This study indicates that the intrahepatic immune responses involved in the clearance of HCV are different between animals in which the immune system has been primed by vaccination and rechallenged animals where the immune system has been primed by natural infection with HCV. Low density arrays may be a useful method to select immune response markers to predict the outcome of HCV infection or the success of a vaccine. Disclosures: Esther Chang – Consulting: SynerGene Therapeutics, Inc. Kathleen F. Pirollo – Grant/Research Support: SynerGene Therapeutics, Inc Stephen Feinstone – Independent Contractor: Dynavax The following people have nothing to disclose: Hongying Duan, Iryna Zubkova, Youkyung Choi, Frances

Wells, Kris Krawczynski, Robert Lanford, Marian E. Major [Background] It has been reported that MDSC and Tregs were major suppressors of the immune response Tyrosine Kinase Inhibitor Library order against Hepatocel-lular carcinoma (HCC). Sorafenib, an oral multi-kinase inhibitor, has been approved for the treatment of HCC. Sorafenib could inhibit the MAPK and VEGF signaling. VEGF signaling might affect MDSC development as well as angio-genesis. [Aim] The aim of this study is to analyze whether sorafenib could suppress MDSC and Tregs development in HCC patients ex vivo and in vitro. [Methods] ex vivo analysis: Thirty-five HCC patients who received selleck screening library sorafenib were enrolled in this study. Sorafenib exhibits inter-individual

pharmacokinetic variability based 上海皓元 on the activity of CYP3A4. Therefore, we quantitated the sorafenib and sorafenib N-oxide in serum by an optimized HPLC-UV led method. The linear range of detection was 0.03–30 μg/ml. Peripheral blood mononuclear cells (PBMCs) were used for the analysis of MDSCs, Tregs and Th1. PBMCs were stained with CD3, CD4, CD25, CD127, CCR5, CXCR3, CD11 b, CD14, CD16, CD33, PD-L1, and HLA-DR antibody and analyzed by FACS canto-II. IL10 or IFN-γ secreting cells were analyzed by cytokine secreting assay. The mRNA expression of PBMCs was analyzed by deep sequence analysis (Transcriptome analysis) and realtime-PCR analysis (GM-CSF, IFN-γ,IL10,

TGF-β1, arginase 1, iNOS, PD-L1). in vitro analysis: Isolated PBMCs were used to analyze the induction of MDSC and Tregs by the soluble factor induced from various hepatoma cell lines (Hep3B, Li3, PLC etc.) in a 0.4μm pore tran-swell system. NOG mice were used for the transplantation of HCC with MDSC. [Results] ex-vivo: The frequency of MDSC in HCC patients was significantly higher than those in healthy subjects. The frequencies of PD-L1 high MDSCs and Tregs were significantly decreased after 8 weeks sorafenib treatment (p<0.01). On the other hand, the frequency of Th1 cells and the ability of IFN-γ secretion in T cells were significantly increased after 8 weeks sorafenib treatment (p<0.01). The expression of GM-CSF mRNA was significantly decreased after 8 weeks sorafenib treatment (p<0.05).

This study indicates that the intrahepatic immune responses involved in the clearance of HCV are different between animals in which the immune system has been primed by vaccination and rechallenged animals where the immune system has been primed by natural infection with HCV. Low density arrays may be a useful method to select immune response markers to predict the outcome of HCV infection or the success of a vaccine. Disclosures: Esther Chang – Consulting: SynerGene Therapeutics, Inc. Kathleen F. Pirollo – Grant/Research Support: SynerGene Therapeutics, Inc Stephen Feinstone – Independent Contractor: Dynavax The following people have nothing to disclose: Hongying Duan, Iryna Zubkova, Youkyung Choi, Frances

Wells, Kris Krawczynski, Robert Lanford, Marian E. Major [Background] It has been reported that MDSC and Tregs were major suppressors of the immune response Alpelisib against Hepatocel-lular carcinoma (HCC). Sorafenib, an oral multi-kinase inhibitor, has been approved for the treatment of HCC. Sorafenib could inhibit the MAPK and VEGF signaling. VEGF signaling might affect MDSC development as well as angio-genesis. [Aim] The aim of this study is to analyze whether sorafenib could suppress MDSC and Tregs development in HCC patients ex vivo and in vitro. [Methods] ex vivo analysis: Thirty-five HCC patients who received MG-132 sorafenib were enrolled in this study. Sorafenib exhibits inter-individual

pharmacokinetic variability based MCE公司 on the activity of CYP3A4. Therefore, we quantitated the sorafenib and sorafenib N-oxide in serum by an optimized HPLC-UV led method. The linear range of detection was 0.03–30 μg/ml. Peripheral blood mononuclear cells (PBMCs) were used for the analysis of MDSCs, Tregs and Th1. PBMCs were stained with CD3, CD4, CD25, CD127, CCR5, CXCR3, CD11 b, CD14, CD16, CD33, PD-L1, and HLA-DR antibody and analyzed by FACS canto-II. IL10 or IFN-γ secreting cells were analyzed by cytokine secreting assay. The mRNA expression of PBMCs was analyzed by deep sequence analysis (Transcriptome analysis) and realtime-PCR analysis (GM-CSF, IFN-γ,IL10,

TGF-β1, arginase 1, iNOS, PD-L1). in vitro analysis: Isolated PBMCs were used to analyze the induction of MDSC and Tregs by the soluble factor induced from various hepatoma cell lines (Hep3B, Li3, PLC etc.) in a 0.4μm pore tran-swell system. NOG mice were used for the transplantation of HCC with MDSC. [Results] ex-vivo: The frequency of MDSC in HCC patients was significantly higher than those in healthy subjects. The frequencies of PD-L1 high MDSCs and Tregs were significantly decreased after 8 weeks sorafenib treatment (p<0.01). On the other hand, the frequency of Th1 cells and the ability of IFN-γ secretion in T cells were significantly increased after 8 weeks sorafenib treatment (p<0.01). The expression of GM-CSF mRNA was significantly decreased after 8 weeks sorafenib treatment (p<0.05).

In addition, both Clone B21 and N12 exhibit the same morphogenesis in Matrigel as the parent (Fig. 5B). We then determined whether the expanded EpCAM+CD49f+ cells could survive and engraft invivo. An ideal location for engraftment would be the native gallbladder. However, because there currently are no protocols that allow for the injection and maintenance of cells in the gallbladder, we attempted engraftment at an ectopic location. http://www.selleckchem.com/products/INCB18424.html Okumura et al.26 have reported the long-term engraftment of invitro explants of human gallbladder in the subcutaneous space of athymic nude mice. We injected the expanded EpCAM+CD49f+ cells mixed with

Matrigel into the subcutaneous neck region of immunodeficient mice. We observed the formation of cyst-like LDE225 structures in the subcutaneous space 1 week postinjection (Fig. 6A). These cysts consisted of cells organized around a central lumen. Seven of seven (100%) mice injected formed cysts. However, engraftment was short term. Only 1 of 3 (33%) mice exhibited cyst formation at 2 weeks. Similar results were obtained with clonal cultures. We then isolated cells from cysts invivo 2 weeks postinjection and cultured them invitro to test their ability to reinitiate cultures with stem cell properties. Flow cytometry

analyses showed that cells isolated from cysts invivo were EpCAM+CD49f+. These cells reexpanded in vitro on feeder cells, forming colonies morphologically identical to parent and clonal cultures (data not shown), and remained EpCAM+CD49f+ (Fig. 6B). These data indicate that expanded EpCAM+CD49f+ cells survive and engraft invivo while retaining their proliferative ability in vitro. There is evidence indicating that intra- and extrahepatic bile duct cells develop separately.7 To date, there are no reports of the molecular differences—if any—between IHBD and gallbladder cells. We first screened primary IHBD cells with the same antibody panel used for primary gallbladder cells (Supporting Table 1). Most IHBD cells express EpCAM12 and we used EpCAM expression to separate IHBD cells from other

liver cells. Briefly, after liver perfusion of GFP+ mice, the high spin fraction was separated and used to isolate IHBD cells. Interestingly, we found differences in integrin expression, including CD49f 上海皓元医药股份有限公司 (Fig. 7A). Other notable markers that showed differences between IHBD and gallbladder cells were CD49e, CD81, CD54, CD26, and CD166 (Fig. 7A). We then determined whether expanded gallbladder cells and IHBD cells were different. IHBD cells are capable of expansion on LA7 feeders, and feeder cells select for EpCAM+ cells (Fig. 7B). In addition, IHBD cells form flat colonies similar to gallbladder cells. The phenotypic profiles of IHBD cells and gallbladder cells converged in culture, and we did not detect any differences using the foregoing panel of antibodies.

Thirty-seven patients received a total of 112 FEIBA treatment courses, 90 for acute bleeding and 22 for surgical haemostasis. The median FEIBA dose per

infusion for acute bleeding was 50 IU kg−1, and for surgery was 100 IU kg−1. For both acute joint and muscle/soft tissue bleeding and in surgery, haemostasis was attained in a median of two FEIBA infusions. FEIBA was judged effective in 92% of treatment courses for acute bleeding, with a 95% confidence interval (CI) of 85–97%. Rates of haemostatic efficacy did not differ significantly between anatomical sites of acute bleeding. The haemostatic efficacy rate of FEIBA in surgery was 86% (CI, 65–97%). No thromboembolic complications or other adverse find more events occurred during any treatment course. FEIBA has been successfully integrated into clinical practice in Turkey, with rates of haemostatic efficacy comparable APO866 solubility dmso to those reported in countries with a longer history of FEIBA usage. “
“Due to an increased life expectancy, besides hemophilia-related comorbidity (e.g. arthropathy, hepatitis C and human immunodeficiency virus infection) nonhemophilia-related medical problems are seen increasingly in hemophilia patients. Treatment recommendations and psychosocial consequences in aging hemophilia patients are discussed. While hypertension is reported to occur more often in hemophilia patients than in the general

population, mortality from cardiovascular disease is lower, although the incidence is increasing. Despite having a higher risk profile, the incidence of myocardial infarction is also lower, especially in severe hemophilia. General indications for medchemexpress cardiac intervention can be applied to hemophilia patients. Treatment of ischemic heart disease using adequate clotting factor concentrate (CFC) correction in combination with an adapted anticoagulant and antiplatelet therapeutical schedule should be tailored to the individual patient, depending on the clinical situation. Recommendations are given on dealing with tooth extraction, surgical intervention,

and sexuality problems in patients with hemophilia. In addition to hemophilia in itself, comorbidity has a major psychological impact, and important effects on sexuality and quality of life. It can also result in complex treatment regimens, in which coordination among healthcare workers is essential. “
“Summary.  The most common bleeding in haemophilic patients is in joints, and joint disability is the most common complications in these patients receiving inadequate treatment. Limited by economy and inadequate treatment, developing countries face huge challenge to reduce disability and improve quality of life (QoL) of haemophilic children. The aim of this study was to investigate the effect of low dose secondary prophylaxis in China.

Arai et al. performed whole transcriptome sequencing in patients affected by intrahepatic CCC without KRAS/BRAF/ROS1 alterations. They used a strategy to identify fusion proteins, then identified two RNA Synthesis inhibitor fusion kinase genes involving fibroblast growth factor receptor 2 (FGFR2). Extending their finding in a group of 66 patients with intrahepatic CCC, they detected FGFR2 fusion in 13% of the cases. These patients did not present with peculiar clinical features, except an association with viral hepatitis, but the numbers are small. FGFR2 fusion kinase seems to be a very rare

event in HCC (1%) and could not be detected in extrahepatic CCC cholangiocarcinoma. Expression of the fusion kinase transformed NIH3T3 cells and FGFR kinase inhibitors reversed these effects. This work illustrates the importance of stratifying cancer patients for driver alterations. A trial testing FGFR2 kinase inhibitor in intrahepatic CCC is very likely to be negative if its population is not selected for FGFR2 activation. (Hepatology 2014;59:1427-1434.) Evidence-based medicine requires demonstration

of benefits with randomized control trials. However, some clinical practices establish themselves nevertheless without such evidence. This is the case for liver transplantation. More controversial is the case of enrolling patients at risk for HCC in a surveillance program. American and European guidelines recommend screening with ultrasonography every 6 months. There is one randomized trial that has the merit MLN0128 to address this issue, but shortcomings in its realization have limited its importance.

Because performing such a trial would currently face major ethical concerns, one of the best ways to address this issue is by mathematical modeling. Mourad et al. developed a sophisticated Markov model in patients with compensated HCV-related liver cirrhosis. They determined life expectancy in a fictitious cohort of 700 patients according to several scenarios. They were first cautious to confirm that the assumptions they had to make result in outcomes that closely fit reality. Then, with this model, they were able to show 上海皓元医药股份有限公司 the complementary importance of access to screening and effectiveness of screening. The researchers artfully took into account lead time bias. These results clearly show a survival benefit with regular screening and add arguments in favor of HCC surveillance. (Hepatology 2014;59:1471-1481.) “
“Alcoholic liver cirrhosis (ALC) is an established indication for liver transplantation (LT). Although the importance of preoperative abstinence is accepted, the optimal period of pretransplant abstinence is unclear. Our previous report in a Japanese cohort revealed a significant negative impact of recidivism on patient survival but failed to show significance of the length of pretransplant abstinence. The aim of this study was to evaluate the optimal period of pretransplant abstinence.

Arai et al. performed whole transcriptome sequencing in patients affected by intrahepatic CCC without KRAS/BRAF/ROS1 alterations. They used a strategy to identify fusion proteins, then identified two http://www.selleckchem.com/products/Deforolimus.html fusion kinase genes involving fibroblast growth factor receptor 2 (FGFR2). Extending their finding in a group of 66 patients with intrahepatic CCC, they detected FGFR2 fusion in 13% of the cases. These patients did not present with peculiar clinical features, except an association with viral hepatitis, but the numbers are small. FGFR2 fusion kinase seems to be a very rare

event in HCC (1%) and could not be detected in extrahepatic CCC cholangiocarcinoma. Expression of the fusion kinase transformed NIH3T3 cells and FGFR kinase inhibitors reversed these effects. This work illustrates the importance of stratifying cancer patients for driver alterations. A trial testing FGFR2 kinase inhibitor in intrahepatic CCC is very likely to be negative if its population is not selected for FGFR2 activation. (Hepatology 2014;59:1427-1434.) Evidence-based medicine requires demonstration

of benefits with randomized control trials. However, some clinical practices establish themselves nevertheless without such evidence. This is the case for liver transplantation. More controversial is the case of enrolling patients at risk for HCC in a surveillance program. American and European guidelines recommend screening with ultrasonography every 6 months. There is one randomized trial that has the merit selleck chemicals to address this issue, but shortcomings in its realization have limited its importance.

Because performing such a trial would currently face major ethical concerns, one of the best ways to address this issue is by mathematical modeling. Mourad et al. developed a sophisticated Markov model in patients with compensated HCV-related liver cirrhosis. They determined life expectancy in a fictitious cohort of 700 patients according to several scenarios. They were first cautious to confirm that the assumptions they had to make result in outcomes that closely fit reality. Then, with this model, they were able to show medchemexpress the complementary importance of access to screening and effectiveness of screening. The researchers artfully took into account lead time bias. These results clearly show a survival benefit with regular screening and add arguments in favor of HCC surveillance. (Hepatology 2014;59:1471-1481.) “
“Alcoholic liver cirrhosis (ALC) is an established indication for liver transplantation (LT). Although the importance of preoperative abstinence is accepted, the optimal period of pretransplant abstinence is unclear. Our previous report in a Japanese cohort revealed a significant negative impact of recidivism on patient survival but failed to show significance of the length of pretransplant abstinence. The aim of this study was to evaluate the optimal period of pretransplant abstinence.

To prevent a future endemic or epidemic of HEV infection, further detection and characterization of HEV strains in animal

and environmental reservoirs are warranted in Mie, as well as in other prefectures of Japan, where domestic hepatitis E has been increasingly reported.[14] This work was supported in part by a grant from the Ministry of Health, Labor and Welfare of Japan. “
“Understanding the anatomy and embryology of the esophagus and stomach is necessary for dealing with clinically important congenital malformations. The esophagus acts as a conduit for transport of food from the oral NVP-LDE225 molecular weight cavity to the stomach which, as a J-shaped dilation of the alimentary canal, connects with the duodenum distally. Sphincters at the upper esophagus, distal esophagus/proximal stomach and distal stomach have strategic functions. Formation of the esophagus (primitive foregut) begins

at six weeks and the stomach is recognizable in the fourth week of gestation as a dilation of the distal foregut. Congenital abnormalities of esophagus are common and of the stomach are rare. “
“Chronic alcohol exposure inhibits insulin and insulin-like growth factor signaling in the liver and brain by impairing the signaling cascade at multiple levels. These alterations produced by alcohol cause severe Rapamycin solubility dmso hepatic and central nervous system insulin resistance as the cells fail to adequately transmit signals downstream through Erk/mitogen-activated medchemexpress protein kinase (MAPK), which is needed for DNA synthesis and liver regeneration, and phosphatidylinositol 3-kinase (PI3K), which promotes growth, survival, cell motility, glucose utilization, plasticity, and energy metabolism. The robust inhibition of insulin signaling in liver and brain is augmented by additional factors involving the activation of phosphatases such as phosphatase

and tensin homologue (PTEN), which further impairs insulin signaling through PI3K/Akt. Thus, intact insulin signaling is important for neuronal survival. Chronic alcohol consumption produces steatohepatitis, which also promotes hepatic insulin resistance, oxidative stress and injury, with the attendant increased generation of “toxic lipids” such as ceramides that increase insulin resistance. The PI3K/Akt signaling cascade is altered by direct interaction with ceramides as well as through PTEN upregulation as a downstream target gene of enhanced p53 transcriptional activity. Cytotoxic ceramides transferred from the liver to the blood can enter the brain due to their lipid-soluble nature, and thereby exert neurodegenerative effects via a liver–brain axis.

To prevent a future endemic or epidemic of HEV infection, further detection and characterization of HEV strains in animal

and environmental reservoirs are warranted in Mie, as well as in other prefectures of Japan, where domestic hepatitis E has been increasingly reported.[14] This work was supported in part by a grant from the Ministry of Health, Labor and Welfare of Japan. “
“Understanding the anatomy and embryology of the esophagus and stomach is necessary for dealing with clinically important congenital malformations. The esophagus acts as a conduit for transport of food from the oral ICG-001 nmr cavity to the stomach which, as a J-shaped dilation of the alimentary canal, connects with the duodenum distally. Sphincters at the upper esophagus, distal esophagus/proximal stomach and distal stomach have strategic functions. Formation of the esophagus (primitive foregut) begins

at six weeks and the stomach is recognizable in the fourth week of gestation as a dilation of the distal foregut. Congenital abnormalities of esophagus are common and of the stomach are rare. “
“Chronic alcohol exposure inhibits insulin and insulin-like growth factor signaling in the liver and brain by impairing the signaling cascade at multiple levels. These alterations produced by alcohol cause severe Dasatinib hepatic and central nervous system insulin resistance as the cells fail to adequately transmit signals downstream through Erk/mitogen-activated 上海皓元 protein kinase (MAPK), which is needed for DNA synthesis and liver regeneration, and phosphatidylinositol 3-kinase (PI3K), which promotes growth, survival, cell motility, glucose utilization, plasticity, and energy metabolism. The robust inhibition of insulin signaling in liver and brain is augmented by additional factors involving the activation of phosphatases such as phosphatase

and tensin homologue (PTEN), which further impairs insulin signaling through PI3K/Akt. Thus, intact insulin signaling is important for neuronal survival. Chronic alcohol consumption produces steatohepatitis, which also promotes hepatic insulin resistance, oxidative stress and injury, with the attendant increased generation of “toxic lipids” such as ceramides that increase insulin resistance. The PI3K/Akt signaling cascade is altered by direct interaction with ceramides as well as through PTEN upregulation as a downstream target gene of enhanced p53 transcriptional activity. Cytotoxic ceramides transferred from the liver to the blood can enter the brain due to their lipid-soluble nature, and thereby exert neurodegenerative effects via a liver–brain axis.

To prevent a future endemic or epidemic of HEV infection, further detection and characterization of HEV strains in animal

and environmental reservoirs are warranted in Mie, as well as in other prefectures of Japan, where domestic hepatitis E has been increasingly reported.[14] This work was supported in part by a grant from the Ministry of Health, Labor and Welfare of Japan. “
“Understanding the anatomy and embryology of the esophagus and stomach is necessary for dealing with clinically important congenital malformations. The esophagus acts as a conduit for transport of food from the oral Alisertib cavity to the stomach which, as a J-shaped dilation of the alimentary canal, connects with the duodenum distally. Sphincters at the upper esophagus, distal esophagus/proximal stomach and distal stomach have strategic functions. Formation of the esophagus (primitive foregut) begins

at six weeks and the stomach is recognizable in the fourth week of gestation as a dilation of the distal foregut. Congenital abnormalities of esophagus are common and of the stomach are rare. “
“Chronic alcohol exposure inhibits insulin and insulin-like growth factor signaling in the liver and brain by impairing the signaling cascade at multiple levels. These alterations produced by alcohol cause severe buy Ivacaftor hepatic and central nervous system insulin resistance as the cells fail to adequately transmit signals downstream through Erk/mitogen-activated medchemexpress protein kinase (MAPK), which is needed for DNA synthesis and liver regeneration, and phosphatidylinositol 3-kinase (PI3K), which promotes growth, survival, cell motility, glucose utilization, plasticity, and energy metabolism. The robust inhibition of insulin signaling in liver and brain is augmented by additional factors involving the activation of phosphatases such as phosphatase

and tensin homologue (PTEN), which further impairs insulin signaling through PI3K/Akt. Thus, intact insulin signaling is important for neuronal survival. Chronic alcohol consumption produces steatohepatitis, which also promotes hepatic insulin resistance, oxidative stress and injury, with the attendant increased generation of “toxic lipids” such as ceramides that increase insulin resistance. The PI3K/Akt signaling cascade is altered by direct interaction with ceramides as well as through PTEN upregulation as a downstream target gene of enhanced p53 transcriptional activity. Cytotoxic ceramides transferred from the liver to the blood can enter the brain due to their lipid-soluble nature, and thereby exert neurodegenerative effects via a liver–brain axis.

2. Angulo P et al. The NAFLD fibrosis score: a non-invasive system that identifies liver fibrosis in patients with NAFLD. Hepatology 2007;45:846–854. M VEYSEY,1,2,3 W SIOW,1,2 S NIBLETT,2,3 K KING,2,3 Z YATES,4 M LUCOCK5 1Department of Gastroenterology and 2Teaching & Research Unit, Central Coast Local Health District and the 3Schools of Medicine & Public Health, 4Biomedical Sciences and 5Environmental & Life Sciences, University of Newcastle, NSW, Australia Introduction: An elevated white cell count is associated with both metabolic syndrome and insulin resistance, with non-alcoholic fatty liver disease (NAFLD) being considered the hepatic manifestation of metabolic

syndrome. There are limited data suggesting an association between raised peripheral white cell counts and NAFLD. The fatty liver index (FLI)1 is a validated, non-invasive method of estimating the MLN0128 solubility dmso likelihood of NAFLD in individuals and is calculated using

an algorithm that incorporates 4 parameters: BMI, waist circumference, GGT and triglyceride levels. We, therefore, set out to examine the relationship between NAFLD, defined as an FLI≥60, and peripheral white cell counts. Methods: We used a prospectively recruited population of 440 community-based participants, aged over 65 (mean age 78 yr, 264 females), who completed a comprehensive assessment of their medical history, metabolic risk factors, medications AZD2014 and alcohol intake. Patients with other liver disease or alcohol intake >20.5 g/day were excluded. All subjects had their FLIs calculated and were classified into three groups, FLI < 30 (No NAFLD), 30

≤ FLI < 60 (Borderline) and FLI ≥ 60 (NAFLD). White cell counts and differentials were measured in peripheral blood collected at the time of FLI estimation. Results: No NAFLD NAFLD p value n = 122 N = 190 White cell count (109/l) 5.89 ± 1.64 6.83 ± 1.66 上海皓元医药股份有限公司 <0.001 Neutrophils (109/l) 3.47 ± 1.29 4.03 ± 1.19 <0.001 Lymphocytes (109/l) 1.69 ± 0.67 1.97 ± 0.81 <0.01 Monocytes (109/l) 0.51 ± 0.17 0.56 ± 0.17 <0.01 Eosinophils (109/l) 0.19 ± 0.16 0.23 ± 0.16 <0.05 Basophils (109/l) 0.02 ± 0.04 0.02 ± 0.05 ns For the whole cohort, there were weak but significant linear relationships between FLI and white cell count (r = 0.25, p < 0.001), neutrophils (r = 0.20, p < 0.001), lymphocytes (r = 0.17, p < 0.001), monocytes (r = 0.15, p < 0.01) and eosinophils (r = 0.12, p < 0.05). Furthermore, there was a linear relationship between FLI and CRP (r = 0.14, p < 0.01), supporting the inflammatory nature of NAFLD. Conclusion: This study confirms that NAFLD is associated with elevation of peripheral white cell counts and supports the inflammatory nature of NAFLD. That all sub-types of white cell, except basophils, are elevated in NAFLD suggests that the inflammatory process may be multifactorial. 1. Koehler E et al. External Validation of the Fatty Liver Index for Identifying Non-alcoholic Fatty Liver Disease in a Population-based Study.