Presumably, inhibitors will form in some patients upon exposure to the deficient factor independent of

any co-existent pro-inflammatory signals, whereas in others these signals will be significant modifiers. In some subjects, only minor inflammatory signals will be needed, whereas in others a more pronounced pro-inflammatory state will be required. A third group of patients will, presumably, never develop inhibitors despite how, when, and with what replacement product they are treated, as long as the agent itself is not immunogenic. One approach is to avoid the deficient factor at start of treatment, since without this exposure antibodies will not be formed. This approach has been tested, but so far without success. Rivard and colleagues evaluated the use of recombinant Ivacaftor factor VIIa to postpone exposure to FVIII until after the age of 2 years, Autophagy pathway inhibitors but succeeded in only 3 of 11 children treated a mean

of 5.5 months (median 4, range 0–12) [28]. Therefore, to use this approach other treatment options than currently available will probably be needed. Another emerging method is the use of low dose prophylaxis in the absence of any tissue damage. This includes very small doses, such as 5–10 IU/kg body weight, as these doses may not only protect against bleeding in a cost-effective manner, but also sensitize the immune system and thereby minimize the risk for inhibitors in the event of a major trauma and bleed. Although, in the context of inhibitors, prophylaxis will be neither required nor of benefit for all, its use should continue to be the state-of-the-art treatment for all patients. In summary, there has been major progress during the last decade in the understanding of how and why patients develop inhibitory antibodies to the deficient factor. However,

a substantial number of issues remain to be resolved including how to better identify patients at high risk before start of treatment using a genetic risk score. New treatment options in the pipeline may emerge in the near future and be offered to patients who are at high risk. Gene therapy may provide another attractive approach. However, from logistic and health-economic selleck compound perspectives, this potentially curative option will likely not be widely available. New – less expensive – therapeutic options need to be continually evaluated and the resources available must be used in the most optimal way. On the basis of current knowledge, this includes low dose prophylaxis initiated prior to the onset of bleeds. Studies to evaluate doses even lower than those currently utilized should be performed in countries in which this treatment modality is not currently available. The authors stated that they had no interests which might be perceived as posing a conflict or bias. “
“Summary.

39 More intrahepatic lymphocytes were detected than expected in normal liver and may represent the response to handling of see more the liver during harvesting and implantation. The reason behind the reduction in sinusoidal cell telomere length with age (in Kupffer cells and hepatic stellate cells) was beyond the scope of this study. Sinusoidal cells have a different origin, namely bone marrow,40, 41 and are subject to constant immune stimulation through contact with portal blood. Others have demonstrated that hepatocyte telomeres shorten in cirrhotic liver

but that hepatic stellate cells and lymphocytes in regions of liver fibrosis have longer telomeres.24 These studies have only looked at small numbers of each hepatic cell lineage and may not be representative, particularly given the heterogeneity seen in liver tissue. They may also reflect the recruitment

of cells with longer telomeres to the injured liver from bone marrow. In chimeric mice, hepatic stellate cells originate from hematopoetic bone marrow stem cells, particularly following hepatic injury.42 Finally, progestogen antagonist telomere shortening in sinusoidal cells may reflect a reduction in hepatic blood flow, which is especially marked after the age of 50.43, 44 It has been suggested that reduced hepatic flow alone could explain delayed hepatic regeneration after injury.45 Kupffer cells populating the liver originate from bone marrow in both mice and humans after bone marrow transplant46 and constitute a large intrahepatic population. Quantitative study of monocyte production in bone marrow and transit through the circulation showed that in the normal steady state, over 50% of monocytes leaving the circulation

become Kupffer cells. Considering the Kupffer cells as kinetically homogeneous, gives a mean turnover time of the total population of Kupffer cells of 21 days.47 Further studies in normal rat liver revealed an age-related decline in antigen presentation ability by Kupffer cells,48 and Liothyronine Sodium these cells in mice have been shown to have a stimulatory role in liver regeneration.49 In conclusion, we developed a robust, high-volume Q-FISH method for analysis of telomeres in different hepatic cell lineages that highlighted the pitfall of using liver homogenates in the study of aging and senescence. Furthermore, we demonstrated very long telomeres in cholangiocytes in normal liver over a wide age range and age-related telomere attrition restricted to sinusoidal cells. Understanding the normal process of aging in the liver is important in many aspects of hepatology from pharmacology to selection of older donors, and the findings encourage careful selection of older liver donors. Additional Supporting Information may be found in the online version of this article.

Methods: In a cohort study, data from 229 well-characterized patients with biopsy-proven NAFLD were collected. Mean follow-up was 26.4 (± 5.6, range 6-33) years. A reference population was obtained from the National Registry of Population, and information on time and cause of death were obtained from the Registry of Causes of Death. Main results: NAFLD patients had an increased mortality compared with the reference population (HR 1.29, CI 1.04-1.59, p=0.020), with increased risk of cardiovascular disease

LY294002 solubility dmso (HR 1.55, CI 1.11-2.15, p=0.01), hepatocellular carcinoma (HR 6.55, CI 2.14-20.03, p=0.001), infectious disease (HR 2.71, CI 1.02-7.26, p=0.046), and cirrhosis (HR 3.2, CI 1.05-9.81, p=0.041). Overall mortality was not increased in patients with NAS 5-8 and fibrosis stage 0-2 (HR 1.41, CI 0.97-2.06, p=0.07), whereas patients with fibrosis stage 3-4, irrespective of NAS, had increased mortality (HR 3.3, CI 2.27-4.76,

p<0.001). Conclusions: NAFLD patients have increased risk of death, with a high risk of death from cardiovascular disease and liver-related disease. The NAS was not able to predict overall mortality, whereas fibrosis stage predicted both overall and disease-specific https://www.selleckchem.com/products/Y-27632.html mortality. 2 (Hepatology 2014;) “
“A 66-year old man with obstructive jaundice was found to have an unresectable pancreatic tumour on contrast-enhanced CT scan. Sagittal (Figure 1) and 3-D (Figure 2) reconstructions of the CT scan images revealed complete agenesis of the coeliac axis, with the splenic and hepatic arteries arising directly from the superior mesenteric artery. The arterial Ribonuclease T1 supply of the gastrointestinal tract develops in week 4 of embryological life. The future blood vessels of the GI tract are formed from the vitelline system, which is composed of two bilateral arterial plexuses which coalesce to form arteries from the dorsal aorta to GI tract. Above the diaphragm the vitelline channels amalgamate to form about 5 pairs of arteries which supply the thoracic oesophagus. Below the diaphragm the vitelline system condenses

to form the three major abdominal arteries of the foregut, midgut and hindgut. The coeliac artery is the most superior of these arteries; it leaves the aorta at the seventh cervical level in the embryo but later descends to the twelfth thoracic level during development. In addition to supplying the abdominal foregut proper, the coeliac artery also supplies its endodermal derivatives; the hepatic diverticulum (future liver), the cystic diverticulum (future gallbladder), and the dorsal and ventral pancreatic bud (future pancreas). It also supplies the mesodermally derived spleen. The anatomical variation in the celiac trunk is assumed to be caused by different patterns of vitelline reduction.

For example, HNF4α and C/EBPα, two important regulators of miR-122 identified in our studies, were not

found to be significant in their data. The physiological role of miR-122 in liver development is currently unknown, primarily because no appropriate targets have been identified. Understanding the molecular mechanisms that regulate cellular proliferation and differentiation is a central theme of developmental biology.9, 23 In this report, we identified that a group of genes involved in proliferation and differentiation regulation are miR-122 targets. Several target genes are considered key regulators of development, such as the two transcription factors (CUTL1 and CCCTC-binding factor [CTCF]) and two mitogen-activated protein kinase kinase kinase (MAP3K) members25, 30, 31 that have been shown to be targets of miRNA. Therefore,

our work this website is significant because it provides important clues for understanding the role of miR-122 during liver development. During the development of a multicellular organism, cells proliferate for a defined length of time before they begin functional differentiation.23 The process of differentiation of primitive cells into more specialized cells involves an increasing restriction in proliferative capacity, culminating in cell cycle exit.23 Precise regulation of terminal cell division is needed to ensure production of proper numbers of differentiated cells at the appropriate time.23 CUTL1, the target we focused on, is a conserved transcriptional repressor that regulates the balance between cell division and differentiation of multiple cell lineages during Selleck Apitolisib embryonic development.20, 25 CUTL1 knockout and transgenic

mouse models have confirmed this role.25 The majority of homozygous mice die at or shortly after birth due to severe hypoplasia, whereas transgenic mice constitutively expressing CUTL1 develop multiorgan organomegaly (including the heart, kidney, testis, spleen, seminal vesicle, and liver).25 In hepatomegaly, constitutively expressing CUTL1 results in an excessive increase in the number of immature hepatocytes.32 These studies suggest that CUTL1 is necessary for embryonic development at an early stage, whereas failure to turn off its activity leads to excessive proliferation, as well as differentiation blocking of primitive cells. Researchers have determined that CUTL1 activity (also known Etomidate as HiNF-D binding activity) is down-regulated during fetal liver development, coinciding with the exit from the cell cycle and terminal differentiation.33 However, the mechanism is unclear. Here, we show that CUTL1 expression is silenced posttranscriptionally during mouse liver development, likely due to repression by miR-122. Therefore, our study not only reveals the mechanism regulating CUTL1 during liver development, but also supports the role of miR-122 in the precise regulation of terminal cell division and differentiation of hepatocytes.

One study has shown the development of anti-HBs to have no influence Vorinostat in vivo over the subsequent occurrence

of HCC.4 Besides providing important clinical data on serologic and virologic parameters before spontaneous HBsAg seroclearance, our present study also offers a reference for future studies investigating the usefulness of serum HBsAg measurements of CHB patients undergoing antiviral therapy. Serum HBsAg levels have already been shown to be useful in predicting favorable outcomes in Peg-IFN therapy.28, 29 In contrast, patients commenced on nucleoside analog therapy do not show significant decline in serum HBsAg up to 2 years,30 although a 0.5-log reduction in HBsAg is also predictive of subsequent HBsAg seroclearance.31 The achievement of low HBsAg levels or a strong reduction in HBsAg should thus be investigated in the future for suitability as treatment endpoints. Future studies should also consider matching baseline HBsAg and HBV DNA levels for a more detailed comparison of HBsAg kinetics. A limitation of our study is that our patient population might not be totally representative of all treatment-naïve CHB populations, with no

HBeAg-positive patients at initial presentation included. Although HBsAg loss is possible shortly after HBeAg seroconversion,16 the average age of HBeAg seroconversion in our population is 35 years32 and the average age of HBsAg seroclearance is 50 years4; hence, the proportion LY294002 manufacturer of patients with HBsAg seroclearance within 3 years of HBeAg seroconversion is likely to be small. Therefore, the validity of our study results, when applied to spontaneous HBsAg

seroclearance, should not be affected by the absence of HBeAg-positive patients. In addition, HBV genotyping was not performed in all patients. Nevertheless, the lack of significant difference in genotype distribution among the two patient groups is in line with findings suggesting HBV Racecadotril genotypes as not being a key factor in determining HBsAg seroclearance.16 Further studies on this aspect are needed. In conclusion, in CHB patients with spontaneous HBsAg seroclearance, low levels of serum HBsAg could be detected up to 3 years before HBsAg seroclearance and were more predictive of HBsAg seroclearance than low levels of serum HBV DNA. Serum HBsAg levels <200 IU/mL already offered a good prediction of eventual HBsAg seroclearance in 3 years. In patients with serum HBsAg ≥200 IU/mL, an annual 0.5-log reduction in serum HBsAg increases the prediction of HBsAg seroclearance. Both absolute and serial measurements of serum HBsAg would offer valuable clinical data in determining the probability of long-term seroclearance. These may also serve as good indicators for the consideration of treatment duration and cessation for CHB. Additional Supporting Information may be found in the online version of this article.

Next, 1:100, Dinaciclib mouse 1:200, and 1:400 dilutions of the same panel of genotype 2 sera were tested against the six genotype 2 Core-NS2 recombinant viruses. Despite the significant ability

to reduce the number of ffu against HVR1-deleted viruses, the sera had limited or no neutralization capacity against the WT genotype 2 viruses. Only five sera showed neutralizing potential. C58(2b), K1118(2c), K2592(2c), and K1475(2j) neutralized J6/JFH1(2a) by ≥50% in 1:100 and/or 1:200 dilutions. In addition, K1118(2c) and C294(2b) neutralized S83/JFH1(2c) and DH8/JFH1(2b), respectively, in 1:200 dilutions. The remaining 14 sera were not able to neutralize any of the studied genotype 2 recombinants ≥50% at 1:100 or higher dilutions. The percentage of ffu reduction at 1:200 dilutions of patient serum samples for HVR1-deleted viruses and the unmodified culture viruses are shown in Table 2. To confirm that the reduction in ffu of HVR1-deleted viruses was IgG dependent, we performed a neutralization assay of J6/JFH1 and J6/JFH1ΔHVR1 with purified IgG and the IgG-depleted serum from sample C294(2b), K2052(2c), K413(2j), and K1475(2j). IgG from these Ku0059436 four sera was able to reduce the number of ffu of J6/JFH1ΔHVR1 in a dose-dependent manner, with IC50 values of 0.1-0.5 μg/mL. In contrast, IgG neutralized J6/JFH1 ≥50% at only the highest concentration of 100 μg/mL for C294, K2052, and K1475; K413 neutralized

J6/JFH1 by 50% at ∼20 μg/mL. IgG-depleted serum was not able to affect the infectivity for J6/JFH1 or J6/JFH1ΔHVR1. Thus, ffu reduction against the HVR1-deleted virus was apparently IgG dependent.

The lack of neutralization of the WT virus could not be explained by infectivity enhancing factors in the human sera. Recently, it was demonstrated that two unique HMAbs (AR4A and HC84.26), recognizing conformational epitopes, had broad neutralizing potential against several HCV genotypes.[9, 10] To study these HMAbs against the genotype 2 panel, each recombinant virus was tested in Ribonucleotide reductase a concentration-response assay with Ab concentrations ranging from 0.008 to 25.0 μg/mL. AR4A neutralized J6(2a), T9(2a), J8(2b), DH8(2b), and S83(2c), with IC50 values of 1.8-8.7 μg/mL; only DH10(2b) had IC50 values >25 μg/mL (Fig. 5A). HC84.26 neutralized the recombinant viruses, with IC50 values of 0.1-8.2 μg/mL; in contrast to ARA4, DH10(2b) was efficiently neutralized by HC84.26 (Fig. 5B). A comparison with the amount of polyclonal IgG purified from selected patients able to neutralize 50% of J6/JFH1 is shown in Table 3. Thus, the genotype 2 virus panel found resistant to NAbs in genotype 2 chronic-phase sera could be neutralized efficiently by HMAbs AR4A and HC84.26. To investigate Ab neutralization susceptibility of HCV, we developed HCV genotype 2a, 2b, and 2c Core-NS2 culture viruses. The S83/JFH1 recombinant represents the first culture system for genotype 2c, a subtype frequently found in Southern Europe.

0%), and mainly found on the right anterior wall (from 0 o’clock to 3 o’clock) of the esophagus (64.0%) (Fig. 5). There were no statistically significant differences in the grade of RE, type of gastric mucosal atrophy, check details and the presence or absence of hiatus hernia between cases of RE on the ridge of mucosal folds or in the valley between folds (Table 2). Although BE is an emerging health problem worldwide, it is also

plagued by controversy regarding its endoscopic diagnosis. A major problem is the significant interobserver variability, partly because of the lack of a universally accepted definition and grading system of SSBE.10,11 To improve the diagnostic concordance in SSBE endoscopically, we focused on the squamous islands and the specific position of columnar epithelium in relation to mucosal folds. Narrow band imaging is a recent optical technique that enhances the diagnostic capability

of endoscopic examination by characterizing tissues using narrow-bandwidth filters in a video system.13,14 Although chromoendoscopy with iodine solution is the gold standard technique for the diagnosis of squamous cell carcinoma of the esophagus,25,26 iodine solution can lead to a transient dysphagia related to esophagospasm, and cause nausea, epigastric discomfort, and allergic reactions.27,28 In the present study, NBI could detect squamous islands in 71 Tofacitinib clinical trial (94.7%) of 75 SSBE cases in which squamous islands were found by iodine chromoendoscopy. WL endoscopy detected only 48 (64%) of the 75 positive cases. Takubo et al. recently reported that the esophageal gland proper, a marker of esophageal mucosa, was found in

squamous islands of columnar epithelium, which suggested the value of squamous islands as a marker of BE.29 Although squamous islands are not reliably recognized by endoscopy with image-enhanced techniques in all cases of SSBE, a diagnosis of SSBE can be made when squamous islands are endoscopically evident in columnar mucosa at locations distant from the squamocolumnar junction. Although the number of identified squamous islands was lower with NBI than with iodine chromoendoscopy in the present study, endoscopic observation using NBI can be recommended as a modality for diagnosing BE because of its 95% detectability of columnar Histidine ammonia-lyase epithelium with squamous islands. Barrett’s esophagus has been generally accepted as a complication of chronic and severe GERD. We have consistently demonstrated that both mucosal breaks and tongue-like SSBE are predominantly found in the right anterior wall of the esophagus.16,17 These findings have been confirmed by other groups.30,31 The asymmetrical lower esophageal sphincter pressure may not effectively prevent gastroesophageal reflux on this side.19 Investigating more precisely the location of tongue-like SSBE and mucosal breaks was the aim of the present study and we found that both are mainly found on the ridges of mucosal folds on the right anterior wall of the esophagus.

1 and SUR2B of KATP channels in the colon devoid of mucosa and submucosa (n = 10, P < 0.05). NaHS (0.01~1 mM) concentration-dependently inhibited the spontaneous Nutlin-3 in vivo contractions of the strips and the NaHS IC50 for the WAS rats was significantly lower than that for the SWAS rats (n = 10, P < 0.0001). The inhibitory effect of NaHS was significantly reduced by glibenclamide (n = 10, P < 0.0001). Conclusion: The colonic hypermotility induced by repeated WAS may be associated with the decreased production of endogenous H2S. The increased expression of the subunits of KATP channels in colonic smooth muscle

cells may be a defensive response to repeated WAS. H2S donor may have potential clinical utility in treating chronic stress- induced colonic hypermotility. Key Word(s): 1. chronic stress; 2. motility; 3. hydrogen sulfide; Presenting Author: A YOUNG SEO

Additional Authors: DONG HO LEE, CHEOL MIN SHIN, SEONG BEOM KIM, WOO-CHAN SON, NAYOUNG KIM, YOUNG SOO PARK, HYUK YOON, HYUN JIN CHO Corresponding Author: A YOUNG SEO Affiliations: Seoul National Univ. Bundang Hospital; Asan Medical Center Objective: Experimental studies have shown the chemopreventive properties of green tea extract (GTE) on colorectal cancer. Colorectal adenomas are precursors to colorectal cancers. Therefore, a randomized trial was conducted to determine the preventive effect of GTE supplements on metachronous colorectal check details adenomas by giving GTE tablets of which are equivalent of 9 cup-of-green tea per day (0.9 g/day GTE, 0.6 g/day epigallocatechin gallate MTMR9 [EGCG]). Methods: The subjects who had undergone complete removal of colorectal adenomas by endoscopic polypectomy were enrolled. They were then randomized into two groups: supplementation group (0.9 g GTE per day for 12 months) or control group without GTE supplementation. Follow-up colonoscopy was conducted in 12 months. A sample size of 176 patients (88 per each group) was calculated to give the study 80% power to detect a difference, assuming a two-sided significance test at the 0.05 level. From June 2010 to March 2013, 68 patients (44 patients with GTE supplementation

and 24 controls) completed the study protocol. Results: Of the 68 patients enrolled in the study, the incidences of metachronous polyps at the end-point colonoscopy were 53.8% (14 of 24) in control group and 23.8% (10 of 44) in GTE group (relative risk [RR], 0.27, 95% confidence interval [CI], 0.09–0.76). Occurrences of metachronous adenoma showed a decreasing trend in GTE group (16.7%, 7 of 44) compared to control group (26.9%, 7 of 24), which was not statistically significant (RR, 0.54, 95% CI, 0.17–1.78). There were no significant findings regarding serum lipid profiles, fasting serum glucose and serum C-reactive protein levels in the two groups. Conclusion: This preliminary study of GTE supplement suggests a favorable outcome for the chemoprevention of metachronous colorectal adenomas. Key Word(s): 1. green tea exrtracts; 2.

Our findings reveal that dysregulation of miRNA-122 (miR-122) contributes to hepatic insulin resistance through PTP1B induction. Flavonoids are being actively studied Selleck Apitolisib as potential treatments for components of the metabolic syndrome. In our previous study, treatment with licorice flavonoid ameliorated liver steatosis.12 In the present study, we additionally discovered the effect of c-Jun

N-terminal kinase 1 (JNK1) inhibition by isoliquiritigenin (IsoLQ) or liquiritigenin (LQ) on miR-122 dysregulation using in vivo models and cell-based assays. Here, we report that they have the ability to abolish hepatic insulin resistance by recovering the constitutive expression of miR-122 responsible

for PTP1B down-regulation. Information on the materials used in this study is described in the Supporting Information. Animal studies were conducted in accordance with the guidelines of the Institutional Selleckchem NU7441 Animal Use and Care Committee. Male C57BL/6 mice at 6 weeks of age were started on a high-fat diet (HFD) for 11 weeks. Detailed information is provided in the Supporting Information. HepG2, H4IIE, C2C12, and 3T3-L1 cell lines were purchased from the American Type Culture Collection (ATCC, Rockville, MD). The isolation of primary rat hepatocytes is described in the Supporting Information. The plasmid containing Luc-PTP1B-3′UTR (3′-untranslated region; Product ID: HmiT015828-MT01) was specifically synthesized (GeneCopoeia, Rockville, MD) and was used in luciferase reporter assay. The plasmid contains firefly luciferase fused to the 3′UTR of human PTP1B, and Renilla luciferase that functions as a tracking gene. pMiR-122a luciferase reporter vector containing the firefly luciferase gene and miR-122 target site at 3′UTR was purchased from Signosis (Sunnyvale, CA). When

miR-122 is expressed, it binds to the sequence and results in repression of the luciferase gene. The sources of other vectors and procedures used in this study for transient transfections and reporter gene assays are provided in the Supporting Information. Total mafosfamide RNA was extracted with TRIzol (Invitrogen, Carlsbad, CA) and was reverse-transcribed. Quantitative real-time PCR (qRT-PCR) was performed with the Light Cycler 1.5 (Roche, Mannheim, Germany). Chromatin immunoprecipitation assay was done using the EZ ChIP kit (Upstate Biotechnology, Lake Placid, NY) according to the manufacturer’s protocol. HFD feeding increased the mRNA and protein levels of PTP1B (Fig. 1A); the change in the level of PTP1B protein was greater than that in its mRNA, suggesting that a posttranscriptional mechanism might be involved in this event. RNA22 and TargetScan programs enabled us to select miRNAs that potentially bind to the 3′-untranslated region (3′UTR) of PTP1B (PTPN1) mRNA (Fig.

Broglio – Consulting: BMS Eric S. Daar – Advisory Committees or Review Panels: Gilead; Consulting: Bristol Myers Squibb, Merck, ViiV, Janssen; Grant/Research

Support: Abbott, Merck, Gilead, ViiV, Pfizer, Bristol Myers Squibb Yong Yuan – Employment: Bristol Myers Squibb Company Anupama Kalsekar- Employment: Bristol Myers Squibb Melanie Quintana – Consulting: BMS Trong Le – Employment: Bristol-Myers Squibb Scott M. Berry-Consulting: BMS The following people have nothing to disclose: Michelle Detry, Brad Spellberg, MAPK inhibitor Roger J. Lewis More than four million people in the US are chronically infected with the hepatitis C virus (HCV), and an estimated 50–75% are unaware of their positive status. Currently, HCV is managed primarily by liver specialists. Few primary care providers (PCPs) have the knowledge and skills to provide HCV care and treatment. As a result of expanded HCV screening recommendations, new testing technologies and more effective treatments, more people infected with HCV will become aware of their status and seek treatment, creating additional demands on an already strained specialty network. In addition, as less complex treatments FK228 molecular weight with more manageable side effects and shorter durations become available, management of HCV infection will move from being a disease managed by specialists to

a disease managed by PCPs. Since 2010, the New York State Department of Health has funded 13 primary care settings to integrate HCV care and treatment. During their first year of providing services, 1,119 patients received HCV care services, of whom 815 (73%) were eligible for treatment. Of those eligible for and offered treatment, 254 (23%) initiated treatment, and 102 (9%) completed treatment. Among those who completed treatment, 37 (33%) achieved a sustained virological response. The overall purpose was to evaluate PCP performance on key

indicators designed to measure the quality of HCV care and treatment. Methods Thirteen HCV Care and Treatment Programs conducted chart reviews on a sample of clients to measure six performance indicators (PI) within four broad categories: HCV treatment, hepatitis vaccination, alcohol counseling and mental health assessment. Data were collected on a spreadsheet and submitted for analysis. Data from the programs were then compared to Elongation factor 2 kinase national data. Results During the review period, 1,119 clients were enrolled in the programs. From these patients, 607 (54%) records were reviewed for PI. 1 00 % had genotype testing prior to treatment; 1 00% had RNA testing prior to treatment; 89 % and 86% received HAV and HBV vaccine, respectively; 89% received alcohol counseling and 83% had mental health assessment prior to treatment initiation. When compared to national data, these programs performed better for each indicator. Conclusions As the demand for HCV care and treatment increases, expanding the capacity to treat HCV beyond liver specialists is critical.