In total, 43% of the patients were smokers. Patients with postoperative strictures were less frequently on anti-TNF therapy (17%, p = 0.023), thiopurines (34%, p = 0.001), and combination therapy (24%, p = 0.001) before surgery, and only 61% were on thiopurines at the time of postoperative colonoscopy (p = 0.040). In CD patients

with postoperative strictures, U0126 price 32% were symptomatic, 68% had an anastomotic stricture, and 18% had an ileal stricture. Endoscopic balloon dilatation was performed in 75% of patients (n = 30) with postoperative strictures, without any procedure complication, with a mean of two dilatations per patient, and mean time between dilatations of 7 ± 4 months. There were no differences between patients with postoperative strictures that were dilatated (n = 30) or not (n = 10), concerning hospital admission and new surgery. CD patients without anti-TNF therapy (OR 5.2 p = 0.033) or thiopurines (OR 5.3, p = 0.002) before surgery and without thiopurines (OR 2.21, p = 0.042) after surgery were at risk for postoperative strictures. Combination therapy before surgery was protective (OR 0.08, p = 0.001). There were no statistically significant differences for sex, Montreal classification, smoking, disease onset time until surgery and time until colonoscopy. Conclusion: Anti-TNF and/or thiopurines therapy before surgery

and thiopurines after surgery Stem Cell Compound Library purchase Phosphoribosylglycinamide formyltransferase are protective factors for postoperative stricture development in patients with Crohn’s disease. Key Word(s): 1. Crohn disease; 2. stricture; 3. surgery; 4. balloon dilatation;

Presenting Author: DUMINDA SUBASINGHE Additional Authors: NAVARATHNA MUDIYANSELAGEMETHTHANANDA NAVARATHNA, DHARMABANDUNANDADEVA SAMARASEKERA Corresponding Author: DUMINDA SUBASINGHE Affiliations: Department of Surgery, The National Hospital of Sri Lanaka Objective: Ulcerative colitis (UC) and Crohn’s disease (CD) are chronic inflammatory conditions related to the gastrointestinal tract. Faecal incontinence (FI) impairs quality of life (QOL), causing embarrassment and limiting daily activities. FI can have a negative impact on the QOL of patients with inflammatory bowel disease (IBD). There is limited published data on FI amongst people with IBD in South Asia. This study looks at the frequency and severity of FI, and its effect on the QOL in IBD patients who presented to a tertiary care center. Methods: Patients with an established diagnosis of IBD were identified and demographics, disease characteristics, FI (Vaizey score), quality of life (IBD-Q) were collected. Data were analyzed using SPSS version 15. Results: A total of 184 patients (women = 101, 54.9%; UC = 153, 83.2%) were included. Female preponderance was observed for UC (male/female ratio = 1 : 1.5) and male for CD (male/female = 2 : 1). Forty eight (26%) reported symptoms of FI.

None of the patients had complications. Conclusion: The majority of very elderly FOBT-positive patients without visible blood in the stool had no abnormalities or low-grade adenoma when the polyp was small, showing that advanced colon cancer was relatively rare. Considering their advanced age, colon polyps are unlikely to Sirolimus cost progress rapidly to cancer in very elderly patients. Thus, instead of offering colonoscopy to all very elderly FOBT-positive patients, non-invasive

abdominal computed tomography may be useful to select those with suspected advanced colon cancer for further examination by colonoscopy. Key Word(s): 1. very elderly patient; 2. FOBT-positive; 3. colonoscopy Presenting Author: HONGJIE ZHANG Additional Authors: XIUFANG CUI Corresponding Author: HONGJIE ZHANG Affiliations: Jiangsu People Hospital Objective: The present study was designed to investigate the effect of GLP-1 analogue exendin-4 on visceral hypersensitivity in rat model, and its possible regulation on SERT expression and 5-HT reuptake. Methods: Neonatal male Sprague-Dawley rats received intra-colonic injection of 0.5% acetic acid. Visceral sensation was determined

by assessing Trichostatin A datasheet abdominal withdrawal reflex (AWR) and electromyography (EMG) activity. Exendin-4 with doses of (1, 5, and 10 μg/kg) was administered by intra-peritoneal injection. SERT expression was detected by quantitative PCR (qRT-PCR)

and Western blotting. SERT function was determined by tritiated 5-HT reuptake experiment in IEC-6 cells. Forskolin, protein kinase A (PKA) inhibitors (H89) or adenylyl cyclase inhibitor (SQ22536) was used to investigate the GLP-1/ cAMP/PKA signaling pathway. Results: Neonatal acetic acid (AA) Cyclin-dependent kinase 3 intra-colonic treatment presented hypersensitivity to CRD in adult rats compared with controls. High levels of 5-HT were detected in plasma and colonic tissues in AA-treated rats (P < 0.05). Stimulated with exendin-4 at 10 μg/kg could reduce visceral sensation. The expressions of SERT reduced in colon of the AA-treated rats, and increased after treatment with exendin-4. The expressions of SERT up-regulated and 5-HT reuptake function enhanced in IEC-6 cells after treatment with exendin-4 in dose- and time-dependently manner. The former effect was abolished by pre-treatment with exendin-9, SQ22536 and H89. Exendin-4 and forskolin increased PKA activity in IEC-6 cells. Conclusion: Exendin-4, a GLP-1 analogue, can attenuate hyperalgesia in rats with neonatal colon sensitivity by up-regulating SERT expression and 5-HT reuptake, and its effect may involve in cAMP/PKA signaling pathway. Key Word(s): 1. irritable bowel syndrome; 2. glucagon-like peptide-1; 3. serotonin transporter Presenting Author: MURDANI ABDULLAH Additional Authors: D. MAKMUN, U.MAIMUNAH, ARLES, KUSNANTO, S.MIRO, SUYATA, NENENG, MARCELLUS S.

To this end, we exposed CXCR3−/− hepatocytes to CXCL10 or vehicle. Interestingly, CXCL10 also induced this website apoptosis in these cells, as evidenced by increased levels of active caspase-3

and caspase-8 (Fig. 6A,B) as well as by prolonged Akt phosphorylation (Fig. 6C and Supporting Fig. 3B). To exclude a contamination of the recombinant CXCL10 by lipopolysaccharide, we preincubated CXCR3−/− hepatocytes with polymyxin B. In fact, this preparation did not change caspase-3 and Akt activation (Supporting Fig. 3C,D), demonstrating a CXCL10-specific effect on hepatocyte apoptosis. Importantly, in contrast to CXCL10, the related chemokine (CXCL9) did not affect hepatocyte apoptosis, as evidenced by measurement of caspase-3 activity (data not shown). Because CXCR3 is not involved in hepatocyte apoptosis, we became interested whether

see more an alternative receptor could trigger CXCL10-induced apoptosis in hepatocytes. Recently, Schulthess et al.24 identified TLR4 as a receptor for CXCL10 in pancreatic β-cells. First, we confirmed the expression of TLR4 on hepatocytes by PCR analysis (Supporting Fig. 4A). Next, we stimulated TLR4−/− hepatocytes with CXCL10 or vehicle. Indeed, we found no caspase-3 and caspase-8 activation (Fig. 6D,E). These results were confirmed by lack of Akt phosphorylation (Fig. 6F and Supporting Fig. 4B) subsequent to CXCL10 stimulation of these cells. Thus, activation of TLR4 signaling appears essential to trigger CXCL10-induced hepatocyte apoptosis. In light of these in vitro data, we hypothesized that systemic administration of CXCL10 might also induce liver cell apoptosis

in vivo. Indeed, a single injection of CXCL10 led to a low, but increased, number of TUNEL-positive liver cells, compared to vehicle treatment (Fig. 7A). The apoptotic response in CXCL10-treated animals was also reflected by increased caspase-3 and caspase-8 activity within livers of these animals (Fig. 7B and Supporting Fig. 4C). Moreover, treatment with CXCL10 increased AST serum levels (Fig. 7C) and reduced intrahepatic mRNA expression of the antiapoptotic factor, BCL-2 PAK5 (Fig. 7D). Importantly, in this experimental setting, TLR4−/− mice were almost completely protected from the proapoptotic effects of CXCL10. In contrast to WT mice, treatment of TLR4−/− mice with CXCL10 neither resulted in augmented cell death (Fig. 7A) nor in caspase-3 or caspase-8 activation (Fig. 7B and Supporting Fig. 4C). In line with these results, lack of TLR4 also triggered no changes in AST and BCL-2 levels after CXCL10 challenge, compared to their vehicle-treated counterparts (Fig. 7C,D), identifying the CXCL10/TLR4 axis as an important chemokine-based apoptotic pathway within the murine liver in vivo. Here, we provide in vitro and in vivo evidence that CXCL10 exerts proapoptotic effects in hepatocytes through its noncognate receptor (TLR4).

However, a significant heterogeneity in survival among RCTs remained even after stratifying patients and study features, and heterogeneity in the survival rates persisted even in the stratum of high-quality studies, implying that this was not explained by study validity alone. Therefore, the evaluation of the methodological quality did not seem to influence the variability of the assessed outcome, because of the mean high quality of the studies (75% of these RCTs were high-quality studies). Heterogeneity of these rates among RCTs may reflect

both inclusion of patients with different stages of disease and variability in the molecular Palbociclib nmr characteristics and biological behavior of the tumor, which are not included in any of the currently available staging systems. In our analysis, when studies were separated according to the BCLC stage, the 1-year survival was much higher in RCTs including only BCLC B or C patients (34%) than in those also including BCLC D patients (11%). This provides further evidence that the BCLC staging system has a good discriminative capacity for prognosticating survival not only in patients with early HCC41 but also in those with intermediate/advanced HCC. However, data on direct selleck BCLC stage were

lacking in several trials, and caution must be exercised when interpreting results from subgroup exploratory analyses. We found by meta-regression analysis that ECOG performance status and portal vein thrombosis are robust predictors of death in untreated patients as reported by Tandon and Garcia-Tsao42 in a recent systematic review of 72 studies on prognostic indicators in HCC. These

CHIR-99021 purchase two individual parameters, both included in the BCLC classification, may explain in large part why this staging system provides accurate information on prognosis in the setting of HCC. A remarkable difference in survival was found between occidental (North American and European) and oriental (Asia-Pacific) studies. The high prevalence of HBV-related liver disease found in Asia-Pacific countries may account for the different survival observed between oriental and occidental studies in which a high prevalence of HCV-related liver disease was observed. However, the potential role of HBV as a prognostic factor disappears when Asian-Pacific location of the studies and HBV-related disease were both included in a multivariate model. The survival differences between occidental and Asian studies may be explained by differences in the distribution of other risk and prognostic factors. In fact, the worse survival observed in the Asia-Pacific study36 could be explained by the higher prevalence of patients in advanced stage than in the SHARP study.

In conclusion, the author reported a projected FNH. The DR of the FNH showed atypical features such as small cells and hyperchromatic nuclei. The DR assumed features of ductal plate-like structures. KIT was positive in the DR in the FNH, suggesting that the cells of DR are liver stem cells, and proliferation of these cells take features of ductal plate-like structures, similar to embryonic biliary development. MUC apomucins are negative in the DR. “
“Background and Aim:  With the rising incidence of digestive cancers in the Asia Pacific region and the advancement in diagnosis, management

and palliation in these conditions, the clinical burden on oncologists is ever increasing. This Summit meeting was called to discuss the optimal management of digestive cancers

and the role of Gastroenterologists Method:  Experts from Asia Pacific countries in the fields of medical, oncologic, surgical and endoscopic management of cancers in selleck products the esophagus, stomach, colon/rectum and the liver reviewed the literature and their practice. 18 position statements were drafted, debated and voted. Results:  It was agreed that the burden on GI cancer is increasing. More research will be warranted on chemotherapy, chemoprevention, cost-effectiveness of treatment and nutrition. Cancer management guidelines should be developed in this region when more clinical data are available. In order to improve care to patients, a multi-disciplinary team coordinated by a “cancer therapist” is proposed. This cancer therapist can be a gastroenterologist, a surgeon Selleck JNK inhibitor or any related discipline who have acquired core competence the training. This training should include an attachment in a center-of-excellence in cancer management for no less than 12 months. Conclusion:  The management of GI cancer should be an integrated multi-disciplinary approach and training for GI cancer therapists

should be provided for. “
“Emerging therapies for chronic hepatitis C viral (HCV) infection involve inhibition of viral enzymes with drug combinations. Natural, or treatment-induced, enzyme polymorphisms reduce efficacy. We developed a phenotyping assay to aid drug selection based on viral transfer from monocytes to hepatocytes. We studied HCV in monocytes from infected patients and developed a model in which patient-derived HCV is “captured” by the cell line THP-1 and replication assessed after fusion to hepatoma cells. We found that monocytes from HCV-infected patients harbour virus that replicates when cells are fused to hepatocytes. THP-1 cells incubated with infected sera ‘capture’ HCV which replicates when fused to hepatocytes. Inhibitable replication of all HCV genotypes was achieved (42 of 52 isolates). We measured sensitivity of telaprevir and alisporivir in different genotypes and showed differences in IC50 correlating with clinical response (telaprevir IC50 for genotype (G)1 was 0.042 ± 0.003 µM, versus 0.

79 Overall, these data indicate that these HLA class II alleles may influence the maintenance of immune tolerance as well as the penetrance of infectious agents, thus having implications in light of the proposed infectious theory in PBC etiology.1 In accordance with this, because the protective HLA alleles are associated with resistance to several infections, it can be hypothesized that the lack of such alleles might contribute to the molecular mimicry of infectious agents, leading to immune tolerance breakdown in PBC.1 The field of human genetics has rapidly changed since the recent completion of the human genome sequence, and novel, challenging

theories have been this website proposed. Decitabine Overall, thanks to dramatic advances in molecular technology linked to the field of genetics,81 we are now witnessing an explosion of new information about the allelic architecture of human complex diseases, such as PBC.82 In particular,

the ability to evaluate the entire human genome for common polymorphisms (i.e., those present in more than 5% of the general population) has allowed us to disclose more than 80 disease-susceptibility loci. The catalog of the National Cancer Institute–National Human Genome Research Institute reports an updated list of published GWAS (http://www. genome. gov/26525384). It is of great interest that the recent GWAS approaches have allowed the identification of an extended major histocompatibility complex, spanning approximately 7.6 megabases of the human genome.83 Indeed, many additional loci (most with a putative immunoregulatory role) were identified outside the well-known HLA class I, II, and III regions.83 A growing number of studies are providing evidence of genetic complexity within the MHC region in a number of disorders. In PBC, the first GWAS was recently performed in cases from Canada and the United States15 and reported significant associations with HLA, as

well as with other non-HLA loci including IL-12A, and IL-12RB2 polymorphisms. This first study manifested a sufficient statistical power by GPX6 including 536 patients with PBC and 1536 controls typed for approximately 300,000 common variants, but more solid data were soon provided by combining data sets from the Canadian–US GWAS with a separate Italian GWAS16 (Fig. 2 and Table 2). More than 610,000 common variants were examined in 457 Italian PBC cases and more than 1 million in 947 controls. When considered alone, the Italian cohort association data set achieves genome-wide significance at the HLA locus, with several other loci showing suggestive association signals (Fig. 2A,B). Analysis of the combined data set (998 cases and 8777 controls) showed many more loci to have reached the conservative genome-wide threshold P value (P < 5 × 10−8), most of these also showed P values < 5 × 10−5 in the Italian-alone cohort.

e., not refrigerated). PPP may be kept at room temperature (20°C–25°C) prior to testing. Plasma that has been hemolyzed during collection and processing should not be analyzed. Many laboratories Tyrosine Kinase Inhibitor Library in vitro now have some

form of semi or fully automated coagulation analyzers. Accurately detecting the clotting end-point using a manual technique requires considerable expertise, particularly if the clotting time is prolonged or if the fibrinogen concentration is low, and the clot is thin and wispy. For manual testing, the tube should be tilted three times every five-seconds through an angle of approximately 90° during observation. The tube should be immersed in a water bath at 37°C between AZD4547 purchase tilting. Platelet count, BT, PT, and APTT may be used to screen a patient suspected of having a bleeding disorder [4]. Bleeding time lacks sensitivity and specificity and is also

prone to performance-related errors. Therefore other tests of platelet function such as platelet aggregometry are preferred when available [5, 6]. Based on the results of these tests, the category of bleeding disorder may be partially characterized to guide subsequent analysis. (Table 3-1). These screening tests may not detect abnormalities in patients with mild bleeding disorders including some defects of platelet function, FXIII deficiency, and those rare defects of fibrinolysis, which may be associated with a bleeding tendency. Correction or mixing studies using pooled normal plasma (PNP) will help define whether prolonged coagulation times are due to factor deficiency or circulating anticoagulants of inhibitors. Correction studies with FVIII/FIX-deficient plasma may be used to identify the particular deficiency if a factor assay is not available. Selleckchem 5 FU 1. Factor assay is required in

the following situations: To determine diagnosis To monitor treatment ○ The laboratory monitoring of clotting factor concentrates is possible by measuring pre- and postinfusion clotting factor levels. The presence of some form of inhibitor is suspected when there is a prolonged APTT that is not fully corrected by mixing patient plasma with PNP. The most frequently encountered functional inhibitors of hemostasis are lupus anticoagulants (LA), which are not directed against specific clotting factors and which should be excluded. Results of APTT testing on mixtures of test and normal plasma can be difficult to interpret, particularly as in acquired hemophilia there may initially be a full correction of APTT in the presence of a potent specific anti-FVIII antibody. Most FVIII inhibitors that occur secondary to replacement therapy in subjects with hemophilia A show a characteristic pattern: the APTT of a patient/PNP mixture is intermediate, i.e., between the APTTs of the two materials, and is further prolonged when the mixture is incubated at 37°C for 1–2 h.

This imbalance could play a role in the immunopathogenesis of HBV-related ACLF. “
“The goal of this study is to evaluate whether an elevated neutrophil–lymphocyte ratio (NLR) at the time of diagnosis predicts survival of patients with hepatocellular carcinoma (HCC) after liver transplantation (LT). We hypothesize that the NLR is predictive of overall survival (OS) and recurrence-free survival (RFS) in patients with HCC who undergo LT. This is a retrospective

analysis of adult patients undergoing LT for HCC between 2000 and 2008 at our institution. We define an elevated NLR as a ratio of 5 or greater. We included 160 patients who underwent LT for HCC in the time period, of whom 28 had an elevated NLR. Seventeen subjects learn more experienced recurrent HCC during buy ICG-001 the study period. The cumulative survival among subjects with an elevated NLR was significantly lower than among subjects with a normal NLR. On univariate analysis, several factors (including an elevated NLR) predicted decreased OS and RFS. However, after multivariate

analysis, only three factors (including elevated NLR) remained significant as predictors of OS. Additionally, multivariate analysis revealed that an elevated NLR was the only significant independent predictor of RFS. Preoperative NLR is a powerful independent predictor of OS and RFS in patients undergoing LT for HCC. Measurement of NLR could serve as a useful and easily obtained adjunct to the Model for End-Stage Liver Disease score and Milan criteria when evaluating this patient population and determining which patients will gain the most survival benefit from transplantation. “
“Caveolin-1 Leukotriene-A4 hydrolase (CAV1) is a structural protein of caveolae involved in lipid homeostasis and endocytosis. Using newly generated pure Balb/C CAV1 null (Balb/CCAV1−/−) mice, CAV1−/− mice from Jackson Laboratories (JAXCAV1−/−), and CAV1−/− mice developed in the Kurzchalia Laboratory

(KCAV1−/−), we show that under physiological conditions CAV1 expression in mouse tissues is necessary to guarantee an efficient progression of liver regeneration and mouse survival after partial hepatectomy. Absence of CAV1 in mouse tissues is compensated by the development of a carbohydrate-dependent anabolic adaptation. These results were supported by extracellular flux analysis of cellular glycolytic metabolism in CAV1-knockdown AML12 hepatocytes, suggesting cell autonomous effects of CAV1 loss in hepatic glycolysis. Unlike in KCAV1−/− livers, in JAXCAV1−/− livers CAV1 deficiency is compensated by activation of anabolic metabolism (pentose phosphate pathway and lipogenesis) allowing liver regeneration. Administration of 2-deoxy-glucose in JAXCAV1−/− mice indicated that liver regeneration in JAXCAV1−/− mice is strictly dependent on hepatic carbohydrate metabolism.

In contrast, they might depend solely on the presence of VS. Some of the additional visual symptoms in patients with VS can also be found in migraineurs. This might, at least in part, explain how a migrainous, but not typical migraine aura, comorbidity Ceritinib might

potentiate these symptoms in VS patients. For migraineurs without VS, the higher prevalence of palinopsia when compared with healthy controls seems to be of minor relevance since it affects only 14.2% of the group and occurs only episodically.[18] However, this predisposition to palinopsia in migraineurs might perpetuate mechanisms of palinopsia in VS resulting in a higher prevalence and continuous presence.[5] For the key migraine symptom photophobia,[6] recent studies have suggested a pain-mediated increase in light sensitivity.[19] In VS, such mechanism is unlikely due to the low prevalence of chronic headache in patients with continuous VS and photophobia.[5] In contrast, photophobia as a symptom of the VS syndrome might be perpetuated by comorbid

migraine in a non-pain-mediated manner. This is less clear for tinnitus, which is not a classical migrainous symptom[20] although migraine attack-associated episodes of tinnitus have been reported.[21] Tinnitus could be interpreted as noise within click here the acoustic system. The similarity to “TV-snow,” ie, “TV-noise,” has previously led to

the interpretation that tinnitus might be the clinical correlate of the affection of the acoustic system by VS-like mechanisms.[5] In our study, tinnitus was also more prevalent in VS patients with comorbid migraine and thus behaved like the additional visual symptoms supporting that the VS syndrome might indeed include the non-visual symptom tinnitus. In [18F]-FDG PET, the right lingual gyrus and the anterior lobe of the left cerebellum were metabolically more active in patients with VS when compared with healthy controls. This first objective correlate of VS strongly suggests the VS Tyrosine-protein kinase BLK syndrome is a neurological condition. This has important consequences for communication with patients, who have been frequently diagnosed as having a psychogenic disorder or as being malingerers. The relevance of the (trend) hypermetabolism of the left cerebellum is unclear. The cerebellum’s key function for vision is extraocular motility.[22] Only little is known about its role in visual perception, but cerebellar disease has been associated with difficulties in depth perception[23] or with a phenomenon called upside-down vision.[24, 25] When analyzed visually, this area seems to extend laterally and rostrally to the left lingual gyrus (Figure) possibly reflecting the relatively low spatial resolution of PET.

Although HCC typically arises in underlying cirrhosis, this is a potential pitfall of hepatobiliary imaging. It is hypothesized that some HCCs overexpress the cellular receptor, OATP1B3, which facilitates

Apitolisib uptake of Eovist.45-51 Additionally, extracellular pooling of contrast within tumors may explain hyperintensity on hepatobiliary phase images, potentially seen with Eovist or Multihance in the setting of fibrotic or necrotic metastases. HCA is an uncommon benign lesion linked to exogenous hormone exposure. Recent advances have facilitated identification of three distinct subtypes of HCA with different biological behavior and potentially different imaging features (Figs. 3, 4).52-56 These subtypes include: hepatocyte nuclear factor-1 check details alpha (HNF-1 alpha)-mutated, beta-catenin, and inflammatory HCA. The majority of HCA are HNF-1 alpha and inflammatory subtypes. Inflammatory HCA has been described as T2 hyperintense with arterial hyperenhancement that persists on portal venous phase (Fig. 4). HNF-1 alpha HCA may show nonpersistent arterial enhancement and intralesional lipid, the presence of which can be diagnosed on in- and opposed-phase imaging. HNF-1 alpha are also called steatotic HCA due to diffuse lipid content. Inflammatory HCA may contain lipid;

however, they potentially have only a small component or demonstrate heterogeneous signal loss on opposed-phase images compared to diffuse signal loss described with steatotic Endonuclease HCA (Fig. 3).56 Studies evaluating the diagnostic performance of MRI in subtyping HCA show high specificity in identifying steatotic and inflammatory subtypes, with specificities ranging from 88%-100%.56, 57 Further investigation is needed to validate the MR criteria for HCA subtyping, especially in defining the imaging features of beta-catenin lesions, which portend the highest

potential risk of malignant transformation.54, 55 Hepatobiliary phase imaging may distinguish HCA from FNH, a common differential in young asymptomatic women. Unlike FNH, HCA with rare exceptions do not retain contrast on hepatobiliary phase images.46 HCC occurs almost exclusively in the setting of chronic liver disease.58 The classic HCC appearance on ECA-enhanced MRI, described in the setting of cirrhosis, is tumoral arterial enhancement, subsequent “washout” during portal venous or equilibrium phases, and delayed enhancing pseudocapsule (Fig. 5).59, 60 It is believed that loss of portal venous blood supply, occurring by way of a multistep carcinogenesis pathway, may explain the imaging appearance of “washout.”61 The presence of “washout” and delayed enhancing pseudocapsule are highly specific features of HCC when using ECA.60, 62, 63 Caution should be exercised in describing a pseudocapsule in the setting of prior hepatic-directed treatment, as granulation tissue can form a ring of peripheral enhancement in this scenario.