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Background Patients with a significant decrease in hepatic venous pressure gradient (HVPG) have a considerable reduction of liver complications and higher survival after HCV eradication. Objectives To evaluate the association between the baseline blood microbiome and the changes in HVPG after successful direct-acting antiviral (DAA) therapy in patients with HCV-related cirrhosis. Methods We performed a prospective study in 32 cirrhotic patients (21 HIV positive) with clinically significant portal hypertension (HVPG ≥10 mmHg). Patients were assessed at baseline and 48 weeks after HCV treatment completion. The clinical endpoint was a decrease in HVPG of ≥20% or HVPG Results During the follow-up, 47% of patients reached the clinical endpoint. At baseline, those patients had a higher relative abundance of Corynebacteriales and Diplorickettsiales order, Diplorickettsiaceae family, Corynebacterium and Aquicella genus and Undibacterium parvum species organisms and a lower relative abundance of Oceanospirillales and Rhodospirillales order, Halomonadaceae family and Massilia genus organisms compared with those who did not achieve the clinical endpoint according to the LEfSe algorithm. Corynebacteriales and Massilia were consistently found within the 10 bacterial taxa with the highest differential abundance between groups. Additionally, the relative abundance of the Corynebacteriales order was inversely correlated with IFN-γ, IL-17A and TNF-α levels and the Massilia genus with glycerol and lauric acid. Conclusions Baseline-specific bacterial taxa are related to an HVPG decrease in patients with HCV-related cirrhosis after successful DAA therapy.

INTRODUCTION: Liver enzyme elevation has been reported for SARS-CoV-2 disease (COVID-19) in heterogeneous cohorts, mainly from China. Comprehensive reports from other countries are needed. We dissect the pattern, evolution and predictive value of such abnormalities in a cohort from Madrid, Spain. METHODS: Retrospective study with prospective 14-day follow-up of 373 patients with confirmed COVID-19 in five Madrid hospitals, including 50 outpatients. COVID-19 severe course was defined as need of mechanical ventilation. RESULTS: A total of 33.1% hospitalised patients showed baseline AST elevation and 28.5% showed ALT elevation, contrasting with 12% and 8% of outpatients (P≤0.001). Baseline AST, ALT and GGT levels correlated with LDH and C-reactive protein levels (CRP) (r≤0.598, P

We aimed to evaluate the association of plasma biomarkers linked to inflammation (bacterial translocation, inflammatory response, and endothelial dysfunction), coagulopathy, and angiogenesis with the severity of liver cirrhosis (assessed by the Child-Pugh-Turcotte score, CTP) and Child-Pugh B cirrhosis (CTP 7-9) in patients with advanced hepatitis C virus (HCV)-related cirrhosis. We carried out a cross-sectional study in 97 patients with advanced HCV-related cirrhosis (32 HCV-monoinfected and 65 HIV/HCV-coinfected). Plasma biomarkers were measured by ProcartaPlex multiplex immunoassays. The outcome variable was the CTP score and the Child-Pugh B cirrhosis (CTP 7-9). HIV/HCV-coinfected patients and HCV-monoinfected patients with advanced HCV-related cirrhosis had near-equivalent values of plasma biomarkers. Higher values of plasma biomarkers linked to an inflammatory response (IP-10, IL-8, IL-6, and OPG), endothelial dysfunction (sVCAM-1 and sICAM-1), and coagulopathy (D-dimer) were related to higher CTP values. The most significant biomarkers to detect the presence of Child-Pugh B cirrhosis (CTP 7-9) were IP-10 (p-value= 0.008) and IL-6 (p-value=0.002). The AUC-ROC values of IP-10, IL-6, and both biomarkers combined (IP-10+IL-6) were 0.78, 0.88, and 0.96, respectively. In conclusion, HIV infection does not appear to have a significant impact on the analyzed plasma biomarkers in patients with advanced HCV-related cirrhosis. However, plasma biomarkers linked to inflammation (inflammatory response and endothelial dysfunction) were related to the severity of liver cirrhosis (CTP score), mainly IP-10 and IL-6, which discriminated patients with Child-Pugh B concerning Child-Pugh A. The HIV BioBank, is supported by Instituto de Salud Carlos III, Spanish Health Ministry (Grant n° RD06/0006/0035, RD12/0017/0037 and RD16/0025/0019) as part of the Plan Nacional R + D + I and cofinanced by ISCIII- Subdirección General de Evaluación y el Fondo Europeo de Desarrollo Regional (FEDER)”. The RIS Cohort (CoRIS) is funded by the Instituto de Salud Carlos III through the Red Temática de Investigación Cooperativa en SIDA (RIS C03/173, RD12/0017/0018 and RD16/0002/0006) as part of the Plan Nacional R + D + I and co-financed by ISCIII-Subdirección General de Evaluacion y e Fondo Europeo de Desarrollo Regional (FEDER). This study was supported by grants from Instituto de Salud Carlos III (ISCII; grant numbers PI14/01094 and PI17/00657 to JB, PI14/01581 and PI17/00903 to JGG, CP17CIII/00007 and PI18CIII/00028 to MAJS, and PI14CIII/00011 and PI17CIII/00003 to SR). The study was also funded by the RD16CIII/0002/0002, RD16/0025/0017, and RD16/0025/0018 projects as part of the Plan Nacional R + D + I and co-funded by ISCIII- Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER). JB is an investigator from the Programa de Intensificación de la Actividad Investigadora en el Sistema Nacional de Salud (I3SNS), Refs INT15/00079 and INT16/00100. Sí

Despite their relatively low prevalence, vascular diseases of the liver represent a significant health problem in the field of liver disease. A common characteristic shared by many such diseases is their propensity to cause portal hypertension together with increased morbidity and mortality. These diseases are often diagnosed in young patients and their delayed diagnosis and/or inappropriate treatment can greatly reduce life expectancy. This article reviews the current body of evidence concerning Budd-Chiari syndrome, non-cirrhotic portal vein thrombosis, idiopathic portal hypertension, sinusoidal obstruction syndrome, hepatic vascular malformations in hereditary haemorrhagic telangiectasia, cirrhotic portal vein thrombosis and other rarer vascular diseases including arterioportal fistulas. It also includes a section on the diagnostic imaging of vascular diseases of the liver and their treatment from a haematological standpoint (study of thrombotic diathesis and anticoagulation therapy). All recommendations are based on published studies extracted from PubMed. The quality of evidence and strength of recommendations were rated in accordance with the GRADE system (Grading of Recommendations, Assessment Development and Evaluation). In the absence of sufficient evidence, recommendations were based on the opinion of the committee that produced the guide.

Introduction: The prevalence of portal vein thrombosis (PVT) in patients that have undergone liver transplantation (LT) is 9.7% (SD 4.5). The aim of our study was to determine the prevalence, assess the factors that are associated with PVT and clarify their association with prognosis in patients with liver cirrhosis (LC) and LT. Aims and methods: From 2005 to 2014, laboratory, radiological and surgical data were collected from patients with LC in our center who had undergone LT for the first time. Results: One hundred and ninety-one patients were included. The mean age was 55 (SD 9), 75.4% of patients were male and 48.7% had HCV. The Child-Pugh scores were A/B/C 41.9%/35.9%/25.5% and the MELD score was 15 (SD 6). Previous decompensations were: ascites (61.4%), hepatic encephalopathy (34.4%), variceal bleeding (25.4%), hepatocellular carcinoma (48.9%) and spontaneous bacterial peritonitis (SPB) (14.3%). The mean post-transplant follow-up was 42 months (0-113). PVT was diagnosed at LT in 18 patients (9.4%). Six patients were previously diagnosed using imaging tests (33.3%): 2 patients (11.1%) by DU and 4 patients (22.2%) by CT scan. All patients with PVT had DU in a mean time of 6 months before LT (0-44) and 90 patients (47.1%) had a CT scan in a median time of 6 months before LT (0-45). PVT was significantly related to the presence of SBP (33.3% vs 12.6%; p = 0.02) and lower levels of albumin (3.1g/dl vs 3.4g/ dl; p = 0.05). MELD was higher in patients with PVT (16.6 vs 14.9; p = 0.3). There were no significant differences with regard to the need for transfusion of blood components. Moreover, the surgery time was similar in both groups. PVT correlated with a higher mortality in the first 30 days (8.8% vs 16.7%; p = 0.2). Conclusion: Prior history of SBP and lower levels of albumin were identified as factors associated with PVT. The pre-transplant diagnosis rate is very low and the presence of PVT may have implications for short-term mortality

espanolIntroduccion: entre los efectos adversos hepaticos secundarios al tratamiento tiopurinico en pacientes con enfermedad inflamatoria intestinal (EII), se ha descrito la posibilidad de desarrollar hipertension portal idiopatica. Esta patologia de etiologia y prevalencia real inciertas puede comprometer el pronostico de estos pacientes, por lo que se debe tener un alto grado de sospecha para su diagnostico precoz. Material y metodos: se ha llevado a cabo un estudio transversal en una cohorte de pacientes con EII en seguimiento en nuestra unidad para determinar la prevalencia del diagnostico de HTP idiopatica (HTPI) y su relacion con el tratamiento tiopurinico. Resultados: en nuestro centro, en el momento del analisis habia 1.419 pacientes en seguimiento por enfermedad inflamatoria intestinal. De estos, 927 pacientes se encuentran bajo tratamiento con farmacos tiopurinicos (o lo han estado durante la evolucion de su enfermedad), lo que supone el 65,3% de la poblacion: 689 pacientes con azatioprina (74,3%) y 238 con 6-mercaptopurina (25,7%). En total, se identificaron 4 pacientes con EII tipo enfermedad de Crohn con hipertension portal idiopatica en probable relacion con el tratamiento tiopurinico, lo que supuso un 4,3% del total, es decir, una incidencia de 4,3 casos por cada 1.000 pacientes con EII tratados con tiopurinicos. Las caracteristicas basales de los pacientes se describen en la tabla I. El 75% de los pacientes debuto con signos o sintomas de hipertension portal: 1 paciente con encefalopatia hepatica y 2 pacientes con hemorragia digestiva por varices esofagicas. Solo un paciente se encontraba asintomatico, pero se sospecho el diagnostico de HTP por trombopenia aislada. No obstante, cabe destacar que todos los pacientes presentaban trombopenia previamente aunque no se habia sospechado el diagnostico de HTP a pesar de un exhaustivo estudio. A todos los se realizo ecografia abdominal con fibroscan, cateterismo de venas suprahepaticas, asi como biopsia hepatica como parte del estudio etiologico de hipertension portal. En la ecografia abdominal se objetivaron datos indirectos de HTP en todos los pacientes (como esplenomegalia), descartandose asimismo cirrosis hepatica. El fibroscan mostraba datos de fibrosis hepatica significativa (F2-F3). Ademas, a todos los pacientes se les realizo una angiorresonancia en la que se descarto trombosis del eje esplenoportal como causa de HTP. Por ultimo, la anatomia patologica de la biopsia hepatica descarto la presencia de cirrosis hepatica, apoyando el diagnostico de HTP idiopatica (Tabla II). Conclusiones: la hipertension portal idiopatica secundaria a tratamiento tiopurinico en pacientes con enfermedad inflamatoria intestinal es un fenomeno poco frecuente, pero ha de ser tenido en cuenta en el diagnostico diferencial para un diagnostico precoz, principalmente en pacientes con tratamiento tiopurinico de larga evolucion. La presencia de trombopenia es a menudo el unico factor predictor de su desarrollo en fases preclinicas. EnglishIntroduction: The possibility of developing idiopathic portal hypertension has been described with thiopurine treatment despite compromises the prognosis of these patients, the fact its true prevalence is unknown. Material and methods: A cross-sectional study was conducted in a cohort of inflammatory bowel disease (IBD) patients followed at our unit, to determine the prevalence of diagnosis of idiopathic portal hypertension (IPH) and its relationship with thiopurine treatment. Results: At the time of the analysis, 927/1,419 patients were under treatment with thiopurine drugs (65%). A total of 4 patients with IBD type Crohn’s disease with idiopathic portal hypertension probably related to the thiopurine treatment were identified (incidence of 4.3 cases per 1,000). Seventy-five percent of patients started with signs or symptoms of portal hypertension. Only one patient was asymptomatic but the diagnosis of IPH because of isolated thrombocytopenia is suspected. However, note that all patients had thrombocytopenia previously. Abdominal ultrasound with fibroscan, hepatic vein catheterization and liver biopsy were performed on all of them as part of the etiology of portal hypertension. In the abdominal ultrasound, indirect portal hypertension data were observed in all patients (as splenomegaly) cirrhosis was also ruled out. The fibroscan data showed significant liver fibrosis (F2-F3). Conclusion: Idiopathic portal hypertension following thiopurine treatment in IBD patients is a rare occurrence, but it must be borne in mind in the differential diagnosis for early diagnosis, especially in patients undergoing thiopurine treatment over a long period. The presence of thrombocytopenia is often the only predictor of its development in the preclinical stage.