It has, therefore, become the screening tool of choice. However, it should be noted that a proportion of cirrhotic patients have intrapulmonary vasodilation detected at echocardiography without gas exchange abnormalities, and in general these patients do not appear to develop hypoxemia

over time.[15, 56] In bubble contrast echocardiography, a sample of liquid (normally saline) is vigorously shaken to produce microbubbles, and then injected into an arm vein while the cardiac chambers are visualized via a transthoracic approach. Normally, mTOR inhibitor these bubbles, which are > 25 μm in diameter, are trapped in the alveolar capillary bed, where the vessels have a diameter of 5–8 μm. Therefore, their appearance in the left atrium after intravenous injection suggests that pulmonary Ruxolitinib price vasodilation has allowed them to traverse the capillary bed, reaching the left side of the heart. A positive study can of course also occur due to the passage of bubbles through a cardiac defect, but in this case the bubbles appear in the left atrium much sooner (within three cycles) after their first appearance in the right atrium. In practice, an intracardiac shunt cannot be definitively excluded in a small proportion of patients with positive studies, and this may require further cardiac investigations. MAA perfusion lung scan is performed by peripheral venous injection of MAA particles that

have been radio-labeled with technetium-99 m, followed MCE公司 by whole body scanning to estimate the extrapulmonary shunt fraction. These radio-labeled particles have a diameter

of 10–90 μm and are removed in the normal pulmonary circulation. Thus, the detection of a significant amount of radiation in the brain or kidneys suggests intrapulmonary vasodilation or intracardiac shunting. MAA scanning appears to be highly specific but less sensitive than bubble contrast echo for detecting intrapulmonary dilatation consistent with HPS, and may fail to detect the presence of intrapulmonary vasodilation in the absence of hypoxia.[15] However, its high specificity makes it useful in diagnosing HPS in patients with coexisting lung disease,[15] and it has the advantage of being quantitative. Chest X-ray may be normal or may show increased vascular markings in the lower zones. High resolution computerized tomography can be helpful in selected patients to exclude intrinsic lung disease, but the absence of vascular abnormalities does not preclude the diagnosis of HPS. A reduced carbon monoxide diffusing capacity is frequently seen in cirrhotic patients and is almost universal in HPS,[10, 12] possibly reflecting diffusion limitation at the alveolus. In the absence of intrinsic lung disease, other pulmonary function tests are normal. Pulmonary angiography can be normal in HPS and is rarely required.

Results: A total of 2275 participants HDAC inhibitor were included in this study (629 patients with adenomatous polyps and 1,646 polyp-free

controls). Old age (p < 0.01), male gender (p < 0.01), current cigarette smoker (p < 0.01), or current alcohol drinker (p = 0.01), and high BMI (>25 kg/m2), Family history of colorectal cancer (p = 0.022) were associated with the development of sporadic colorectal neoplasm of 40s patients. In the point of view of a family history of malignant neoplasm, colorectal cancer (OR:1.50, CI:1.05–2.14), kidney cancer (OR:2.55, CI:1.00–6.50) were associated with adenomas development especially more than 3 adenomas. Family history of colorectal cancer is associated with advanced adenoma development (OR:3.02, CI:1.42–6.40) at the multivariate analysis adjusted for sex, age, BMI, smoking and alcohol check details consumption. Especially, colon adenoma is more affected than rectal adenoma by family history of colorectal cancer. Conclusion: This study shows family history of colon cancer, family history of kidney cancer were a risk factor for the colorectal adenoma in persons aged 40–49 years. Therefore, earlier screening

colonoscopic surveillance might be needed for individual 40–49 years aged relatives than none of family history. Key Word(s): 1. colorectal neoplasm; 2. aged 40–49 years; 3. colon cancer; 4. kidney cancer; Table 2 The association between family history of cancer and risk for colorectal adenomas according to the location of adenomas   Colon Rectum (n = 564) (n = 98) N (%) OR* (95% CI) N (%) OR* (95% CI) *Adjusted for sex, age, BMI, smoking status, alcohol consumption Presenting Author: RASOUL SOTOUDEHMANESH Additional Authors: NAIMEH NEJATI, MARYAM FARSINEJAD,, SHADI KOLAHDOOZAN, ROYA RAHIMI, JAVAD MIKAELI, MORTEZA KHATIBIAN Corresponding Author: RASOUL SOTOUDEHMANESH Affiliations: digestive DiseaseResearchCenter; Digestive Disease Research Center Objective: Not infrequently, the usual imaging modalities fail to identify the cause of CBD dilation and

endoscopic ultrasonography (EUS) becomes necessary. The aim of this study was to assess the value of EUS in identifying the cause of CBD dilatation undiagnosed by transabdominal ultrasonography Methods: During 18 months, 152 consecutive patients who were referred for evaluation medchemexpress of dilated CBD (diameter ≥7 mm) discovered incidentally during transabdominal ultrasonography were included. Final diagnoses were confirmed by ERCP, EUS-guided FNA, surgical exploration, or clinical follow up of at least 10 months. Patients with choledocholithiasis were referred for ERCP and sphincterotomy, and patients with operable tumors were referred for surgery. Patients with inoperable tumors underwent biliary stenting with or without chemoradiotherapy. Results: One hundred and fifty (54% female) with dilated CBD were included. Mean age of patients was 60 ± 17 years. The final diagnoses was choledocholithiasis in 32 (21.

It has recently been shown in a model of atherosclerosis that sustained induction of apoptosis in lesional macrophages results in significant increases in inflammation and lesion size.31 In this model, the defective clearance of apoptotic macrophages in advanced lesions favors

enhanced recruitment of monocytes and thus leads to enhanced atherogenesis.31 It is thus very likely that in our model increased hepatic macrophage apoptosis provides a strong signal for the click here infiltration of additional monocytes and thereby perpetuates the inflammatory response. By dissecting the expression of proapoptotic and antiapoptotic genes in different hepatic cell populations, our results suggest that bcl2 is the specific molecular target for CX3CR1-mediated survival signals

in hepatic monocytes/macrophages. In agreement, bcl2 down-regulation has also been reported in circulating CX3CR1−/− monocytes and inflamed tissue macrophages by other investigators.22, 24 Moreover, overexpression of bcl2 in CX3CR1-deficient monocytes/macrophages could restore their survival,22 and enforced cell survival by the transduction of CX3CR1-deficient BM with bcl2-overexpressing constructs restored Selleck Atezolizumab the phenotype of CX3CR1−/− mice in an atherosclerosis model.22 Moreover, in the absence of CX3CR1, hepatic monocytes/macrophage displayed a more proinflammatory TNF/iNOS-producing phenotype. Interestingly, this skewing toward the proinflammatory M1-type macrophage subtype1 was apparent already after acute injury, and this MCE公司 suggests that CX3CL1 limits the

activation of macrophages in vivo. This conclusion is strongly supported by recent in vitro experiments using murine liver macrophages, which demonstrated increased TNF expression and reduced arginase 1 expression by CX3CR1-deficient macrophages upon CCl4 stimulation.32 Furthermore, CX3CL1 induced preferential arginase 1 expression in WT liver macrophages.32 Similarly, the pretreatment of (BM-derived) macrophages with fractalkine suppressed the release of TNF upon lipopolysaccharide stimulation.33 Collectively, the in vitro data and our in vivo models provide evidence that CX3CR1-deficient macrophages deviate toward a proinflammatory M1 phenotype upon activation and that in turn CX3CL1 inhibits skewing toward an M1 phenotype in WT macrophages. By activating antiapoptotic and anti-inflammatory signals in hepatic macrophages, the fractalkine-CX3CR1 pathway represents a protective mechanism that limits liver inflammation and fibrosis in vivo. Thus, pharmacological augmentation of this pathway may represent a possible therapeutic antifibrotic strategy for patients with chronic liver inflammation.

3A) and in the subgroup of 83 patients with a nodule 2-3 cm (Fig. 3B): again, no significant survival difference was observed among the three alpha-fetoprotein

classes (HCC ≤2 cm: χ2 = 0.6744, P = 0.714; HCC 2-3 cm: χ2 = 2.0926, P = 0.351). We also compared survival between patients with normal (≤20 ng/mL) and elevated (>20 ng/mL) alpha-fetoprotein (Fig. 4A), and between patients with an alpha-fetoprotein above or below 200 ng/mL (Fig. 4B). Even with these cutoffs, no statistically significant differences were observed. Lastly, we evaluated treatment and survival of the seven patients with extremely high alpha-fetoprotein levels (>400 ng/mL): three (42.9%) had a tumor ≤2 cm, four underwent hepatic resection, and three percutaneous ablation. Four patients Paclitaxel concentration died after a median of 56 months (range, 17-79 months) and three were alive after a median of 60 months (range, 6-100 months). Taking into account the caveat selleck such an analysis may bear, due to the very small sample size, there was no survival difference between patients with alpha-fetoprotein above and below 400 ng/mL (χ2 = 0.137, P = 0.712). The ROC curve showed that alpha-fetoprotein had inadequate accuracy to discriminate survivors and deceased patients (area under the ROC curve = 0.536, 95% confidence interval

[CI] = 0.465-0.606). A ROC curve-identified alpha-fetoprotein cutoff of 100 ng/mL had good specificity (88%, 95% CI = 81%-94%) but unacceptably low sensitivity (23%, 95% CI = 15%-33%) for discriminating survivors and deceased patients MCE (Fig. 5). Prevalence-adjusted positive and negative predictive values for death of this cutoff were 63.6% and 56.5%, respectively, whereas positive and negative likelihood ratios were 1.96 and 0.86, respectively. Moreover, there was no significant survival difference between patients with an alpha-fetoprotein below or above this cutoff (χ2 = 0.8301; P = 0.367). Lastly, we also evaluated the predictors of death in this

very homogenous population of cirrhosis patients with HCC and found that the type of curative treatment (hepatic surgery, median survival 86 months versus ablative treatment, median survival 64 months, P = 0.019) was the only predictor of survival, whereas there was no significant survival difference associated with gender, age below 65 years, etiology of liver disease (viral versus nonviral), presence of esophageal varices (datum available in 163 patients), and size of HCC (≤2 or 2-3 cm). The usefulness of serum alpha-fetoprotein as a surveillance and diagnostic test for HCC has been dramatically challenged by the impressive technical improvement of abdominal ultrasound and contrast medium-enhanced diagnostic imaging that have led to great accuracy in the early identification and noninvasive characterization of small HCCs.

g., after pinealectomy and exposure to dark to stimulate melatonin release from the pineal gland) in the regulation of biliary functions are ongoing. Having demonstrated that AANAT is expressed by cholangiocytes and that AANAT expression is up-regulated by BDL and melatonin administration, we proposed to demonstrate that reduction of biliary AANAT expression (by Vivo-Morpholino) increases cholangiocyte proliferation and IBDM as well as the expression of SR, CFTR, and Cl−/HCO AE2 in cholangiocytes. After BDL, the increase of biliary proliferation and IBDM is followed

by the extension of the peribiliary plexus and the increase of surrounding connective tissue, which is organized selleckchem around bile ducts and vessels.10 In our model, we only observed a slight 3-deazaneplanocin A difference in collagen tissue content in BDL rats treated with mismatch Morpholino versus BDL rats treated with AANAT Vivo-Morpholino. This low increase of connective tissue cannot determine a clear hepatic fibrosis in our model of short time of BDL. Further studies are needed to evaluate the long-term effects of BDL on the modulation of melatonin synthesis on liver fibrosis. Also, the novel concept that AANAT regulates SRCFTRCl−/HCO AE2 expression is supported by our previous study16 showing that in vivo administration of melatonin to BDL rats decreases secretin-induced choleresis. To determine that the effects of down-regulation of AANAT

on biliary growth depend on direct effects on bile ducts, cholangiocytes 上海皓元医药股份有限公司 were treated in vitro with melatonin that decreased the biliary proliferation and expression of SR, CFTR, and Cl−/HCO AE2. We overexpressed AANAT in cholangiocytes and demonstrated a decrease

in biliary proliferation and secretin-stimulated cAMP levels and Cl− efflux. In vitro, overexpression of AANAT in cholangiocytes leading to decreased biliary proliferation and secretin receptor-dependent ductal secretion (in the absence of intestinal secretin supply) was likely the result of the fact that cholangiocytes express SR and express the message for secretin and secrete secretin,7, 39, 40 which (similar to what is observed in vivo) is an important autocrine factor sustaining biliary proliferation. We propose that the modulation of biliary melatonin secretion (by chronic administration of melatonin or changes in AANAT expression; Fig. 6) may be a valuable therapeutic approach for regulating the balance between biliary growth/apoptosis. In support of this view, we have shown that in the first stage of primary biliary cirrhosis, there is an increase of cholangiocyte proliferation that resulted in a positive balance between growth and apoptosis.41 By contrast, the end stage is characterized by the collapse of the proliferative capacity of cholangiocytes, resulting in the reduction (high apoptosis rate) of the number of bile ducts (vanishing bile duct syndrome).

Here we present a series of studies conducted by our group (Fig 1) and review the literature. Methods: We first determine whether certain serum miRNAs tested by qRT-PCR could represent potential diagnostic and prognostic

biomarkers for PDAC on 2010. Then the value of such miRNAs compared with serum CA19-9 was evaluated. We used serum samples to screen the differentially expressed serum miRNAs with Illumina sequencing by synthesis technology using pooled selleck chemicals llc serum samples followed by validation of a large number of samples arranged in multiple stages. Finally, the role of PDAC-specific miRNA was also studied by using transfection and animal model. Results: Of the serum miRNAs detected, miR-21, miR-155 and miR-196a were identified as differentially expressed in PDAC and control groups (chronic pancreatitis or normal). Selleck FK506 Furthermore, serum miR-196a expression level was found to have a potential value in predicting median survival time of PDAC

patients. The combination of miR-16, miR-196a and CA19-9 was more effective for discriminating PDAC from normal (sensitivity 92.0%; specificity 95.6%) compared with CA19-9 alone. Most significantly, the combination was effective at identification of tumors in Stage 1 (85.2%). A 7 miRNA – based biomarker can serve as a novel noninvasive approach for PDAC diagnosis and prognosis. Mir-196a was found to modulate PDAC progression via its target gene of inhibitor of growth 5 (ING5). Conclusion: Circulating miRNAs show promising value in diagnosis of PDAC. The origin and their roles on PDAC formation and invasion warrant further studies. Key Word(s): 1. pancreatic cancer; 2. miRNA; Presenting Author: RAJESH GUPTA Additional Authors: SUNIL SHENVI, YELLAKANTIRAGHAVENDRA medchemexpress BABU, PRASANNA C, SURINDER RANA, DEEPAK BHASIN, MANDEEP KANG, RAKESH KAPOOR Corresponding Author: RAJESH GUPTA Affiliations: PGIMER Objective: Despite advances in surgery and perioperative care that have resulted in markedly reduced postoperative mortality after pancreaticoduodenectomy(PD), the median survival for pancreatic cancer patients has changed minimally over the past two decades. Apart from SMA margin and Neoadjuvant

chemotherapy which have effect on long term survival of patients; reducing early mortalityfurthur following PD can also lead to improved results. Present study analysis the reasons and outcome for early mortality following PD. Methods: We retrospectively reviewed details of patients undergoing pancreatico-duodenectomy between January 2002 and Dec 2011 at Division of Surgical Gastroenterology, PGIMER, Chandigarh. A total of 101 patients underwent pancreaticoduodenectomy. Indications being Carcinoma head of pancreas/Periampullary carcinoma in 81, PNET in 11, chronic pancreatits in 6, duodenal GIST in 1, adenoma with high grade dysplasia in 2 patients. Results: There were 60 male patients. Mean age was 52±12.9 SEM (Range 25-78 years).Mean post op stay was 13.8days±6.5 SEM.

Presence of fibrosis is a sign of chronicity. Thus, the diagnosis of NAFL/NASH rests on clinicopathological criteria; it always requires both clinical and biopsy-based information. NAFLD could be both the result MK-2206 chemical structure and the cause of metabolic syndrome,

with a vicious cycle operating between these conditions. Remaining challenges are: (i) the lack of a clear threshold alcohol intake for defining “non-alcoholic”; (ii) a lacking consensus for the classification of fatty liver disease; and (iii) absence of a histological definition of NASH, which currently remains the gold standard for the diagnosis. Further challenges include the overlap of the criteria for NAFLD and alcoholic liver disease as many obese individuals also consume considerable volumes of alcohol. “
“Ulinastatin is a drug used effectively selleck kinase inhibitor to alleviate symptoms and improve the pathophysiology of various types of pancreatitis. However, the molecular mechanism responsible for its action remains unknown. Therefore, we further explore the therapeutic effects of ulinastatin and investigate possible molecular pathways modulated by this drug in the development of severe acute pancreatitis (SAP). SAP mouse model was created by administering intraperitoneal injections of cerulein and lipopolysaccharide.

Pancreatic injury was assessed by performing biochemical and histological assays and by measuring the inflammatory response of the pancreas. Specifically, we examined changes in the expression of components MCE of the rennin–angiotensin system (RAS), including angiotensin-converting enzyme (ACE)-angiotensin II (Ang II)-angiotensin type 1 receptor (AT-1R), and ACE2-Ang-(1–7)–Mas receptor. When SAP mouse models were treated with ulinastatin at a dosage of 50 000 U/kg body weight, we found, through

biochemical and histopathological analyses, that the pancreatic injury was significantly ameliorated. Administration of ulinastatin to SAP mice led to increased expression of ACE2, Ang-(1–7), and Mas receptor, decreased expression of serum Ang II and pancreatic AT-1R, and no alterations in the expression of pancreatic ACE and Ang II when compared to cerulein-treated control group that did not receive ulinastatin. This study shows that ulinastatin has differential effects on the two axes of the RAS during SAP. Our results further suggest that upregulation of components of the ACE2-Ang-(1–7)–Mas pathway might be an important mechanism contributing to the therapeutic role of ulinastatin in alleviating pancreatitis-associated symptoms. “
“Hereditary tyrosinemia type I (HT1) results in hepatic failure, cirrhosis, and hepatocellular carcinoma (HCC) early in childhood and is caused by a deficiency in the enzyme fumarylacetoacetate hydrolase (FAH).

32 (SD 0.45) and 2.56 (SD 2.71) mL, respectively. The median follow-up period of patients was 44.3 (range, 1–77.5) months. Treatment-related complications occurred in 7 (9.6%) patients; massive variceal bleeding during the EVO in 3 (4.1%), septic thrombophlebitis in 1 (1.3%), pulmonary embolism in 1 (1.3%), intraperitoneal leakage of cyanoacrylate in 1 (1.3%), symptomatic splenic infarction in 1 (1.3%). By Kaplan-Meier analysis, the cumulative rebleeding rate were 3.4%, 14.1%, 25.4% and 33.8% at 1, 12, 36 and 60 months respectively. By univariate analysis, Child-Pugh class C liver function was associated with increased rate of rebleeding. However,

no independent risk factor for rebleeding was identified by multivariable analysis. find more Conclusion: EVO using N-butyl-2-cyanoacrylate for bleeding fundal varices shows favorable long-term effectiveness and safety profile. Key Word(s): 1. Fundal varices; 5-Fluoracil 2. Variceal obturation; 3. Cyanoacrylate; Presenting Author: JIANGYUAN WANG Additional Authors: YULAN LIU Corresponding Author: YULAN LIU Affiliations: Department of Gastroenterology, Peking University People’s Hospital Objective: To explore the etiology, clinical features and prognostic factors of hepatorenal syndrome (HRS) in cirrhosis patients with ascites. Methods: A retrospective analysis was performed on clinical data of 74

patients with HRS admitted to Peking University People’s Hospital from August 2007 to December 2012. Clinical features and laboratory findings were compared before and after onset of HRS. Survival curves of HRS were estimated by Kaplan-Meier method, and multivariable Cox proportional hazards 上海皓元 model was used to analysis the predictive

factors of death. Results: Totally 74 patients were included in this study, with a male-female ratio of 3.6:1 and mean age of 64 ± 13. Patients with Child-Pugh A, B and C are 0(0%), 10(13.5%) and 64(86.5%), respectively. There are 42(56.8%) patients with type I HRS and 32(43.2%) with type II. Infection, upper gastrointestinal hemorrhage and electrolyte disorder are the main risk factors of HRS, and 67(90.5%) patients had one or more precipitating factors. Significant differences of CRE, BUN, GFR, TBIL, DBIL, ALB, INR, Na, Child-Pugh classification and MELD score are found between before and after the onset of HRS. There are significant differences of NE, CRE, BUN, GFR, TBIL, DBIL, INR, Child-Pugh classification and MELD score between two types of HRS. The median survival time of type I and type II HRS are 7 days and 120 days respectively (P < 0.001). In single-factor Cox proportional hazards model, CRE, BUN, GFR, TBIL, DBIL, INR, MELD score are all associated with prognosis. According to multivariable Cox model, only MELD score is associated with prognosis (P < 0.001, OR = 1.078). Conclusion: HRS usually occurs in end-stage live disease with some precipitating factors, and can greatly deteriorate liver and renal function.

(1-B) 41. Establish an etiology of PALF in order to identify conditions that are treatable without LT or contraindicated for LT. (1-B) Gold standard treatment of hepatoblastoma (HB) is perioperative chemotherapy followed by complete resection of all viable tumor.[182, 183] The Children’s Oncology Group protocol

for hepatoblastoma (COG-AHEP0731) suggests that tumors with potential for complete resection can be identified after 2-4 rounds of cisplatin-based selleck screening library chemotherapy. Those who undergo primary LT for unresectable HB have an 82% 10-year survival, while those who receive an LT for recurrence of HB following chemotherapy and resection (“rescue” LT) have a 30% 10-year survival.[184] The PRETEXT (Pretreatment Extent of disease)[185] is used to gauge extent of disease at the time of diagnosis and triage patients for early referral to a program with experience in both pediatric hepatobiliary surgery and liver transplantation. Patients with PRETEXT IV disease (disease involving all four sections of liver), complex PRETEXT

III disease (multifocal or presence of venous thrombosis), or centrally located tumors whose location makes a tumor-free excision plane unlikely have poor outcomes with chemotherapy and surgical resection alone.[186] A recent report from a single MCE institution reported 93% survival with aggressive resection MK-8669 in POST-TEXT III and IV patients with hepatoblastoma.[187] Patients with pulmonary metastases (PM) at the time of diagnosis have recurrence-free survival following LT that is similar to those without PM at the time of diagnosis if either of the following occurs following chemotherapy: 1) PM are no longer seen by computerized tomography (CT) or 2) residual PM are completely resected and tumor-free margins are identified.[184] In the absence of significant response to chemotherapy that would

allow surgical resection of the liver tumor with clear margins and sufficient functional residual hepatic mass, total hepatectomy with LT has been demonstrated to have satisfactory long-term outcomes.[188-191] 42. Children with nonmetastatic and otherwise unresectable hepatoblastoma should be referred for LT evaluation at the time of diagnosis or no later than after 2 rounds of chemotherapy. (1-B) 43. Patients with HB and pulmonary metastases can be considered for LT if, following chemotherapy, a chest CT is clear of metastases or, if a tumor is identified, the pulmonary wedge resection reveal the margins are free of the tumor.

Hence, the suppressed immune networks, including a halt of cellular senescence and autophagy due to TLR4 deficiency, fail to clean ROS and repair DNA damage.5, 18 It is the unclean ROS and unrepaired DNA damage contributing to DNA mutation, development of precancerous cells, and HCC progression (Fig. 7F). In conclusion, an intact TLR4-mediated immune network is critical for initiating and sustaining cellular senescence, autophagy flux, and expression of DNA damage repairing proteins that together build the barrier against hepatocellular carcinogenesis. Our studies show that Ku70 is down-regulated in TLR4mut liver tissue,

which correlates significantly with enhanced initiation and progression of HCC in TLR4mut mice. Our work Y-27632 manufacturer thus suggests an underlying mechanism in which Ku70 may act as a tumor suppressor in the liver by restoring immunity, senescence, and autophagy flux by activating p53/p21- and P16/pRb-dependent pathways. A further revelation of the molecular mechanism of the TLR4-regulated Ku70 expression and of potential strategies to induce Ku70 expression may provide a new therapeutic target for prevention and treatment of HCC. We thank Ya-Bing Gao (Academy of Military Medical Sciences of China) for preparing frozen liver sections.

Additional Supporting Information may be found in the online version of this article. “
“Background & Aims: Oltipraz is a synthetic dithiolethione with an antisteatotic effect by inhibiting the activity of liver X receptor alpha (LXR-α). Recent experimental studies clearly Cabozantinib cost demonstrated the disruptive role of oltipraz on LXR-α-dependent lipogenesis in hepatocytes and a high-fat diet mouse model. This study aimed to evaluate the efficacy and safety of oltipraz for reducing

liver MCE fat in subjects with non-alcoholic fatty liver disease (NAFLD). Methods: We performed a multicenter, double-blind, placebo-controlled, phase II study. Subjects with liver fat content of >20% and elevated aminotransferase levels were randomly allocated to three groups given either placebo (n=22), 30 mg (n=22), or 60 mg (n=24) oltipraz twice daily for 24 weeks. The change of liver fat amount from baseline to 24 weeks was quantified using magnetic resonance spectroscopy. We also assessed changes of body mass index (BMI), liver enzymes, lip-ids, insulin resistance, cytokines, NAFLD fibrosis scores (NFS), and NAFLD activity scores (NAS). Results: Absolute changes in liver fat content tended to increase in a dose-dependent manner (-3.21±11.09% in a placebo group, -7.65±6.98% in a low dose group, and -13.91±10.65% in a high dose group). Percent reduction in liver fat content was also significantly greater in a high dose group than in a placebo group. BMI and NFS also significantly decreased in a high dose group compared with in a placebo group.