMPK, ALK targets it is also remarkable that FA synthesis and its main regulator SREBP1c are inhibited in burned-out NASH patients.13 It is thus possible that adiponectin activation of adipoRI leads to AMPK activation which subsequently inhibits

SREBP1c expression by phosphorylation of a serine residue near the cleavage site of SREBP1c, thereby repressing endogenous FA synthesis and forcing lipid droplet catabolism in the liver (Fig. 1). Conversely, low adipoRII expression may concomitantly promote oxidative stress and inflammation (Fig. 1). Unfortunately, potential changes of hepatic adipoRI or RII receptors expressions were not addressed in the current study. A key question concerns potential mechanisms which might cause elevated adiponectin levels in advanced NASH. Adiponectin levels are known to be elevated in experimental models and patients with liver cirrhosis,14 with the highest levels being observed in cholestasis,15 suggesting a potential link to biliary constituents such as BAs. Previous studies established that adiponectin levels correlated with fibrotic markers such as transient elastography, hyaluronate, and serum BA.16 Serum BA levels are increased

Janus kinase (JAK) in NASH patients and correlate with disease progression.17 Adiponectin is secreted into the bile, which represents an important way of elimination, as reflected by increased levels in cholestatic patients and bile duct-ligated mice.15 It is therefore plausible that parallel increases of serum adiponectin and BA levels might simply reflect progressive liver dysfunction leading to burnt-out NASH. Apart from their detergent properties in lipid digestion, BAs have more recently been recognized to possess additional hormonal actions that control a range of metabolic and immune functions throughout the body by way of the farnesoid X receptor (FXR) and the G-protein coupled BA receptor (GPBAR1/TGR5).18 As such, BA-activating FXR and TGR5 regulate cholesterol, triglyceride and glucose metabolism, as well as energy expenditure.

Clinical efficacy of therapy was assessed as the number needed to Selumetinib cell line treat (NNT) to prevent 1 death in 5 years, which was calculated with the adjusted hazard ratio (HR) of SVR for all-cause mortality and the individual’s estimated 5-year survival based on our externally validated mortality risk score (including solely objective variables). [NNT=(1/(estimated 5y-survival without SVR^(HR of SVR) – estimated 5y-survival without SVR))*(100/ SVR rate)] RESULTS In total, 530 patients were followed for a median of 8.4 (IQR 6.4-11.4) years. Median age was 48 (IQR 42-56) years,

143 (27%) patients had bridging fibrosis and 387 (63%) had cirrhosis. SVR was attained by 192 (36%) patients. Cox analyses showed that SVR was independently associated with reduced all-cause mortality (adjusted HR 0.25, 95%CI 0.12-0.53), without significant interactions with any baseline variables. Among patients without SVR, the 5-year mortality rate was 8.6 (95%CI 5.7-11.5). For calculating the NNT, the HR of SVR was fixed at 0.25 and the SVR rate at 95%. The NNT to prevent 1 death in 5 years was

29, 15, 10 or 8 in case of a 5-year mortality risk of 5, 10, 15 or 20%, respectively. The figure shows the estimated NNT and 5-year mortality risk, according to the individual’s mortality risk score. CONCLUSION These results indicate that the clinical efficacy of interferon-free therapy varies extensively this website among patients with advanced liver disease, which might provide guidance when prioritizing patients for treatment with these costly regimens. Mortality Risk Score=age (in years)- platelets (per 109/L) + (258.8*log10(AST/ALT))

+ (64.5 for males) Disclosures: Adriaan J. van der Meer – Speaking and Teaching: MSD, Gilead Raoel Maan – Consulting: AbbVie Jordan J. Feld – Advisory Committees or Review Panels: Idenix, Merck, Janssen, Gilead, AbbVie, Merck, Theravance, Bristol Meiers Squibb; Grant/Research Support: AbbVie, Boehringer Ingelheim, Janssen, Gilead, Merck Heiner Wedemeyer – Advisory Committees or Review Panels: Transgene, MSD, Roche, Gilead, Abbott, BMS, Falk, Abbvie, Novartis, GSK; Grant/Research Support: MSD, Novartis, Gilead, Roche, Abbott; Speaking and Teaching: BMS, MSD, Novartis, ITF, Abbvie, Gilead Jean-Francois Dufour – Advisory Committees or Review Panels: Bayer, BMS, Gil-ead, Janssen, Novartis, Roche, Jennerex, Merck; Speaking and Teaching: Bayer, Alanine-glyoxylate transaminase Boehringer-Ingelheim, Novartis, Roche Andres Duarte-Rojo – Advisory Committees or Review Panels: Gilead Sciences; Grant/Research Support: Vital Therapies Michael P. Manns – Consulting: Roche, BMS, Gilead, Boehringer Ingelheim, Novartis, Idenix, Achillion, GSK, Merck/MSD, Janssen, Medgenics; Grant/ Research Support: Merck/MSD, Roche, Gilead, Novartis, Boehringer Ingelheim, BMS; Speaking and Teaching: Merck/MSD, Roche, BMS, Gilead, Janssen, GSK, Novartis Stefan Zeuzem – Consulting: Abbvie, Boehringer Ingelheim GmbH, Bristol-Myers Squibb Co., Gilead, Novartis Pharmaceuticals, Merck & Co.

An acceptable recipient survival rate and a guarantee of donor safety are prerequisites that ethically justify the risks taken by adult LDLT donors.14 By multivariate

analyses, after adjusting for variables such as age and MELD we found that both adult LDLT and DDLT greatly reduced the 1-year mortality rate of patients when compared with patients who did not undergo LT, with HRs of 0.10 and 0.12, respectively. Our finding that the 1-year survival rate of adult LDLT recipients was 85% Selleckchem Acalabrutinib was similar to the 1-year survival rate of 82% in patients who underwent DDLT for ALF in the United States3, 15 and to worldwide data on the effect of adult LDLT in ALF patients (70% to 87.5% survival).7–9 The short time from diagnosis

to death (median, 7 days) among patients in the no-LT group who died waiting for a graft highlights the limited window during which transplantation is possible. Interestingly, we found that all significant factors predicting 1-year posttransplantation mortality were associated with renal impairment or metabolic derangement. These included Aloxistatin mw dialysis, creatinine concentration, arterial pH, and lactate concentration measured just prior to LT. These results indicate that, for patients with ALF, delayed transplantation may be associated with poor posttransplantation survival and indicate the importance of expediting emergency LT before deterioration of renal function and metabolic status. In this context, adult LDLT would offer an advantage over DDLT, by reducing waiting time and providing more optimal timing of surgery. In the present study the median waiting time from diagnosis to LT was 2.5 days for adult LDLT and 5.5 days for DDLT. Although this difference was not significant, probably because of the small numbers of patients who underwent MRIP DDLT, our findings are consistent with previous reports showing that adult LDLT was associated with shorter waiting times.7, 9, 16 In the present study,

some of our patients received dual-graft LDLTs, using the same surgical techniques previously described.17 However, we do not advocate the routine use of dual-graft transplantation for patients with ALF because of the potential for an increased risk to donors. Dual-graft transplantation was considered as a last resort when single-graft transplantation did not appear feasible after considering donor safety (remnant volume <30% of total liver volume and/or severe steatosis) and small-for-size graft for recipient. The patients in the LT group were significantly younger than those in the no-LT group, suggesting that younger patients were more likely to receive LT than were older patients and that this may have contributed, at least in part, to the higher likelihood of death observed in older patients. Multivariate analysis showed, however, that age was a prognostic factor for 1-year mortality independent of LT and MELD.

Results: The cohort included 3,815 pts (mean age 57, 98% male, 74% Caucasian, 50% HCV +/− alcohol, 28% alcohol only, 56% decompensated, 13% HCC). A total of 84 (2.2%) pts were referred to hospice. Of those who died within 6 mos of cirrhosis diagnosis, 27 (6.2%) were referred to hospice [median survival 100 days (IQR 74-139)]. IWR-1 order Of those with MELD ≥20, 9 (2.4%) were referred to hospice [median survival 119 days (IQR 86-296)]. Presence of HCC was the only covariate associated with hospice referral. Neither age, decompensation symptoms, MELD score,

nor comorbidities predicted hospice referral. Conclusions: In this large cohort of patients with cirrhosis, only 6.2% of those who survived less than 6 mos after cirrhosis diagnosis were referred to hospice. HCC was the only predictor of hospice referral, indicating the discomfort of physicians in referring patients with non-malignant conditions to hospice and need for guidelines on end of life care for patients with advanced cirrhosis. Table. Hospice referral by HCC status in all patients with cirrhosis, patients who died within 6 months of cirrhosis diagnosis, and patients with MELD>=20. Disclosures: Anna S. Lok – Advisory Committees selleck products or Review Panels: Gilead, Immune Targeting System, MedImmune, Arrowhead, Bayer, GSK, Janssen, Novartis, ISIS, Tekmira; Grant/Research Support:

Abbott, BMS, Gilead, Merck, Roche, Boehringer The following people have nothing to disclose: Mina Rakoski, Grace L. Su, Michael Volk Introduction: The prevalence of Tryptophan synthase antibody to hepatitis E virus (anti-HEV) was found to be 21% in NHANES III. The seroprev-alence of HEV in subjects with chronic liver disease (CLD), a population who may share risk factors for HEV transmission, is unknown. Aims: To determine the seroprevalence of HEV in patients with CLD using three different assays. Methods: 229 of 758 adult patients who visited the liver clinic at the NIH from 2/1/12 to 2/1/13 were randomly selected for anti-HEV IgG testing using 2 commercial ELISAs, Wantai (Beijing Wantai) and Focus Diagnostics (Quest, Mayo Laboratory) and, an in house ELISA (NIH), that uses a 55KDa recombinant

ORF-2. Results: Mean age of the 229 patients was 51 years, 47% were women, 44% White, 19% Black, 29% Asian and 9% other. Seroprevalence of HEV varied substantially with the 3 assays, 26% with the NIH, 18% with the Wantai and 14% with the Focus assays. 11% of samples tested positive and 71% tested negative by all 3 assays. Kappa statistic was 75% between NIH and Wantai assays, 59% between Focus and Wantai assays and 45% between Focus and NIH assays. Subjects positive by all 3 assays were significantly older than those positive by Focus alone but similar to those positive by NIH alone (see table). Using Wantai assay, prevalence of anti-HEV increased with age: 4% for patients <40, 14% for 40-49, 22% for 50-59 and 26% for >60 years, (p=0.

133 Such models bear some limitations because enzymes and transporters may not have similar functions in mouse and human systems and the crosstalk of NRs cannot be sufficiently determined because only one or two genes are humanized.131 PXR and CAR are the most prominent NRs involved in regulation of drug disposition. Other nuclear factors involved in drug metabolism and the defense against oxidative stress are the aryl hydrocarbon receptor (AhR) and nuclear factor-E2-related factor (Nrf2).134 PXR and CAR play important roles in clinically

relevant drug interactions. Prescription drugs activating these NRs can either lead to Talazoparib datasheet increased clearance and decreased therapeutic efficacy of other drugs or can induce drug bioactivation with formation of reactive intermediate metabolite causing hepatotoxicity.135 Acetaminophen (APAP) hepatotoxicity is a prototypic example for drug interactions due to NR activation. Various inducers of CYP gene expression worsen APAP liver toxicity by increasing phase I oxidation of APAP to the reactive metabolite N-acetyl-p-benzoquinone-imine

(NAPQI).136 Increased APAP toxicity has been reported after administration of the CYP3A inducer dexamethasone and PXR was identified as a further culprit.137 CAR and RXRα also play a role in the pathophysiology of APAP toxicity, because CAR and RXRα knockout mice and mice treated with a CAR antagonist are resistant against APAP toxicity.138,139 In addition, activation of PPARα Z-IETD-FMK cell line by clofibrate treatment and stimulation of Nrf2 by oleanolic acid has protective properties.140,141 Drugs inhibiting CAR and PXR target gene expression and inducers of RXRα, PPARα, and Nrf2 may represent innovative therapeutic approaches for the treatment of APAP-induced selleckchem liver injury. Taken together, NRs play a key role in drug interactions

and in drug-induced liver injury. Such interactions can cause liver damage even when the drug is not directly hepatotoxic. A variety of transcription factors, including NRs, regulate HBV promoters and enhancers and thereby control HBV pregenomic RNA synthesis and transcription.142 Thus, future antiviral strategies may take advantage of NR effects on viral replication. As summarized in Supporting Table 6, most NRs increase rather than decrease HBV replication. The antiinflammatory effects of NRs should further assist potential direct antiviral effects. FXR, HNF4, and PPARα up-regulate synthesis of pregenomic RNA and viral DNA.143,144 Two FXR response elements in the hepatitis B virus enhancer and core promoter regions have been identified143 and bile acids promote transcription and expression of HBV in hepatic cell lines by way of FXR.145 Thus, bile acids can antagonize the antiviral effects of interferons through promotion of HBV transcription and gene expression.145 In contrast, the PPARγ agonist rosiglitazone has an inhibitory effect on HBV replication in vitro.

Recently, loss of SMAD4, especially loss of nuclear SMAD4 expression, was described in GC progression [22]. Given the role of SMAD4 in gastric tumor suppression, Wu et al. [23] searched for genetic variants in the SMAD4 gene that could be associated with the risk of GC. Of the five SNPs studied, the authors found an association between the allele C at position rs17663887 and the allele G at position rs12456284 with increased expression of SMAD4 protein and decreased risk of GC. Proteolytic breakdown of the extracellular

matrix is an essential event involved in tumor invasion, metastasis, and angiogenesis [24]. Serpin peptidase inhibitor, clade E, member 1 (SERPINE1), plays a key role in tumorigenesis, because it prevents excessive proteolysis, which is necessary for capillary Venetoclax nmr morphogenesis, cell migration, and invasion [25]. According to Ju et al. [26] a polymorphism in intron 7 (c.1162 + 162C>T) of SERPINE1 is strongly associated with susceptibility to diffuse-type GC. Using luciferase reporter assays, the authors detected an increase in gene expression associated with the risk haplotype when compared with nonrisk haplotype.

The results obtained are interesting, because expression levels of SERPINE1 are elevated in GC tissues compared with normal stomach tissue [27]. In the last year, numerous articles were Cobimetinib published establishing an association between genetic polymorphisms and the risk of GC. It is becoming evident that host genetic factors are key agents in the risk for the development of cancer and that the interaction of different polymorphisms combined with environmental triggers may provide crucial clues to explain diverse risks in various populations. Understanding the molecular mechanisms and alterations behind the initiation and progression of gastric tumorigenesis is crucial for the early detection of the disease and to identify novel Decitabine therapeutic and clinical targets for GC. A number of molecular abnormalities have been identified in GC, namely gene overexpression and gene silencing. Nevertheless, it is of vital importance to decipher the mechanisms of gastric

carcinogenesis, because the molecular pathogenesis of GC is still incompletely understood. In the last years, a vast amount of articles reporting the overexpression and/or amplification of various genes in GC were published. Recently, Zheng et al. [28] reported the overexpression of the inactive form of glycogen synthase kinase (GSK)-3β and p-GSK3β-ser9 in GC when compared with normal mucosa. Noteworthy, the authors addressed that the overexpression of p-GSK3β-ser9 was positively correlated with a poor prognosis. Interestingly, Mishra et al. [29] described that p-GSK3β-ser9 is gastrin induced and that inhibition of GSK3β leads to an increase in expression of Snail, nuclear translocation of β-catenin, and an increase in GC cell migration.

Surprisingly, Topoisomerase inhibitor the levels of IL-22 mRNA expression were undetectable in the liver from chronic-binge–treated mice or from patients with alcoholic hepatitis (Fig. 8A,B). On the contrary, hepatic expression of IL-22R1

was up-regulated from chronic-binge–fed mice or from patients with alcoholic hepatitis (Fig. 8A,B). Expression of IL-10R2 that is also required for IL-22 activation of downstream signaling was up-regulated in the liver from ethanol-fed mice but remained unchanged in the patients with alcoholic hepatitis (data not shown). Two important findings are presented in the current study. First, we developed a murine model of alcoholic liver injury induced by chronic-binge ethanol feeding, which induces significant steatosis and liver injury. Second, using this model, we have demonstrated that treatment with

IL-22 ameliorates ethanol-induced liver injury, suggesting therapeutic potential of IL-22 in treating alcoholic liver disease. Currently, the most commonly used model for alcoholic liver injury in rodents is voluntary feeding with the liquid diet containing ethanol; however, this model only induces minor liver injury with slight elevation of serum ALT.17-22 In particular, male mice seem to be more resistant to liver injury induced by voluntary ethanol feeding than female mice. Thus many laboratories used female mice instead of male mice to investigate ethanol-induced hepatocellular damage; however, serum ALT levels were still only slightly elevated in female mice, ranging from 50-116 IU/L.18, 22 In Lenvatinib cell line the present study, we demonstrated that chronic-binge ethanol feeding significantly elevated serum ALT and AST levels with the peak levels of approximately 250 IU/L ALT and 420 IU/L AST in male C57BL/6 mice,

which are equivalent to the levels obtained from mice fed Inositol monophosphatase 1 intragastrically ethanol diet,29 and are much higher than that from mice fed a voluntary ethanol diet.17-21 Because chronic alcohol feeding increases CYP2E1 protein expression, whose role in alcoholic liver injury has been well documented,30, 31 we speculate that chronic ethanol feeding elevates CYP2E1 protein, which subsequently accelerates binge ethanol-induced hepatocellular damage in this chronic-binge model. Using this model, we demonstrated that IL-22 treatment reduces ethanol-induced liver injury (Figs. 4-6). IL-22 treatment induces activation of STAT3, whose role in protecting against liver injury has been well documented.32 This leads us to speculate that the hepatoprotection of IL-22 is likely mediated via activation of STAT3 in hepatocytes. In deed, deletion of STAT3 in hepatocytes abolished the hepatoprotective effects of IL-22 (Fig. 6), confirming the critical role of STAT3 in IL-22 protection against alcoholic liver injury.

Conclusions: Our novel data identify hepatocyte-derived ATP and uric as pro-inflammatory triggers that activate the NLRP3 inflammasome in immune cells to promote the development of ALD. Our results demonstrate immediate clinical relevance of the ATP/uric acid NLRP3 molecular pathways for therapeutic interventions in ALD. Disclosures: The following people have nothing to disclose: Jan Petrasek, Arvin Iracheta-Ve丨丨ve, Shashi

Bala, Karen Kodys, Evelyn A. Kurt-Jones, Gyongyi Szabo Background: Stem cell-derived microvesicles (MVs) and their related microRNAs mediate genetic changes that promote recovery of liver disorders. The present study aims to characterize the functional role of liver stem cell-derived MVs and specific miRNAs in the regulation of hepatic stellate cell activity during alcoholic-induced liver injury. Methods:

microRNA expression check details was assessed using microarray and real-time PCR assays in isolated microvesicles from human mesenchymal stem cells (MSCs) and liver stem cells (LSCs), in LPS treated human hepatic stellate cells and liver specimens from Toll-like receptor 4 (TLR4) knockout mice or mice intragastrically fed alcohol or vehicle for 4 weeks. Human hepatic stellate cell (HHSC) activation and transdifferentiation was evaluated by Western blot and Raf inhibitor real-time PCR analysis through specific markers such asα SMA, laminin, fibronectin, TLR4, TIMP-3 and MMPs. Results: We found that the expression of several miRNAs was consistently up-regulated in both MSCs and LSC- derived MVs compared to normal hepatocyte-derived MV controls, including miR-181 family members. Meanwhile,

the total liver histopathology score was increased in 4-week PJ34 HCl ethanol fed mice relative to control mice, along with HHSC activation and significant reduction of miR-181a and miR-181b. The expression of miR-181a and miR-181b was also considerably decreased in activated HHSCs after cultured in uncoated plastic culture dishes for 5 wk. Treatment of HHSCs with LPS (20 ng/ml) for 72 hr induced a significant decrease of miR-181a and miR-181b in both the activated and control state. Transfection of miR-181a and miR181b precursors markedly attenuated the expression of laminin and fibronectin mRNAs and additionally blunted the increased expression of a-SMA, MMP-2 and MMP-9 (key genes involved in the activation of HHSCs) by LPS treatment. Treatment with MSC/LSC derived MVs (30 μg/ml, 72 hr) phenocopied the effects of miR-181 overexpression in activated HHSCs by LPS. A complementary mass spectrometry-based proteomics approach with luciferase reporter assay identified TLR4, the key LPS receptor, as putative miR-181 cluster target.

6%, 44.0%, and 77.4%, respectively. Of 87 patients with rs8099917 genotype TT, 84 (97%) achieved SVR (Fig. 1a). By contrast, 28 of 50 check details (56%) patients with genotype TG/GG had SVR (P = 3.29 × 10−9). As for pre-existence of cirrhosis (Fig. 1b), 89 of 100 (89%) patients without cirrhosis and 23 of 37 (62%) patients with cirrhosis achieved SVR (P = 3.05 × 10−4). Concerning prior treatment response, 53 of 60 (88%) naïve patients achieved SVR (Fig. 1c). In this study, all of prior relapsers and NVRs had previously received combination therapy with peg-IFN alfa-2a or -2b/RBV for 48 or 72 weeks. Fifty of 54 (93%) prior relapsers showed SVR. When prior NVRs were further divided into prior partial

and null responders, 9 of 13 (69%)

prior partial responders achieved SVR (Fig. 1c). None of 10 (0%) prior null responders showed SVR. Regarding attainment of RVR, 96 of 108 (89%) RVR patients and 16 of 29 (55%) non-RVR patients showed SVR (Fig. 1d, P = 2.99 × 10−5). As described earlier, IL28B SNP rs8099917 genotype was the strongest among significantly independent factors. The SNP had an impact on each category of significantly independent contributors to SVR: pre-existence of cirrhosis, prior treatment response, and RVR (Table 4). Except for prior relapsers and prior partial responders, http://www.selleckchem.com/products/PLX-4032.html most of categories in these contributors were significantly influenced by the IL28B SNP. Specifically, the impact on prior null responders was remarkable (Table 4). Among viral variables analyzed in this study, only core 70 was significantly associated with SVR in bivariate analysis (Table 1), although it was excluded from the final multivariable analysis. In 60 naïve patients, 37 of 42 (88%) with wild core 70 and 16 of 18 (89%) with mutant core 70

achieved SVR (P = 0.651). In 54 prior relapsers, 36 of 37 (97%) with wild core 70 and 14 of 17 (82%) with mutant core 70 achieved SVR (P = 0.0871). Aged and/or female patients generally have a susceptibility to treatment-induced anemia and have poor response to peg-IFN/RBV therapy.[18, Avelestat (AZD9668) 19] In this study, median patient age was around 60 years in both SVRs and non-SVRs, indicating that over-60s accounted for nearly one-half of the community-based patient cohort in Japan. Female frequently achieved SVR with the addition of telaprevir comparable with male. This study regimen differed from phase 3 trials[9, 10] in that reduction and modification of telaprevir dose was approved, probably leading to reduction of the discontinuation rate and increase of the SVR rate. This study showed that close monitoring and proper management, including dose modifications, make it possible for aged and/or female patients to safely receive telaprevir-based triple therapy, with further improvement of the SVR rate. Response of HCV genotype 1 patients to peg-IFN/RBV therapy is strongly associated with host genetic variations, such as SNPs rs12979860 and rs8099917 nearby the IL28B gene.

Although Helicobacter pylori eradication can decrease the development of metachronous EGCs,1,2 newly developed cancers are not infrequently observed among patients successfully treated for H. pylori infection after ESD for PD98059 solubility dmso EGC. Severe corpus atrophy, high grade atrophy at the mid-point of the lesser curvature, and pepsinogen I concentration <25 ng/mL before

H. pylori eradication, are independent risk factors for developed metachronous EGC after eradication.3 Some studies have shown that H. pylori eradication improves gastric atrophy and prevents the progression of intestinal metaplasia.4,5 However, atrophic gastritis and intestinal metaplasia usually continue to exist after successful eradication for H. pylori in the stomach of the patients undergoing ESD KPT330 for EGC. Further such continuous atrophy and intestinal metaplasia appear to be the background for further metachronous EGCs in these patients. The representative method used to diagnose corpus atrophic gastritis has been endoscopic mucosal biopsies. However, a biopsy specimen shows only a small area of the entire gastric mucosa. Even though multiple biopsies are taken from multiple areas of the mucosa, we cannot be convinced of the area of true atrophy or intenstinal metaplasia. In this month’s issue of the Journal of Gastroenterology and Hepatology (JGH), Hanaoka et al.6 demonstrated the usefulness of autofluorescence imaging

for detecting atrophic fundic gastritis in the patients undergoing ESD for EGC. Autofluoresence imaging (AFI) produces real-time pseudocolor images by computating detected natural tissue fluorescence from endogenous fluorophores, such as flavins (riboflavin, flavin mononucleotide and flavin dinucleotide), nicotinamide adenine dinucleotide, collagen, and pyridoxal 50-phosphate. These metabolites could be responsible

for the observed differences in the autofluorescence spectra of normal and diseased tissues.7 So far, the use of AFI has been limited to the diagnostic field for HAS1 gastric neoplasia.6–11 Otani A et al. noted that AFI might reliably determine the depth of gastric cancer or invasion.8 Uedo N et al. suggested that AFI seemed to be a clinically useful system for the diagnosis of the lateral extension of EGCs.9 More than 50% of EGCs appear on AFIs as well-defined pink colored lesions with a green background, the latter indicating areas with chronic atrophic fundic gastritis.10,11 We have scored the atrophic gastritis in patients with gastric neoplasm in a recent study. The patients with green background color had higher scores of atrophy compared with those with pink background color using AFI.10 On the other hand, Kato M et al. suggested that the color of depressed EGCs would be green in AFI because they are thin.11 Therefore, the results of these previous studies is evidence for using AFI as a useful and noninvasive endoscopic imaging technique to detect atrophic gastritis.