7 The mechanism for this unexpected detrimental effect remains unclear. It has been postulated that high-dose UDCA treatment allows unabsorbed drug to enter the colon and be modified into hydrophobic, hepatotoxic bile acids, such as lithocholic acid (LCA).8-10 LCA is hepatotoxic in animal models and leads to segmental bile duct obstruction, destructive cholangitis, and periductal fibrosis.11, 12 Nonetheless, a recent study testing the effects of various, escalating UDCA doses on biliary composition showed only minimal

changes in all bile acids except UDCA, which was proportionally enriched.13 The aim of our Tipifarnib cell line study was to determine the serum bile acid composition after high-dose UDCA treatment during a randomized, find more double-blind controlled trial and to correlate the changes in bile acid levels with clinical outcomes. ΔCA, cholic acid after treatment minus cholic acid at entry; ΔCDCA, chenodeoxycholic acid after treatment minus chenodeoxycholic acid at entry; ΔDCA, deoxycholic acid after treatment minus deoxycholic acid at entry; ΔLCA, lithocholic acid after treatment minus lithocholic acid at entry; ΔtBA, total bile acids after treatment minus total

bile acids at entry; ΔUDCA, ursodeoxycholic acid after treatment minus ursodeoxycholic acid at entry; CA, cholic acid; CDCA, chenodeoxycholic acid; DCA,

deoxycholic acid; GCMS, gas chromatography-mass spectrometry; LCA, lithocholic acid; NS, not significant; PSC, primary sclerosing cholangitis; UDCA, 上海皓元医药股份有限公司 ursodeoxycholic acid; ULN, upper limit of normal. Patients were entered into the present study according to the criteria followed for our randomized, double-blind controlled trial of high-dose UDCA versus placebo.7 Difficulties related to the multicenter nature of the study and the long enrollment period did not allow all of the initial study patients to be analyzed with respect to the bile acid composition. The study was approved by the institutional review boards at each site. A PSC diagnosis was based on the following criteria: (1) chronic cholestatic disease of at least 6 months’ duration; (2) a serum alkaline phosphatase level at least 1.5 times the upper limit of normal (ULN); (3) retrograde, operative, percutaneous, or magnetic resonance cholangiography findings consistent with PSC within 1 year of study entry; and (4) a liver biopsy sample in the previous year that was compatible with the diagnosis of PSC and was available for review.

Based on the results of this study, we hope to demonstrate in the future whether famotidine is more effective than teprenone for reducing gastroduodenal mucosal injuries under use of LDA in the long term. In conclusion, famotidine is better than teprenone in terms of reducing the number of the erosions under use of LDA, yet it does not necessarily mean famotidine is better than teprenone in prevention of peptic ulcer under use of LDA. The authors thank the following investigators for their participation in the study: Masahiro Sakaguchi, Hisato Higuchi, Yasuhiko Fujioka, Ryosaku Harada, Shinichi Nakayama, Kanako Yamaguchi, Shuichi Terao, and Keishi Kojima. Guarantor

of the article: Toshihisa Takeuchi. Specific author contributions: principal investigator, subject recruitment, subject evaluation, data collection, statistical analysis, and manuscript preparation: Toshihisa Takeuchi; manuscript preparation: Wnt antagonist Kazuhide Higuchi; subject recruitment, subject evaluation, and data collection: Kazuhiro Ota, Satoshi Harada, Yuichi Kojima, Takuya Inoue, Ryuichi Iwakiri, Yasuhisa Sakata, Kazuma Fujimoto, Tsuyoshi Fujita, and Takeshi Azuma. This research did not receive any specific grant from any

funding agency in the public, commercial, or not-for-profit sector. “
“Hepatitis E refers to liver disease caused by the hepatitis E virus (HEV), a small, nonenveloped virus with a single-stranded RNA Rucaparib purchase genome. The virus has four genotypes, but only one serotype. Genotypes 1 and 2 exclusively infect humans, whereas genotypes 3 and 4 also infect pigs and several other mammalian species. Though

HEV does 上海皓元医药股份有限公司 not grow well in cell culture, several aspects of its biology and pathogenesis have been worked out using animal models and cell transfection studies, and by analogy with other related viruses. HEV itself appears noncytopathic, and the liver injury during hepatitis E may be mediated by the host immune response. In areas with poor sanitation, HEV infection is common and presents as outbreaks and also as sporadic cases with acute self-limited hepatitis. The transmission is feco-oral, usually through contaminated drinking water. The disease often affects young adults and is particularly severe among pregnant women and persons with preexisting liver cirrhosis. In the developed world, the disease is being increasingly recognized. It occurs as occasional sporadic cases, most often among elderly men with coexisting illnesses. These appear to be related to zoonotic transmission. Chronic infection is known among immunosuppressed persons in these regions and may progress to liver cirrhosis. Serological tests for diagnosis of HEV exposure and recent infection, namely immunoglobulin (Ig)G and IgM anti-HEV, respectively, need further improvement in sensitivity and specificity, particularly when used in developed countries.

Thus, we envision that future approaches to treating and preventing liver disease will consider the liver-microbiota axis. “
“Background and Aim:  Focal nodular hyperplasia (FNH) and FNH-like lesions are hypervascular masses that can mimic hepatocellular carcinoma (HCC). We have investigated the clinical, radiological and pathological features of FNH and FNH-like lesions of the liver, with particular focus on the aspect of diagnosis. Methods:  A total of 84 patients, 77 with pathologically-proven FNH and seven with FNH-like lesions of the liver, were

analyzed retrospectively. Results:  Of the 84 patients, seven had underlying liver cirrhosis, including two with Budd-Chiari syndrome and one with cardiac cirrhosis. These cases were NVP-LDE225 nmr therefore classified as

having FNH-like lesions. Two of the remaining 77 patients selleck without underlying liver cirrhosis were positive for hepatitis B surface antigen. Seven of 50 (14.0%) patients evaluated by four-phase computed tomography (CT) showed portal or delayed washout, and three of 28 (10.7%) patients analyzed by three-phase CT showed washout on the portal phase. Collectively, three of nine (33.3%) patients with risk factors for HCC could have been wrongly diagnosed with HCC based on the non-invasive diagnostic criteria for HCC. A central scar was observed in 30 patients (35.7%) radiologically. Among 62 patients who underwent percutaneous needle biopsy, four patients (6.5%) were misdiagnosed as having HCC and two patients (3.2%) medchemexpress had inconclusive results by a first needle biopsy. Conclusions:  The presence of a hepatic lesion with arterial hypervascularity and/or portal/delayed washout is not necessarily diagnostic of HCC, particularly in patients without risk factors for HCC. These radiological findings can also occur in cirrhotic patients with FNH-like lesions, including those with hepatic outflow obstruction. “
“Previous studies have suggested that patients with chronic hepatitis C with a low pretreatment hepatitis C virus (HCV) level have a high sustained

virological response (SVR) rate, and that there would be a subpopulation of patients in which HCV can be eradicated with pegylated interferon (PEG IFN) alone without a decrease in SVR. However, the efficacy of PEG IFN monotherapy in patients with low HCV RNA levels is unclear. Several studies have reported that interferon sensitivity-determining region (ISDR) and the single-nucleotide polymorphism (SNP) of interleukin-28B (IL-28B) contribute to IFN response, but these relationships are controversial. The aim of this study was to determine whether the SNP of IL-28B (rs8099917) and amino acid substitutions in the ISDR among patients with low HCV levels affect the response to PEG IFN monotherapy. One hundred and four patients with low-level HCV infection were studied. Low HCV level was defined as 100 KIU/mL or less. SVR was achieved in 94 patients (92.2%).

Red meat intake is the most important source of endogenous formation of nitrosamines, probably due to the heme-iron content. In a population-based case–control study in Nebraska, USA [32], including 154 GC cases and 449 controls, a significant positive association between a high rate of GC and a Bafilomycin A1 high intake of heme iron and total iron from meat was observed. In a prospective study in Finland [33] in which prediagnostic serum iron, ferritin, and unsaturated iron-binding capacity

were measured, a “u”-shaped relationship with total iron-binding capacity and an inverse association between serum ferritin and serum iron was observed in patients with GC. In the Netherlands cohort [34] including 497 noncardia GC, 166 cardia GC and 110 esophageal squamous cell carcinoma (ESCC), a positive association between N-nitrosodimethylamine

intake (the most important nitrosamine, considered as a probable carcinogen for humans) and noncardia GC and ESCC in men was observed. Heme-iron intake was associated with ESCC but not with noncardia GC. On the other hand in a prospective study (EPIC Spain), a positive association between aromatic DNA adducts from leukocytes and GC risk was observed [35]. Aromatic compounds are formed during cooking of meat but also occur in tobacco smoking. There is important evidence showing that regular aspirin use may reduce the progression of preneoplastic lesions and reduce the incidence of GC

and other gastrointestinal cancers. A wide systematic review comparing Napabucasin nmr results from observational and randomized trials [36] confirms this evidence. Regular use of aspirin reduces the long-term risk of GC and also the risk of distant metastasis. Results were consistent MCE among both types of studies. There is strong evidence showing the positive association between esophageal adenocarcinoma and general and abdominal obesity, but it remains unclear whether there is an association with GC. In a large prospective study in the USA [37] including 191 cardia and 125 noncardia GC, a positive association between cardia GC and BMI (HR highest vs referent 3.67, 95% CI 2.0–6.7) and waist circumference HR 2.22, 95% CI 1.4–3.5) was observed. However, as expected, obesity was not associated with noncardia GC. It is well known that people infected with human immunodeficiency virus have an increased risk of some cancers, but little is known about the effect on GC. In a large study in the USA [38], the risk of GC in patients with AIDS and those from the general population was compared. There was a positive association for both cardia and noncardia GC. In a meta-analysis of 29 case–control studies in Latin America (so far no cohort studies have been published) from countries with high GC incidence, the role of different GC risk factors was investigated [39].

20 The following were used for analysis between LEE011 supplier groups: pre- and postoperative PS of each subject; prevalence rates of pre-existing comorbidities; characteristics of the lesion; treatment outcome (en bloc plus R0 resection rates); duration of hospitalization; operating time; incidence rates of complications and duration of hospitalization; postoperative hemorrhage in patients administered anticoagulant therapy; and duration of hospitalization for patients on anticoagulant therapy. We performed ESD using an upper gastrointestinal endoscope (Olympus 1-channel endoscope [Olympus GIF H260 or GIF Q260J], Olympus Medical Systems, Tokyo, Japan).

A hood (Elastic touch, slit and hole hood, TOP Co., Tokyo, Japan) was placed on the tip of the scope to maintain a good visual field at the site of submucosal dissection. VIO 300D (Erbe Elektromedizin, Tubingen, Germany) was used as the high-frequency generator. We mainly used an IT knife (KD-610L, KD-611L, Olympus Medical Systems) and a flush knife (DK2618JN15, DK2618JB15, Fujinon, Tokyo, Japan). The area of submucosal dissection was maintained at the required distance from the muscle layer by submucosal injection of 1% hyaluronic acid solution (Mucoup, Johnson & Johnson K.K., Tokyo, Japan). Long-lasting submucosal elevation was maintained

during ESD.21,22 Hemostatic forceps (Coagrasper, FD410LR, FD411QR, Olympus Medical Systems) were used for controlling active hemorrhage during ESD or for

pre-coagulation of large vessels. Conscious sedation was used Autophagy Compound Library during ESD with a combination of flunitrazepam (Rohypnol, Chugai Pharmaceutical, Tokyo, Japan), pentazocine (Pentagin, Daiichi Sankyo, Tokyo, Japan), and propofol (Diprivan, AstraZeneca, Osaka, Japan). It has been reported that the standard dose can be unsafe for the elderly, so the doses were decreased compared with those used for the non-elderly.23 The patients were monitored during ESD using an ECG monitor, percutaneous oxygen saturation monitor, automatic blood pressure monitor, and bispectral index monitor (BIS monitor, Aspect Medical Systems, Norwood, MA, USA). For sedation, we adjusted the aforementioned drugs so that the BIS value during ESD was 50–60.24 Anticoagulant therapy 上海皓元 was discontinued for ESD according to the recommended cessation period.25 After ESD, re-examination by EGD was performed 1 week postoperatively for patients without complications. If there was no evidence of exposed vessels in the artificial ulcer, anticoagulant therapy was resumed. We evaluated all together both using warfarin and/or antiplatelet agents as an anticoagulant therapy. We decided to make heparin infusion during the discontinuation period of warfarin and/or antiplatelet agents, and we considered to need or not heparin infusion individually.

HMGB1 BAY 73-4506 ABM mice were not protected from APAP-induced injury, excluding a biologically relevant influence of HMGB1 from this compartment. Deficiency of RAGE, a putative HMGB1 receptor, strongly reduced APAP-induced ALT elevation (p<0.05), necrosis (p<0.01) and neutrophilic infiltration (p<0.01)24h after APAP intoxication. In contrast, deficiency of TLR4, a second putative HMGB1

receptor, did not ameliorate APAP-induced liver injury. CONCLUSION: The HMGB1-RAGE axis is a key injury-sensing system that amplifies acute liver injury through the initiation of sterile inflammation. Disclosures: The following people have nothing to disclose: Peter Huebener, Pradere JeanPhilippe, Geum Youn Gwak, Robert Schwabe High mobility group box-1 (HMGB1) is secreted into the extracellular milieu during liver ischemia/reperfusion (I/R) and initiates proinflammatory cascades that lead to organ injury. However, the intracellular role of HMGB1 during oxidative stress is not understood. We sought to determine the role of intracellular HMGB1 in hepatocytes (HGs) following liver I/R. HG specific HMGB1 knockout (HMGB1-HG KO)and WT mice were subjected to a non-lethal warm liver I/R.

HMGB1-HG K〇 mice have markedly elevated sALT, necrosis, inflammatory cytokines production as well as infiltration BGJ398 manufacturer of innate immune cells in ischemia lobes compared to WTs after I/R injury. HMGB1 K〇 HGs demonstrate significantly more oxidative stress as measured by 4-hydroxynonenal staining. HMGB1-HG KO mice also express lower levels of superoxide dismutases (SOD) 1/S〇D2 than

WTs after liver I/R. In vitro, HMGB1 deletion in HCs leads to more total cellular ROS and mitochondria R〇S production under hypoxia. Significantly medchemexpress more release of histones and phosphorylation of histone H2A. X. HMGB1 K〇 mice were found compared to WT mice after liver I/R. Significantly more LDH was observed in HMGB1 K〇 HGs compared to WT HCs under hypoxia, all suggesting more cell damage in K〇 HGs. Excessive activation of PARP1 and poly(ADP-ribose)ylation of proteins in HMGB1 K〇 HGs under oxidative stress, exhausting NAD and ATP, exacerbating mitochondrial instability, consequently led to more mitochondrial damage and cell death compared with WT HGs. Inhibition of PARP1 significantly ameliorated the liver damage in HMGB1-HG K〇 mice after liver I/R. Therefore, although released HMGB1 may function as a DAMP in ischemic liver injury, our study demonstrates the importance of intracellular HMGB1 in the response to oxidative stress. Lack of HMGB1 in HGs leads to diminished R〇Sscavengers and over-activation of PARP1 which may exacerbate organ damage and cells death after liver I/R. Disclosures: The following people have nothing to disclose: Hai Huang, Gary Nace, Sheng Tai, John R.

TRAF2 can recruit IκB kinase (IKK) and promote NF-κB–mediated inflammation.16, 17 Proapoptotic Bcl2 proteins, which regulate apoptotic cell death via altering calcium homeostasis, have been linked to the ER stress response and in particular to the IRE1α branch.12, 18 When activated, these Bcl2 proteins can lead to calcium release, calpain activation which can cause mitochondrial depolarization, and increased reactive oxygen species (ROS),19 as well as the activation of caspase-4 which along with JNK modulates apoptosis. On the other hand, BAX and BAK have been shown to form a complex with the

cytosolic domain of IRE1α and Selleck MI-503 regulate IRE signaling in cells undergoing ER stress. Double knockouts of BAX and BAK apoptotic factors demonstrate a phenotype similar to that of IRE1α-deficient mice.18 ER-associated caspase-12 plays an important role in ER stress

response–induced apoptosis in rodents but not in humans20; Calcium release is Pifithrin-�� clinical trial a critical factor in affecting mitochondrial function, particularly in areas in which the ER is in close association with the mitochondria, so-called mitochondria-associated membrane21, 22; PERK-induced ATF4 as well as ATF6 can increase the expression of CHOP, which promotes ER stress response through numerous mechanisms. CHOP promotes oxidative stress and inflammation, and results in down-regulation of antiapoptotic Bcl2 proteins and increased transcription of proapoptotic Bcl2 member Bim.23 CHOP induces GADD34 (Growth arrest and DNA damage-inducible protein 34), which associates with protein phosphatase-1 and promotes dephosphorylation

of P-eIF2α (phosphorylated eIF2α) a mechanism aiming to recover ER homeostasis by resuming protein synthesis but which could be harmful if protein overload were to continue. In addition, CHOP and ATF4 together induce TRB3 (tribbles homolog 3), which inhibits the cytoprotective, insulin-sensitizing Akt kinase.13, 24 Hepatocytes, like other secretory cells, are rich in ER. Because of their high protein synthesizing capacity, it is easy to postulate that UPR/ER stress medchemexpress response plays an important role either in preventing or mediating pathological changes in various liver diseases. Despite the identification of up-regulation or dysregulation of ER stress signaling mediators in various forms of liver injury and the rapid growth in the field of ER stress research in liver diseases, the exact contribution of ER stress response to many forms of hepatic injury remains to be fully established.25 Here, we review and update some well-established associations between ER stress response and liver disease (Fig. 2).

Even triptans, mainstay of effective, specific migraine treatment, can,

when overused, provoke chronic migraine. Acute medications taken for another pain disorder, such as back pain or fibromyalgia, go into the same bloodstream. Combining these medications can result in chronic daily headache. How can one avoid the pitfall of too much acute medication and rebound? Remember Torin 1 the rule of 2′s with acute medications: no more than 2 doses/day, 2 days/week. Avoid treating migraines with narcotics or butalbital combinations at all. Address modifiable risk factors, such as poor sleep, obesity, depression, anxiety, caffeine overuse, and lack of exercise. An ounce of prevention is worth a pound of cure; that is, it is far better to stay in episodic migraine than try to treat established chronic migraine. In the United States, most people with chronic migraine are overusing acute medications. There are health consequences to overusing acute medications, consequences to the gastrointestinal tract, kidneys, and other body systems. Rebound will not get better while this stew of medications is consumed. Withdrawal from medication overuse can result in headaches worsening before improvement. OnabotulinumtoxinA (brand name Botox) is the only

FDA-approved medication for treatment of chronic migraine. Treatment involves 155 units injected in defined locations of head and neck with an evidence-based FDA-approved protocol find more (PREEMPT) every 3 months. OnabotulinumtoxinA can wear off, with ongoing injections often required. Later, injections can be stopped or delayed, evaluating whether migraines return and, if so, at what frequency. Other medications may be of benefit for chronic migraine but are not FDA-approved for this indication, and include topiramate and other antiseizure medications and antidepressants, such as amitriptyline or venlafaxine. Your headache care provider could match other health conditions with one prevention that helps both problems. Someone with depression might consider antidepressants, while an overweight individual, topiramate. Those with past, 上海皓元医药股份有限公司 resolved, chronic migraine are at risk for relapsing back into a frequent pattern;

follow up is important. Increased relapse risks are male gender, higher headache frequency, longer medication overuse duration, especially combination medications, poor sleep, and other pain disorders. Effective treatment of chronic migraine is aimed at returning to an episodic pattern of headache occurrence. It will not cure migraine, but will reduce the frequency to 14 or fewer days per month, and allow for effective acute treatment of the headaches when they do occur. Chronic migraine is treatable. Patient and provider need to actively control its impact. If the above interventions do not work, consider a multidisciplinary headache treatment program combining cognitive behavioral strategies with medications and physical therapy to regain headache control. “
“(Headache 2010;50:479-480) “
“Background.

ERAT; 4. minimally invasive; Presenting Author: HYUNG HUN KIM Additional Authors: JI HYUN KIM, GWANG HA KIM, MYUNG-KYU CHOI Corresponding Author: GWANG HA KIM Affiliations: The Catholic University of Korea College of Medicine; Inje University College of Medicine; Selleckchem CDK inhibitor Pusan National University College of Medicine Objective: Unlike surgery, endoscopic submucosal dissection (ESD) removes gastric

epithelial neoplasms within a tight margin, leaving most normal tissue around the neoplasm intact, thus resulting in a high risk for missed synchronous gastric epithelial neoplasms (mSGENs). The purpose of this study was to evaluate the characteristics and risk factors for missed SGENs (mSGENs) compared to simultaneously identified SGENs (siSGENs) in http://www.selleckchem.com/products/GDC-0980-RG7422.html patients who underwent ESD. Methods: We retrospectively examined 312 SGENs from 275 patients treated by ESD at 3 hospitals in Korea between January 2004 and May 2011. The incidence and clinicopathological features of SGENs, mSGENs, and siSGENs were investigated. Any second epithelial neoplasm found within 1 year of the first

ESD procedure was defined as an mSGEN and any neoplasm detected simultaneously with the first neoplasm was defined as a siSGEN. Results: The overall incidence of ESD patients with SGENs was 9.1% (275/3018 patients). Of the SGENs, 45.2% were siSGENs and 54.8% were mSGENs. Independent risk factors for mSGENs were adenoma as the first gastric lesion (Exp (B) = 2.154, 95% CI = 1.282–3.262), and duration of endoscopic examination before the first ESD (Exp (B) = 1.074, 95% CI = 1.001–1.141). The results suggest that 33% of mSGENs could have been identified during the endoscopic examination prior to ESD. Conclusion: Additional effort needs to be expended in identifying siSGENs, particularly prior to ESD for less serious adenomas. This should include sufficient time for endoscopic examination, prior to ESD, to ensure a thorough examination for siSGENs. MCE Key Word(s): 1. Synchronous; 2. Neoplasm; 3. Gastric cancer; Presenting Author: KHIENVAN VU Corresponding Author: KHIENVAN VU Affiliations: 108 Hospital Objective: Transjugular Intrahepatic Portosystemic Shunt (TIPS) is useful in the treatment of patients

who develop rebleeding despite adequate medical or endoscopic therapy. From 2009 to now, we have made TIPS technique for pantients with oesophageal variceal bleeding many time, no respond to endoscopic treatment. Methods: 57 patients with cirrosis with eosophageal variceal bleeding many time have been included in this study. TIPS technique was performed at the Department of Intervention. Results: Clinical: Male 84.9%; Mean age: 45.3 (23–70 year). Cirrhosis stage Child A, Child B, Child C proportion accounted for: 40%; 29.5% and 30.5%. Endoscopy: Form of varices grade III: 96%; red colour signs: 90%. There are 5/57 patients with gastric variceal, with form F2 and F3 corresponding percentage: 42.8% and 57.2%. Effective treatment: Technique success: 57/57 (100%); Clinical success: 55/57 (96.4%).

Prospective trials are needed to ascertain whether it is useful to predict thrombosis in patients with cirrhosis. HEPATOLOGY 2010 Chronic liver disease is characterized by impaired synthesis of most coagulation Vismodegib solubility dmso factors and prolonged conventional coagulation tests such as the prothrombin and activated

partial thromboplastin time.1 Recently, the long and widely used belief that there is a causal relationship between abnormal coagulation tests and the risk of bleeding has been challenged by showing that under appropriate experimental conditions, liver disease patients generate as much thrombin as healthy subjects provided that platelets numbers are sufficient (>60 × 109/L) to support the normal thrombin generation elicited by plasma.2-4 More recently, it has been shown that patients with cirrhosis display a procoagulant imbalance that may be detected by measuring thrombin generation performed with and without thrombomodulin.5 These observations are in keeping with an earlier observation that patients with

chronic liver disease, despite their substantial prolongation of the conventional coagulation times, are not protected from venous thromboembolism (VTE)6 and with those Tanespimycin mouse of a recent population-based case-control study showing that patients with chronic liver disease (both cirrhotic and noncirrhotic) have a relative risk of VTE nearly

two-fold higher than that of the general population.7 The detection of the procoagulant versus anticoagulant imbalance might have important practical implications in assessing the risk of VTE, especially in patients with cirrhosis awaiting liver transplantation. Cirrhosis is the main cause of portal vein thrombosis (PVT),8 with a prevalence of 1%9 in compensated cirrhosis, but much higher in advanced cirrhosis 上海皓元医药股份有限公司 or in patients awaiting transplantation (from 8%-25%).10 PVT is a multifactorial process, in which local inflammatory foci and systemic prothrombotic factors concur. Its pathogenetic factors are those recognized for a long time as leading to deep vein thrombosis of the lower limbs: damaged vessel wall, slowing of blood flow, and procoagulant versus anticoagulant imbalance. Thus far, the laboratory method available to detect the procoagulant imbalance in cirrhosis is the thrombin generation test5 which requires expertise and equipment that are not readily available in clinical laboratories. This article reports results on a large series of patients with chronic liver disease investigated for their procoagulant imbalance by means of a standardized, easy-to-run, and commercially available method. ETP, endogenous thrombin potential; PVT, portal vein thrombosis; OD, optical density; PICI, Protac-induced-coagulation inhibition; VTE, venous thromboembolism.