Portal Vein Thrombosis in Patients with Liver Cirrhosis

The myth that patients with liver cirrhosis are “auto‐anticoagulated” is outdated, and evidence shows that these patients frequently experience thrombosis. Portal vein thrombosis (PVT), although considered as rare, it gradually increases complications that are more likely to occur during late‐stage liver cirrhosis. The aim of this chapter is to perform a review of nonmalignant portal vein thrombosis in cirrhosis, in terms of prevalence, pathogenesis, diagnosis, clinical course, and management. Studies were identified by a search strategy using MEDLINE and EMBASE databases. For the MEDLINE search, we used the following terms: (“liver cirrhosis” [MeSH Terms] OR “cirrhosis” [All Fields] OR “cirrhosis” [All Fields]) AND (“portal vein” [MeSH Terms] OR “portal vein” [All Fields]) AND (“Thrombosis” [MeSH Terms]). For the EMBASE search, we used the following terms: (cirrhosis OR phrase liver cirrhosis) AND (phrase thrombosis/OR phrase vein thrombosis/OR phrase thrombosis prevention/OR phrase portal vein thrombosis/OR phrase liver vein thrombosis/OR phrase mesenteric vein thrombosis/OR thrombosis). Studies were considered eligible if they referred to any aspect of prevalence, pathophysiology, clinical presentation, diagnosis and management, or therapy of PVT in cirrhosis. We put forward possible responses to these unsettled issues starting with prevalence, pathogenesis, and treatment options

Gastrointestinal Manifestations of IgA Vasculitis-Henoch-Schönlein Purpura

Immunoglobulin A vasculitis, formerly called Henoch-Schönlein purpura (HSP), is the most common systemic vasculitis in childhood. It is a small-vessel vasculitis mediated by type III hypersensitivity, manifested as rash accompanied by gastrointestinal (GI) symptoms, arthritis, and nephritis. The etiology of this disease (a leukocytoclastic vasculitis) is still uncertain, but immune complexes of IgA and unidentified antigens seem to have a central pathogenic role. Most often the diagnosis is established after the clinical examination; it is easy at first glance when the clinical presentation includes the classic tetrad of rash (nonthrombocytopenic palpable purpura), arthralgia/arthritis, abdominal pain, and renal manifestations but may be difficult when the gastrointestinal manifestations precede the skin purpuric rash. Gastrointestinal involvement is frequently seen and varies from mild symptoms to severe complications; sometimes the gastrointestinal symptoms (colicky abdominal pain, nausea, vomiting, diarrhea, gastrointestinal bleeding) are the first manifestations of the disease. Immunoglobulin A vasculitis is usually a self-limited disease with a benign course, and the treatment is often symptomatic; in severe cases corticosteroids are necessary

Natural course of nonmalignant partial portal vein thrombosis in cirrhotic patients

Background/Aim: Portal vein thrombosis (PVT) has a high incidence in patients with liver cirrhosis and determines a poor prognosis of hepatic disease. The aim of our study was to define the natural course of partial PVT in cirrhotic patients, including survival and decompensation rates. Patients and Methods: We performed a prospective, cohort study, in a tertiary referral center. There were 22 cirrhotic patients with partial nonmalignant PVT, without anticoagulant treatment, who were followed-up between January 2011 and October 2013. All patients were evaluated by Doppler abdominal ultrasound and computed tomography. Kaplan-Meier method was used to determine the difference in clinical events between the study subgroups. Results: After a mean follow-up period of 20.22 months, partial PVT improved in 5 (22.73%), was stable in 11 (50%), and worsened in 6 (27.27%) patients. Hepatic decompensation rate at 6 and 18 months was higher in patients with worsened PVT than in those with stable/improved PVT (50% vs. 25%, P < 0.0001 and 100% vs. 56.25%, P < 0.0001, respectively). The survival rate at 6 months was 66.66% in worsened PVT group vs. 81.25% (P = 0.005) in stable/improved group, and 16.66% vs. 81.25% (P < 0.0001) at 18 months, respectively. Multivariate analysis showed that Model of End-Life Disease was the independent predictor of hepatic decompensation [hazard ratio (HR) 1.42; 95% confidence interval (CI): 1.08-1.87, P = 0.012] and survival (HR 1.76; 95% CI: 1.06-2.92, P = 0.028). Conclusions: Nonmalignant partial PVT remained stable/improved in over half of cirrhotic patients and aggravated in more than one fourth in whom it negatively influenced the survival and decompensation rates

Nonalcoholic Fatty Liver Disease and Cardiovascular Diseases: The Heart of the Matter

Nonalcoholic fatty liver disease (NAFLD) has emerged as the most frequent cause of liver disease worldwide, comprising a plethora of conditions, ranging from steatosis to end-stage liver disease. Cardiovascular disease (CVD) has been associated with NAFLD and CVD-related events represent the main cause of death in patients with NAFLD, surpassing liver-related mortality. This association is not surprising as NAFLD has been considered a part of the metabolic syndrome and has been related to numerous CVD risk factors, namely, insulin resistance, abdominal obesity, dyslipidemia, hyperuricemia, chronic kidney disease, and type 2 diabetes. Moreover, both NAFLD and CVD present similar pathophysiological mechanisms, such as increased visceral adiposity, altered lipid metabolism, increased oxidative stress, and systemic inflammation that could explain their association. Whether NAFLD increases the risk for CVD or these diagnostic entities represent distinct manifestations of the metabolic syndrome has not yet been clarified. This review focuses on the relation between NAFLD and the spectrum of CVD, considering the pathophysiological mechanisms, risk factors, current evidence, and future directions

The Prevalence of Liver Steatosis and Fibrosis Assessed by Vibration-Controlled Transient Elastography and Controlled Attenuation Parameter in Apparently Healthy Romanian Medical Students

Vibration-Controlled Transient Elastography (VCTE) with Controlled Attenuation Parameter (CAP) is used as a non-invasive method for evaluating liver steatosis and fibrosis simultaneously. In this prospective study, we aimed to assess the prevalence of liver steatosis and fibrosis, as well as the associated risk factors in Romanian medical students by VCTE and CAP score. We used a cut-off CAP score of ≥248 dB/m for the diagnosis of mild steatosis (S1), ≥268 dB/m for moderate steatosis (S2), and ≥280 dB/m to identify severe steatosis (S3). For liver fibrosis, the cut-off values were: ≤5.5 kPa, indicating no fibrosis (F0), 5.6 kPa for mild fibrosis (F1), 7.2 kPa for significant fibrosis (F2), 9.5 kPa for advanced fibrosis (F3), and 12.5 kPa for cirrhosis (F4). In total, 426 Romanian medical students (67.8% females, mean age of 22.22 ± 1.7 years) were evaluated. Among them, 352 (82.6%) had no steatosis (S0), 32 (7.5%) had mild steatosis (S1), 13 (3.1%) had a moderate degree of steatosis (S2), and 29 (6.8%) had severe steatosis (S3). Based on liver stiffness measurements (LSM), 277 (65%) medical students did not have any fibrosis (F0), 136 (31.9%) had mild fibrosis (F1), 10 (2.4%) participants were identified with significant fibrosis (F2), 3 (0.7%) with advanced fibrosis (F3), and none with cirrhosis (F4). In conclusion, the prevalence of liver steatosis and fibrosis is low among Romanian medical students

Association between Nonalcoholic Fatty Liver Disease and Endocrinopathies: Clinical Implications

Nonalcoholic fatty liver disease (NAFLD) has a rising prevalence worldwide. Its potential for evolution towards liver cirrhosis and hepatocellular carcinoma, as well as associations with extrahepatic manifestations, represents a double burden for patients and physicians alike. Recently, there has been increasing evidence of the association between NAFLD and a number of endocrinopathies, such as hypothyroidism, polycystic ovarian syndrome (PCOS), hypopituitarism, growth hormone deficiency (GHD), hypogonadism, and hypercortisolism. Definite correlations are supported by clear evidence so far, but further studies are needed in order to completely clarify the pathogenic mechanisms and, especially, to identify therapeutic implications. In this review, we present the main relationships between NAFLD and endocrinopathies, emphasizing the reciprocal causality, evolutive interconnections, and current clinical scenarios of presentations of which the clinicians should be aware

Nonalcoholic Fatty Liver Disease and Type 2 Diabetes Mellitus: A Bidirectional Relationship

Worldwide, the leading cause of chronic liver disease is represented by nonalcoholic fatty liver disease (NAFLD) which has now become a global epidemic of the 21st century, affecting 1 in 4 adults, and which appears to be associated with the steadily increasing rates of metabolic syndrome and its components (obesity, type 2 diabetes mellitus (T2DM), and dyslipidemia). NAFLD has been reported to be associated with extrahepatic manifestations such as cardiovascular disease, T2DM, chronic kidney disease, extrahepatic malignancies (e.g., colorectal cancer), endocrine diseases (e.g., hypothyroidism, polycystic ovarian syndrome, psoriasis, and osteoporosis), obstructive sleep apnea, and iron overload. The prevalence of NAFLD is very high, affecting 25–30% of the world population and encloses two steps: (1) nonalcoholic fatty liver (NAFL), which includes steatosis only, and (2) nonalcoholic steatohepatitis (NASH) defined by the presence of steatosis and inflammation with hepatocyte ballooning, with or without fibrosis which can progress to liver fibrosis, hepatocellular carcinoma, and liver transplantation. Current data define a more complex relationship between NAFLD and T2DM than was previously believed, underlining a bidirectional and mutual association between the two entities. This review aims to summarize the current literature regarding the incidence of T2DM among patients with NAFLD and also the prevalence of NAFLD in T2DM patients, highlighting the recent key studies. Clinicians should screen, diagnose, and treat T2DM in patients with NAFLD in order to avoid short- and long-term complications

Vibration-Controlled Transient Elastography and Controlled Attenuation Parameter for the Diagnosis of Liver Steatosis and Fibrosis in Patients with Nonalcoholic Fatty Liver Disease

Vibration-Controlled Transient Elastography (VCTE) with Controlled Attenuation Parameter (CAP) is a widely used non-invasive technique for concomitant assessment of liver steatosis and fibrosis in patients with nonalcoholic fatty liver disease (NAFLD). We aimed to evaluate the level both of hepatic steatosis and fibrosis as well as the associated risk factors in patients referred to our unit with clinically suspected NAFLD or diagnosed by abdominal ultrasonography. Two hundred four patients were prospectively included in this study and assessed by VCTE with CAP. The final analysis included 181 patients with reliable liver stiffness measurements (LSMs) (53% female, mean age 57.62 ± 11.8 years and BMI 29.48 ± 4.85 kg/m2). According to the cut-off values for steatosis grading, there were 10 (5.5%) patients without steatosis (S0), 30 (16.6%) with mild (S1), 45 (24.9%) moderate (S2), and 96 (53%) severe (S3) steatosis. Based on LSM, there were 73 (40.3%) patients without fibrosis (F0), 42 (23.2%) with mild (F1), 32 (17.7%) significant (F2), 19 (10.5%) advanced (F3) fibrosis, and 15 (8.3%) with cirrhosis (F4). In addition, we found an association between several metabolic components and hepatic steatosis and fibrosis. Thus, in the multivariate analysis, higher BMI, fasting plasma glucose, triglycerides, low-density lipoprotein cholesterol, and serum uric were associated with increased CAP. Furthermore, higher serum uric acid and alpha-fetoprotein together with lower platelets count and albumin levels were associated with increased LSM. The assessment of steatosis and fibrosis using VCTE and CAP should be performed in all patients with suspected or previously diagnosed NAFLD in units with available facilities

Changes in Liver Steatosis Using Controlled Attenuation Parameter among Patients with Chronic Hepatitis C Infection Treated with Direct-Acting Antivirals Therapy Who Achieved Sustained Virological Response

Chronic hepatitis C virus (HCV) infection induces hepatic steatosis due to viral and host factors. However, information regarding the effects of direct-acting antivirals (DAAs) therapy on liver steatosis and fibrosis is limited. Vibration-controlled transient elastography (VCTE) with a controlled attenuation parameter (CAP) represents a non-invasive method, which has been used in the last few years for the detection of hepatic steatosis and fibrosis before and at a sustained virological response at 12 weeks (SVR12). The aim of this study was to assess the modifications of liver steatosis and fibrosis in HCV-infected patients who achieved SVR12. Consecutive patients with chronic HCV infection that were treated with DAAs in a tertiary gastroenterology center from Romania were included. Demographics, laboratory data, and VCTE evaluation were recorded in all patients. Patients with previous hepatic decompensation and those who did not achieve SVR were excluded. Two hundred and eighty patients (67.1% females) who achieved SVR12 were included. Regarding the changes in biological parameters, including liver enzymes such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), reduced to normal levels at SVR12 compared to the baseline (28.72 &plusmn; 24.71 U/L vs. 40.72 &plusmn; 27.34 U/L for ALT, p &lt; 0.013 and 27.21 &plusmn; 11.15 U/L vs. 33.35 &plusmn; 23.37 U/L for AST, p = 0.029). On the contrary, the levels of triglycerides increased significantly from the baseline to SVR12 (124.03 &plusmn; 113.49 mg/dL to 153.78 &plusmn; 94.53, p = 0.004). Regarding hepatic steatosis by CAP evaluation, at SVR12, 186 (66.4%) of the individuals had a CAP score of &ge;248 dB/m, an increase of 4.6% from the baseline. After viral eradication with DAAs, we observed an increase in hepatic steatosis. Hence, a long-term follow-up is mandatory to identify HCV-infected patients with hepatic steatosis post-SVR and the risk factors for more severe outcomes