Vascular Liver Diseases Research Articles

National 10-year trends and outcomes of isolated and concomitant tricuspid valve surgery.

The data on the trends and comparative outcomes after isolated and concomitant tricuspid valve repair/replacement (TVR) is scarce. The International Classification of Diseases - 9th version was used to identify the patients who underwent TVR, using the National Inpatient Sample. Outcomes were evaluated using the analysis of variance and Chi-square test, and trends across the years were tested via Cochran-Armitage Test. Of 6868 patients who underwent TVR between 2005-14, 1601 (23%) were isolated. Over the 10-years period, the number of total and isolated TVR has steadily increased (P<0.001). The proportion of patients undergoing repair has increased compared to replacement. Overall in-hospital mortality was 8.5% and 7.7% (p=0.28), permanent pacemaker requirement was 11.24% and 10.69% (P=0.53), blood transfusion rates were 32.6% and 37.9% (P<0.001), and the post-procedure length of stay (LOS) was 14.1±0.44 and 12.5±0.17 days (P<0.001) after isolated and concomitant TVR respectively. High (26.25%) number of patients were discharged to skilled facility. The operative mortality associated with TV repair was lower than with replacement (6.8% versus 11.15%, P<0.001), but the mortality trend over the 10-years has stayed relatively stable. Independent predictors of mortality were age >50 years, heart failure, cerebrovascular accident, end-stage renal disease, peripheral vascular disease, liver disease, and TV replacement. Both isolated and concomitant TVR has increased over the last 10 years, however is associated with high mortality, complications, need for skilled facility placement, and longer LOS. The mortality after TV replacement was significantly higher than that after repair.

Hepatocellular nodules in vascular liver diseases.

Hepatocellular nodules have been recognized in vascular liver diseases for a long time and mostly described and studied in the imaging literature. Some confusions in their identification and overlap in their definitions exist, especially in this specific clinical context. Pathology descriptions report the development of nodular regenerative hyperplasia, large regenerative nodule, and focal nodular hyperplasia, as adaptive responses of the liver parenchyma to the modified blood flow. True neoplastic hepatocellular nodules such as hepatocellular adenoma and hepatocellular carcinoma can also appear, mainly in Budd-Chiari syndrome, and have to be correctly diagnosed. This is more difficult for the radiologist in these diseased livers, leading more frequently to perform liver biopsies. We describe the histology of each type of well-differentiated hepatocellular nodules and provide some clues for their differential diagnosis. A review of the literature gives an historical perspective of the problem and enlightens the frequency and the subtypes of hepatocellular nodules found in the most common vascular liver diseases.

Comorbidities Can Predict Mortality of Kidney Transplant Recipients: Comparison With the Charlson Comorbidity Index

BackgroundComorbid conditions are important in the survival of kidney transplant recipients. The weights assigned to comorbidities to predict survival may vary based on the type of index disease and advances in the management of comorbidities. We aimed to develop a modified Charlson comorbidity index (CCI) in renal allograft recipients (mCCI-KT), thereby improving risk stratification for mortality. MethodsA total of 3765 recipients in a multicenter cohort were included to develop a comorbidity score. The weights of the comorbidities, per the CCI, were recalibrated using a Cox proportional hazards model. ResultsPeripheral vascular disease, liver disease, myocardial infarction, and diabetes in the CCI were selected from the Cox proportional hazards model. Thus, the mCCI-KT included 4 comorbidities with recalibrated severity weights. Whereas the CCI did not discriminate for survival, the mCCI-KT provided significant discrimination for survival using the Kaplan-Meier method and Cox regression analysis. The mCCI-KT showed modest increases in c-statistics (0.54 vs 0.52, P = .001) and improved net mortality risk reclassification by 16.3% (95% confidence interval, 3.2–29.4; P = .015) relative to the CCI. ConclusionThe mCCI-KT stratifies the risk for mortality in renal allograft recipients better than the CCI, suggesting that it may be a preferred index for use in clinical practice.

Pathology of idiopathic non-cirrhotic portal hypertension.

Idiopathic non-cirrhotic portal hypertension is an under-recognized vascular liver disease of unknown etiology, characterized by clinical signs of portal hypertension in the absence of cirrhosis. By definition, any disorder known to cause portal hypertension in the absence of cirrhosis and any cause of chronic liver disease must be excluded to make a diagnosis of idiopathic non-cirrhotic portal hypertension. However, the diagnosis is often difficult because the disease resembles cirrhosis and there is no gold standard test. Liver biopsy is an essential tool: it is able to exclude cirrhosis and other causes of portal hypertension and it allows the identification of the characteristic lesions. Nonetheless, the histological diagnosis of idiopathic non-cirrhotic portal hypertension is not always straightforward, in particular by needle biopsy samples, because there is no pathognomonic lesion, but rather a variety of vascular changes which are unevenly distributed, very subtle, and not all necessarily identified in a single specimen. Pathologists should be able to recognize several patterns of injury, involving portal/periportal areas as well as parenchymal structures.The histological features of idiopathic non-cirrhotic portal hypertension are described in this review, focusing on their interpretation in needle biopsy specimens.

Vascular liver diseases on the clinical side: definitions and diagnosis, new concepts.

The components of the hepatic vascular system (hepatic arteries, portal and hepatic veins, sinusoids, and lymphatics) can be damaged by various types of injury. Each of the resulting conditions is rare, which has limited knowledge and awareness. In the last two decades, international collaborations have allowed to reach critical masses of data, which has driven significant progresses in understanding and management of vascular disorders of the liver. The present paper discusses definitions, denominations, and diagnosis of such vascular disorders with the exception of those affecting hepatic arteries. Evolving pathogenic or pathophysiologic views relevant to the clinical aspects are also overviewed.

Benign and malignant hepatocellular lesions in patients with vascular liver diseases.

A variety of vascular liver disorders can induce hepatocellular tumors. They may be related to portal venous deprivation, venous outflow obstruction, or arterial diseases. Their common feature is an imbalance between hepatic arterial and portal venous blood flow leading to an increased hepatic arterial inflow. Consequently, hepatocellular tumors may arise, most commonly focal nodular hyperplasia-like lesions but hepatocellular adenomas and hepatocellular carcinoma may be seen as well. This article will review the most common vascular liver diseases associated with hepatocellular nodules (Budd-Chiari syndrome, congenital portosystemic shunt, hereditary hemorrhagic telangiectasia, and portal cavernoma). For each condition, imaging findings will be described as well as the differential diagnosis and the diagnostic clues.

Cholangiopathy in critically ill patients surviving beyond the intensive care period: a multicentre survey in liver units.

The outcome of cholangiopathy developing in intensive care unit (ICU) is not known in patients surviving their ICU stay. To perform a survey in liver units, in order to clarify the course of cholangiopathy after surviving ICU stay. The files of the liver units affiliated to the French network for vascular liver disease were screened for cases of ICU cholangiopathy developing in patients with normal liver function tests on ICU admission, and no prior history of liver disease. Between 2005 and 2015, 16 cases were retrieved. Extensive burns were the cause for admission to ICU in 11 patients. Serum alkaline phosphatase levels increased from day 11 (2-46) to a peak of 15 (4-32) × ULN on day 81 (12-511). Magnetic resonance cholangiography showed irregularities or frank stenosis of the intrahepatic ducts, and proximal extrahepatic ducts contrasting with a normal aspect of the distal common bile duct. Follow-up duration was 20.6 (4.7-71.8) months. Three patients were lost to follow-up; 2 patients died from liver failure and no patient was transplanted. One patient had worsening strictures of the intrahepatic bile ducts with jaundice. Nine patients had persistent but minor strictures of the intrahepatic bile ducts on MR cholangiography, and persistent cholestasis without jaundice. One patient had normal liver function tests. In patients surviving their ICU stay, ICU cholangiopathy is not uniformly fatal in the short term or clinically symptomatic in the medium term. Preservation of the distal common bile duct appears to be a finding differentiating ICU cholangiopathy from other diffuse cholangiopathies.

Predictors of readmissions after head and neck cancer surgery: A national perspective

ObjectivesSurgical oncology patients have multiple comorbidities and are at high risk of readmission. Prior studies are limited in their ability to capture readmissions outside of the index hospital that performed the surgery. Our goal is to evaluate risk factors for readmission for head and neck cancer patients on a national scale. Material and methodsA retrospective cohort study of head and neck cancer patients in the Nationwide Readmissions Database (2013). Our main outcome was 30-day readmission. Statistical analysis included 2-sided t tests, χ2, and multivariate logistic regression analysis. ResultsWithin 30days, 16.1% of 11,832 patients were readmitted and 20% of readmissions were at non-index hospitals, costing $31million. Hypopharyngeal cancer patients had the highest readmission rate (29.6%), followed by laryngeal (21.8%), oropharyngeal (18.2%), and oral cavity (11.6%) cancers (P<0.001). Half of readmissions occurred within 10days and were often associated with infections (27%) or wound complications (12%). Patients from lower household income areas were more likely to be readmitted (odds ratio [OR], 1.54; 95% confidence interval [CI], 1.16–2.05). Patients with valvular disease (OR, 2.07; 95% CI, 1.16–3.69), rheumatoid arthritis/collagen vascular disease (OR, 2.05; 95% CI, 1.27–3.31), liver disease (OR, 2.02, 95% CI, 1.37–2.99), and hypothyroidism (OR 1.30; 95% CI, 1.02–1.66) were at highest risk of readmission. ConclusionThe true rate of 30-day readmissions after head and neck cancer surgery is 16%, capturing non-index hospital readmissions which make up 20% of readmissions. Readmissions after head and neck cancer surgery are most commonly associated with infections and wound complications.

Comorbidity and dementia: A nationwide survey in Taiwan.

BackgroundComorbid medical diseases are highly prevalent in the geriatric population, imposing hardship on healthcare services for demented individuals. Dementia also complicates clinical care for other co-existing medical conditions. This study investigated the comorbidities associated with dementia in the elderly population aged 65 years and over in Taiwan.MethodsWe conducted a nationwide, population-based, cross-sectional survey; participants were selected by computerized random sampling from all 19 Taiwan counties between December 2011 and March 2013. After exclusion of incomplete or erroneous data, 8,456 subjects were enrolled. Of them, 6,183 were cognitively normal (control group), 1,576 had mild cognitive impairment (MCI), and 697 had dementia. We collected information about types of comorbidities (i.e., vascular risk factors, lung diseases, liver diseases, gastrointestinal diseases, and cancers), Charlson comorbidity index score, and demographic variables to compare subjects with normal cognition, MCI, and dementia.ResultsRegardless of the cognitive condition, over 60% of the individuals in each group had at least one comorbid disease. The proportion of subjects possessing at least three comorbidities was higher in those with cognitive impairment (MCI 20.9%, dementia 27.3%) than in control group (15%). Hypertension and diabetes mellitus were the most common comorbidities. The mean number of comorbidities and Charlson comorbidity index score were greater in MCI and dementia groups than in control group. Logistic regression demonstrated that the comorbidities significantly associated with MCI and dementia were cerebrovascular disease (OR 3.35, CI 2.62–4.28), cirrhosis (OR 3.29, CI 1.29–8.41), asthma (OR 1.56, CI 1.07–2.27), and diabetes mellitus (OR 1.24, CI 1.07–1.44).ConclusionMultiple medical comorbid diseases are common in older adults, especially in those with cognitive impairment. Cerebrovascular disease, cirrhosis, asthma, and diabetes mellitus are important contributors to cognitive deterioration in the elderly. Efforts to lower cumulative medical burden in the geriatric population may benefit cognitive function.

P-selectin, endocan, and some adhesion molecules in obese children and adolescents with non-alcoholic fatty liver disease

There is increasing evidence for a direct relationship between the vascular system and non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate endocan and adhesion molecules such as P-selectin derived from the endothelium and platelets in obese children and adolescents with NAFLD. One hundred obese patients and 40 lean controls were enrolled. The obese subjects were divided into two subgroups based on the presence or absence of fatty liver. Blood samples were assayed for endocan, P-selectin, platelet-derived growth factor (PDGF), intercellular cell adhesion molecule (ICAM)-1, and vascular cell adhesion molecule (VCAM)-1. Obese patients with NAFLD presented higher ALT and insulin levels, as well as more profound dyslipidemia when compared with their counterparts without NAFLD. Serum levels of high-sensitivity C-reactive protein, VCAM-1 and ICAM-1 were found increased in both obese groups, regardless of NAFLD. In obese subjects with NAFLD, decreased P-selectin levels (51.6 ± 4.14 ng/mL) were detected as compared with the obese (72.3 ± 4.23) and control (74.2 ± 6.97) subjects. Furthermore, circulating P-selectin levels were closely associated with endocan levels (r = 0.852, p < 0.001). Childhood obesity leads to vascular inflammation and therefore may cause a predisposition to atherosclerosis at an early age. The possible outcome of decreased P-selectin levels with NAFLD development must be further investigated.

Mouse and Rat Models of Induction of Hepatic Fibrosis and Assessment of Portal Hypertension.

Portal hypertension either develops due to progressive liver fibrosis or is the consequence of vascular liver diseases such as portal vein thrombosis or non-cirrhotic portal hypertension. This chapter focuses on different rodent models of liver fibrosis with portal hypertension and also in few non-cirrhotic portal hypertension models. Importantly, after the development of portal hypertension, the proper assessment of drug effects in the portal and systemic circulation should be discussed. The last part of the chapter is dedicated in these techniques to assess the in vivo hemodynamics and the ex vivo techniques of the isolated liver perfusion and vascular contractility.

Antithrombotic treatment with direct-acting oral anticoagulants in patients with splanchnic vein thrombosis and cirrhosis.

Direct-acting oral anticoagulants (DOACs) are used in patients with splanchnic vein thrombosis (SVT) and cirrhosis, but evidence for safety and efficacy in this setting is limited. Our aim was to identify indications and reasons for starting or switching to DOACs and to report adverse effects, complications and short-term outcome. Data collection including demographic information, laboratory values, treatment and complications through the Vascular Liver Disease Interest Group Consortium. Forty-five centres (90%) of the consortium completed the initial eCRF. We report here a series of 94 patients from 17 centres. Thirty-six patients (38%) had cirrhosis. Child-Pugh score was 6 (range 5-8), and MELD score 10.2 (range 6-19). Indications for anticoagulation were splanchnic vein thrombosis (75%), deep vein thrombosis (5%), atrial fibrillation (14%) and others (6%). DOACs used were rivaroxaban (83%), dabigatran (11%) and apixaban (6%). Patients were followed up for a median duration of 15months (cirrhotic) and 26.5months (non-cirrhotic). Adverse events occurred in 17% of patients and included one case of recurrent portal vein thrombosis and five cases of bleeding. Treatment with DOACs was stopped in three cases. The major reasons for choosing DOACs were no need for monitoring or inadequacy of INR to guide anticoagulation in cirrhotic patients. Renal and liver function did not change during treatment. A consistent number of patients with SVT and/or cirrhosis are currently treated with DOACs, which seem to be effective and safe. These data provide a basis for performing randomized clinical trials of DOACs vs. low molecular weight heparin or vitamin K antagonists.

Sinusoidal obstruction syndrome

Sinusoidal obstruction syndrome (SOS) is characterized by damage to small hepatic vessels affecting particularly sinusoidal endothelium. Damaged sinusoids can be associated with a partial or complete occlusion of small hepatic veins, hence the previous denomination of hepatic veno-occlusive disease (VOD). Exposure to certain exogenous toxins appears to be specific to this condition and is frequently included in its definition. Typical histopathological features of SOS in a liver biopsy specimen are presented in the text. The purpose of this article is to provide an overview on the different entities corresponding to this general definition. Such entities include: (i) liver disease related to pyrrolizidine alcaloids; (ii) liver injury related to conditioning for hematopoietic stem cell transplantation; (iii) vascular liver disease occurring in patients treated with chemotherapy for liver metastasis of colorectal cancer; and (iv) other liver diseases related to toxic agents.

European Association for the Study of the Liver clinical guidelines for vascular diseases of the liver in 2016

European Association for the Study of the Liver clinical guidelines for vascular diseases of the liver in 2016

Ductular Reaction and the K7-19 Progenitor Cell Sequence in Vascular Liver Disease: A New Perspective to Pathogenetic Mechanisms of Injury and Repair

Background:Ductular reaction (DR), a process intricately connected with hepatocyte progenitor cells (HPCs) at the canal of Hering evokes considerable scientific interest. The present study was undertaken to (a) identify DR patterns in different subsets of hepatic vascular disease, (b) localize intermediate hepatobiliary progenitors activated in response to stresses to vascular flow while studying their K7/19 immunoexpression profiles, and (c) possibly provide new insights to pathogenesis. Methods: Forty-six cases of hepatic vasculopathy including Budd-Chiari syndrome [BCS] (11), acute hemorrhagic necrosis [AHN] (6), veno-occlusive disease [VOD] (7), non-cirrhotic portal fibrosis [NCPF] (10), extrahepatic portal vein obstruction [EHPVO] (10) and chronic venous congestion [CVC] (2) were randomly selected. Mean DR was scored as 1: 2–5, 2: 6–8, 3 > 8 after counting ductules per portal tract (D/ PT) separately on K7 and 19 immunostains. Extraportal ‘‘progenitors’’ were semiquantitatively graded as 0: None, 1: Occasional, 2: Significant number. This was done separately for hepatocytic and ductular cells on K7 & 19. Zonation effect, if any was noted. Results: DR, intermediate hepatocytic progenitors and extraportal ductules were seen in 69.5/45.6%, 84.7/30.4% and 65.2/50% cases respectively on K7/ 19 stain. DR was seenmost frequently in the subset of AHN (100%) and least in EHPVO (40%). All cases of BCS, AHN and CVC showed intermediate K7+ hepatocytic cells. Extraportal ductular cells (K7+/K19 ) were most common in AHN (100%) and showed a distinct centrilobular pattern. Conclusions: Derangements in vascular flow trigger prominent ductular reaction in all subsets of hepatic vasculopathy barring EHPVO. Severe parenchymal loss as seen in AHN activates both biliary and hepatocytic intermediate cells possibly as a response to extensive parenchymal cell loss. Vascular liver diseases show heterogeneity in K7/19 expression profiles of extraportal progenitors across all subsets, emphasizing that as a group vasculopathies may be trickier to reverse. Timely diagnosis hence is paramount tominimize damage. Corresponding author Tel: +91 9718599073: Puja Sakhuja. E-mail: pujasak@gmail.com

WS16.5 Pathological analysis of native liver in cystic fibrosis (CF) with severe portal hypertension reveals a vascular liver disease without cirrhosis

The prevalence of CF related liver disease (CFLD) ranges from 26% to 45%. The pathogenesis is allegedly related to small bile duct obstruction leading to focal biliary cirrhosis and cirrhosis. Portal hypertension (PHT) without hepatocellular insufficiency is the main presentation of CFLD. The aim of this study was to establish the pathologic pattern in CFLD patients with severe PHT. Patients and Methods In 2 CF centers, all consecutive patients who underwent liver transplantation were retrospectively analysed. Results Eight patients (7 males; 14–32 y) were analysed. All presented with severe PHT: esophageal varices more than grade 2 (bleeding in 2 patients), splenomegaly 18–30 cm, collaterals or ascites. None had signs of hepatocellular insufficiency. Liver tests were less than 1.5 times elevated. Macroscopically, all explants (mean weight 1.6 kg) were dysmorphic with left atrophy and irregular macronodular aspect. There was no thrombosis of the large veins and large bile ducts were normal. Microscopically, all explants showed septal fibrosis without cirrhosis (F2 or F3 Metavir Score, n = 4 each). Diffuse obliterative portal venopathy with sinusoidal dilatation and regenerative nodular hyperplasia was observed in all, associated with frequent ductopenia in small portal tracts, without cholestasis or inflammation. Biliary plugs with ductular reaction were scarce, medium or large biliary ducts were normal. Conclusion According to histological examination of the native livers, CFLD with PHT is not related to biliary cirrhosis but responds to vascular damages as observed in idiopathic non-cirrhotic PHT. The mechanism leading to vascular lesion in CF is unknown.

Multimodality imaging of primary extrahepatic portal vein obstruction (EHPVO): what every radiologist should know.

Portal vein thrombosis (PVT) is a frequent complication of liver cirrhosis, but it can also occur as a primary vascular disorder amid absent liver disease. Extrahepatic portal vein obstruction (EHPVO) refers to the obstruction of the extrahepatic portal vein with or without involvement of the intrahepatic portal vein branches, splenic and/or superior mesenteric vein. It is a distinct disorder that excludes PVT occurring in concurrence with liver cirrhosis or hepatocellular carcinoma. The term "EHPVO" implies chronicity and is principally reserved for a long-standing condition characterized by cavernous transformation of the portal vein. The most characteristic imaging manifestation is the formation of portoportal collaterals (via the venous plexi of Petren and Saint) that allow hepatopetal flow. However, this collateral circulation is insufficient resulting in clinically significant pre-hepatic portal hypertension, wherein the liver function and structure remain preserved until late. Although the long-term (more than 10 years) survival with controlled variceal bleeding is up to 100%, affected individuals have an impaired quality of life owing to portal cavernoma cholangiopathy, hypersplenism, neurocognitive dysfunction and growth retardation. Imaging diagnosis is not always straightforward as the collaterals can also present as a tumour-like solid mass that can be inadvertently biopsied. Moreover, EHPVO has its implications for the biliary tree, arterial circulation, liver/splenic volumes and stiffness, which merit proper understanding but have not been so well described in literature. In this review, we present the complete spectrum of the vascular, biliary and visceral changes with a particular emphasis on what our medical/surgical hepatology colleagues need to know from us in the pre-operative and post-operative settings.

The Role of PB1 Domain Proteins in Endothelial Cell Dysfunction and Disease.

There are a limited number of proteins containing the Phox-Bem1 (PB1) protein interaction domain, and almost all of them play some role in endothelial cell (EC) function, health, and homeostasis. Most of these proteins have been shown to physically interact through PB1-PB1 binding and, as such, are linked together to form complexes that are responsive to hemodynamic force. These complexes range from redox regulation to inflammation to autophagy and back, and they employ multiple feedback mechanisms that are reliant on PB1 domain proteins. Pathologic roles for PB1 domain-containing proteins have been demonstrated in multiple diseases, including vascular disease, cancer, liver disease, and myriad other concerns. Findings cited in this review show that dimerization of PB1 proteins exerts novel effects on EC function that may be important in multiple cardiovascular diseases, including atherosclerosis, thrombosis, inflammation, and hypertension. As mechanistic understanding of the component pathways (redox regulation, cell polarity, inflammation, atheroprotection, and autophagy) is continually increasing, the larger picture of how these pathways interact with one another is evolving rapidly. We can now evaluate the PB1 domain proteins as a family in the context of multiple phenotypic readouts in EC function as well as evaluate them as drug targets against disease.

Benign and malignant hepatocellular lesions in patients with vascular liver disease.

The liver is a unique organ because of its dual blood supply, 70%-80% being derived from the portal vein and 20%-30% being derived from the hepatic artery. These two vessels communicate at different levels, explaining that a decrease in the portal vein is compensated by an increase in arterial flow. 1 When the hepatic venous system is chronically compromised, the portal vein tends to behave as a draining vein, leading to an increase in the hepatic arterial flow (Fig. 1). Finally, some arterial disorders are responsible by themselves for an increase in arterial flow. This increased hepatic arterial flow likely favors the development of hepatocellular liver tumors. In this article, we will describe the most common vascular liver diseases inducing hepatocellular tumors (Table 1). Budd-Chiari Syndrome Budd-Chiari syndrome (BCS) is characterized by an obstruction of the hepatic venous outflow tract in the absence of right heart failure or constrictive pericarditis. Benign regenerative nodules in association with BCS have been described in the literature since the 1990s, probably due to the major improvements in patient survival and advances in liver imaging. These benign regenerative nodules are seen only in patients with chronic BCS, and mostly correspond to focal nodular hyperplasia (FNH). Some imaging features are different from those of FNH seen on normal liver, such as hyperintensity on T1- and T2-weighted magnetic resonance (MR) images, but they also are homogeneous, hypervascular, and the largest lesions often contain a central scar (Fig. 2). 2,3 In most cases, these lesions are multiple and their size does not exceed 3 cm in diameter. Progression either by size or number is often observed. In some cases, benign nodules display morphological features of hepatocellular adenomas characterized by welldifferentiated liver plates associated with increased number of unpaired arteries. Patients with BCS are also at risk of hepatocellular carcinoma (HCC) (11 of 97 patients in a recent cohort followed up for a mean of 5 years), suggesting that BCS patients should be monitored for HCC development. 4 Serum alphafetoprotein seems quite specific for HCC in this setting. Patients with long-standing inferior vena cava obstruction carry a much higher risk of developing HCC than those with pure hepatic vein involvement. At imaging, HCC usually appears hypervascular, heterogeneous, and solitary. Diagnosis of these two lesions might be challenging at imaging and hepatobiliary MR contrast agents are helpful. Liver biopsy is indicated in atypical cases or when significant changes occur over time. There is no evidence to date that benign regenerative nodules arising in patients with BCS degenerate into malignancy. 5

Diagnosis of thrombophilia/prothrombotic conditions in patients with liver disease.

Introduction Thromboses of splanchnic veins are encountered increasingly by clinicians, either as a complication of chronic liver disease (typically cirrhosis with or without hepatocellular carcinoma) or as the first presentation of a primary form of vascular liver disease, such as noncirrhotic portal vein thrombosis (PVT) or Budd-Chiari syndrome (BCS), in a previously healthy person. PVT forms part of the spectrum of idiopathic noncirrhotic portal hypertension (INCPH).