Absence Of Cirrhosis Research Articles

Description of patient with telangiectasis and palmar erythema without any structural liver changes or changes of liver laboratory parameters due to treatment of Her -2 -positive breast cancer with Ado-Trastuzumab-Emtansine

Ado- Trastuzumab-Emtansine is approved by EMA and FDA for treatment of HER-2-positive metastatic breast cancer. The drug combines the cytotoxic activity of emtansine with trastuzumab [1,2,3]. Here we are describing 50- year old woman with 3-ple positive left breast cancer with metastasis to left axillary lymph nodes treated with the drug. The patient had normal liver and spleen structure on CT of the abdomen with I.V. contrast, along with a normal liver function test. However she did have a mild elevation of her indirect bilirubin after the initiation of the drug. Despite the normal liver and spleen and absence of Cirrhosis the patient developed drug induced spider angiomas on the upper chest, upper back, shoulders along with palmar erythema. The association of the Ado-Trastuzumab-Emtansine with spider angiomas and palmar erythema in those with normal liver and spleen function, with only a mild elevation of indirect bilirubin is discussed in the article [1].

Key features of the environment promoting liver cancer in the absence of cirrhosis

The prevalence of obesity and non-alcoholic fatty liver disease (NAFLD) associated hepatocellular carcinoma (HCC) is rising, even in the absence of cirrhosis. We aimed to develop a murine model that would facilitate further understanding of NAFLD-HCC pathogenesis. A total of 144 C3H/He mice were fed either control or American lifestyle (ALIOS) diet, with or without interventions, for up to 48 weeks of age. Gross, liver histology, immunohistochemistry (IHC) and RNA-sequencing data were interpreted alongside human datasets. The ALIOS diet promoted obesity, elevated liver weight, impaired glucose tolerance, non-alcoholic fatty liver disease (NAFLD) and spontaneous HCC. Liver weight, fasting blood glucose, steatosis, lobular inflammation and lipogranulomas were associated with development of HCC, as were markers of hepatocyte proliferation and DNA damage. An antioxidant diminished cellular injury, fibrosis and DNA damage, but not lobular inflammation, lipogranulomas, proliferation and HCC development. An acquired CD44 phenotype in macrophages was associated with type 2 diabetes and NAFLD-HCC. In this diet induced NASH and HCC (DINAH) model, key features of obesity associated NAFLD-HCC have been reproduced, highlighting roles for hepatic steatosis and proliferation, with the acquisition of lobular inflammation and CD44 positive macrophages in the development of HCC—even in the absence of progressive injury and fibrosis.

NAFLD-Related Hepatocarcinoma: The Malignant Side of Metabolic Syndrome.

Hepatocellular carcinoma (HCC) is the seventh most common cancer worldwide and the second leading cause of cancer-related mortality. HCC typically arises within a cirrhotic liver, but in about 20% of cases occurs in absence of cirrhosis. Among non-cirrhotic risk factors, non-alcoholic fatty liver disease (NAFLD) currently represents the most important emerging cause of HCC in developed countries. It has been estimated that annual incidence of HCC among patients with non-cirrhotic NAFLD is approximately 0.1–1.3 per 1000 patients/year and ranges from 0.5% to 2.6% among patients with non-alcoholic steatohepatitis (NASH) cirrhosis. However, only a few clinical trials enrolling HCC patients actually distinguished NAFLD/NASH-related cases from other non-cirrhotic causes and therefore evidence is still lacking in this subset of patients. This review aims to describe the biology underpinning NAFLD development, to investigate the main molecular pathways involved in its progression to NASH and HCC and to describe how different pathogenetic mechanisms underlying the onset of HCC can have an impact in clinical practice. We hereby also provide an overview of current HCC treatment options, with a particular focus on the available data on NAFLD-related cases in practice-changing clinical trials.

Usage of Direct Acting Oral Anticoagulants in Cirrhotic and Non-Cirrhotic Portal Vein Thrombosis: A Systematic Review.

Thrombosis of the portal vein (PVT) is generally seen in the setting of liver cirrhosis and to a lesser extent in the absence of cirrhosis. There is no clear guidance in relation to approaching treatment with anticoagulation in this condition. The professional societies and guidelines recommend treatment with traditional anticoagulation like low-molecular-weight heparin and vitamin-K antagonists in patients presenting with acute portal vein thrombosis. There is no clarity in relation to treatment in the setting of chronic PVT and in patients with cirrhosis. Also, the role of direct-acting oral anticoagulants (DOACs) that are becoming a preferred choice for anticoagulation for various other indications is not clear in the case of PVT. There are a very few studies in the medical literature that have investigated the role of DOACs in patients with PVT in different settings. Thus, we performed a systematic review of the literature to study the use of DOACs in PVT in patients with and without cirrhosis. The results of the available studies show that DOACS appears to be a promising choice for the treatment of patients with PVT. The availability of more data in the future along with better availability of the approved reversal agents for various DOACs is expected to make DOACS a preferred choice for the clinicians to treat patients with PVT.

A PDCD1 Role in the Genetic Predisposition to NAFLD-HCC?

Simple SummaryMany more people are dying each year from primary liver cancers arising in obesity-related fatty liver disease. Often these cancers are a consequence of fatty liver disease progression, with inflammation, scarring and cirrhosis. Less often, cancers develop in the presence of fat without cirrhosis. Evidence from animal models suggests the immune response to fat is important. We have explored genetic variations in candidate immunoregulatory genes. Our study of nearly one-thousand patients with fatty liver disease, comparing 391 with cancers to 594 without, indicates that genetic variation in a gene (PDCD1) that codes for the T cell receptor PD-1 may be important. Inherited variations that affect function of immunoregulatory proteins like PD-1 may underpin why some patients with fatty liver disease—whether they have cirrhosis or not—are more likely to develop liver cancer.Obesity and non-alcoholic fatty liver disease (NAFLD) are contributing to the global rise in deaths from hepatocellular carcinoma (HCC). The pathogenesis of NAFLD-HCC is not well understood. The severity of hepatic steatosis, steatohepatitis and fibrosis are key pathogenic mechanisms, but animal studies suggest altered immune responses are also involved. Genetic studies have so far highlighted a major role of gene variants promoting fat deposition in the liver (PNPLA3 rs738409; TM6SF2 rs58542926). Here, we have considered single-nucleotide polymorphisms (SNPs) in candidate immunoregulatory genes (MICA rs2596542; CD44 rs187115; PDCD1 rs7421861 and rs10204525), in 594 patients with NAFLD and 391 with NAFLD-HCC, from three European centres. Associations between age, body mass index, diabetes, cirrhosis and SNPs with HCC development were explored. PNPLA3 and TM6SF2 SNPs were associated with both progression to cirrhosis and NAFLD-HCC development, while PDCD1 SNPs were specifically associated with NAFLD-HCC risk, regardless of cirrhosis. PDCD1 rs7421861 was independently associated with NAFLD-HCC development, while PDCD1 rs10204525 acquired significance after adjusting for other risks, being most notable in the smaller numbers of women with NAFLD-HCC. The study highlights the potential impact of inter individual variation in immune tolerance induction in patients with NAFLD, both in the presence and absence of cirrhosis.

International Liver Cancer Association (ILCA) White Paper on Biomarker Development for Hepatocellular Carcinoma

International Liver Cancer Association (ILCA) White Paper on Biomarker Development for Hepatocellular Carcinoma

English

Massive splenomegaly presenting with hypersplenism, pancytopenia and portal hypertension, without any underlying known cause is known as Banti’s syndrome. There are various causes of splenomegaly. When all the known causes of portal hypertension are ruled out, it is termed as Banti’s syndrome. This syndrome was discovered by Guido Banti in 1882 and is named after him. Banti’s syndrome is also known as idiopathic portal hypertension or non-cirrhotic portal fibrosis.1 Banti’s syndrome is commonly found in India and Japan than in the West. 2 There is absence of any haematologic cause, primary hepatic cause or any tumour or mass lesion involving the spleen. Banti had stated that the primary organ involved was spleen and not the liver leading to secondary splenomegaly. Other features include normal liver function tests, varices seen in endoscopy, cytopenia of one or more cell lines, absence of cirrhosis, patent hepatic veins and elevated portal pressure with multiple collaterals. The complications include rupture of varices and massive bleeding. 3 We report a case of a 20-year-old male who presented to us with a history of fever for 7 days and one-episode of hematemesis on the day of admission. All known causes of hypersplenism were ruled out and he was diagnosed to have idiopathic massive splenomegaly with portal hypertension and hypersplenism.

Performance of Ultrasound Techniques and the Potential of Artificial Intelligence in the Evaluation of Hepatocellular Carcinoma and Non-Alcoholic Fatty Liver Disease.

Simple SummaryThe increasing prevalence of non-alcoholic fatty liver disease (NAFLD) represents a challenge for the current medical systems. If NAFLD is left undetected and untreated, it can progress towards fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). To date, ultrasonography (US) is the first-line examination indicated to NAFLD patients that also screens for other focal liver lesions (FLLs). The downside of conventional B-mode US is that it cannot accurately quantify steatosis and fibrosis and cannot further characterize FLL certainly—is it cancer or is it not? Ultrasound contrast agents (UCAs) allowed physicians to further evaluate the FLL for the diagnosis of HCC. This review discusses the performance of US techniques in NAFLD and NAFLD-related HCC diagnosis, as well as of artificial intelligence (AI)-based methods, specifically the usefulness and assistance of deep learning algorithms for improving liver US image processing.Global statistics show an increasing percentage of patients that develop non-alcoholic fatty liver disease (NAFLD) and NAFLD-related hepatocellular carcinoma (HCC), even in the absence of cirrhosis. In the present review, we analyzed the diagnostic performance of ultrasonography (US) in the non-invasive evaluation of NAFLD and NAFLD-related HCC, as well as possibilities of optimizing US diagnosis with the help of artificial intelligence (AI) assistance. To date, US is the first-line examination recommended in the screening of patients with clinical suspicion of NAFLD, as it is readily available and leads to a better disease-specific surveillance. However, the conventional US presents limitations that significantly hamper its applicability in quantifying NAFLD and accurately characterizing a given focal liver lesion (FLL). Ultrasound contrast agents (UCAs) are an essential add-on to the conventional B-mode US and to the Doppler US that further empower this method, allowing the evaluation of the enhancement properties and the vascular architecture of FLLs, in comparison to the background parenchyma. The current paper also explores the new universe of AI and the various implications of deep learning algorithms in the evaluation of NAFLD and NAFLD-related HCC through US methods, concluding that it could potentially be a game changer for patient care.

Hepatocellular carcinoma in non-alcoholic fatty liver disease-a review of an emerging challenge facing clinicians.

Non-alcoholic fatty liver disease (NAFLD) is a rapidly growing cause of chronic liver disease and is becoming a leading cause of hepatocellular carcinoma (HCC) in many developed countries. This presents major challenges for the surveillance, diagnosis and treatment of HCC. To discuss the clinical challenges faced by clinicians in managing the rising number of NAFLD-HCC cases. MEDLINE, PubMed and Embase databases were searched using the keywords; NAFLD, HCC, surveillance, hepatectomy, liver transplantation, percutaneous ablation, transarterial chemoembolization (TACE), selective internal radiotherapy treatment (SIRT) and sorafenib. Relevant clinical studies were included. Current HCC surveillance programmes are inadequate because they only screen for HCC in patients with cirrhosis, whereas in NAFLD a significant proportion of HCC develops in the absence of cirrhosis. Consequently NAFLD patients often present with a more advanced stage of HCC, with a poorer prognosis. NAFLD-HCC patients also tend to be older and to have more co-morbidities compared to HCC of other etiologies. This limits the use of curative treatments such as liver resection and orthotopic liver transplantation (OLT). Evidence suggests that although NAFLD-HCC patients who undergo liver resection or OLT have worse perioperative and short-term outcomes, overall long-term survival is comparable to HCC of other etiologies. This highlights the importance of careful patient selection, pre-habilitation and perioperative planning for NAFLD-HCC patients being considered for surgical treatment. Careful consideration is also important for non-surgical treatments, although the evidence supporting treatment selection is frequently lacking, as these patients tend to be poorly represented in clinical trials. Locoregional therapies such as percutaneous ablation and TACE may be less well tolerated and less effective in NAFLD patients with obesity or diabetes. The tyrosine kinase inhibitor sorafenib may also be less effective. This review highlights how international guidelines, for which NAFLD traditionally has made up a small part of the evidence base, may not be appropriate for all NAFLD-HCC patients. Future guidelines need to reflect the changing landscape of HCC, by making specific recommendations for the management of NAFLD-HCC.

Effect of disease stage and treatment outcomes on the dynamics of liver functions during and after treatment of hepatitis C with directly acting antivirals.

Virus C infection is recently treated successfully with plenty of direct antiviral agents (DAAs). We aimed to evaluate the effect of disease stage and treatment outcome on the dynamics of liver functions during treatment of hepatitis C with DAAs. We reported the liver function in 2354 subjects diagnosed as chronic hepatitis C before, during and after treatment with different DAAs regimens. Patients were classified into two groups according to treatment response with further subclassification according to the presence or absence of cirrhosis, and changes in liver functions were compared in each group and subgroup. Totally 2213 (94%) achieved sustained virological response (SVR) to DAAs therapy with significant improvement in all liver biochemistry. Also, there was an improvement in the non-SVR group's liver enzymes in relapsers during and after treatment; however, there was no improvement in serum albumin. We noticed a slight increase in serum bilirubin at weeks 4 and 8 for both groups. DAAs therapy is associated with improvement of the liver biochemical profile and improved outcome in the majority of chronic hepatitis C virus patients due to suppression of viral replication. However, the long-term impact of DAAs therapy needs to be further evaluated.

Nonalcoholic Fatty Liver Disease and Recent Guideline Updates.

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Effectiveness of Sofosbuvir and Daclatasvir in treatment of Hepatitis-C: An experience of tertiary care hospital in Karachi.

Objective:To assess the effectiveness of Sofosbuvir (SOF) and Daclatasvir (DCV) in patients with chronic hepatitis C (CHC), compensated cirrhosis (CC) and decompensated cirrhosis (DCLD) either treatment naïve or experienced.Methods:This was a prospective, observational study, conducted from January 2017 to December 2018 at Jinnah Postgraduate Medical Centre, Karachi. All patients above 12 years of age with detectable HCV RNA PCR were included. Patients were divided into three groups: CHC, CC and DCLD. SOF and DCV for 12 or 24 weeks were given. Ribavirin (RBV) was given to treatment experienced and cirrhotic patients. Primary outcome was End of Treatment Response (ETR) and secondary outcome was Sustained Virological Response (SVR) at post treatment week 12 or 24.Results:Total 300 patients with mean age of 40.49 ± 13.86 were enrolled. Majority were females 174 (58%). CHC were 200 (66.6%) while cirrhotic were 100 (33.4%). Treatment naïve patients were 267 (89%) and 33 (11%) patients were experienced. Most common genotype was 3 (83%). ETR was achieved in 292 (97.33%) and SVR in 265 (88.33%) patients respectively.Conclusion:SOF plus DCV with or without RBV is a highly effective treatment for chronic HCV and is still used in many centers of Pakistan. This regimen has excellent results for GT-3. The outcomes are mainly influenced by the presence or absence of cirrhosis.

Comparison of Vasopressor Duration in Septic Shock Patients With and Without Cirrhosis.

Patients with cirrhosis have immune dysfunction, altered inflammatory response, and hemodynamic changes which increase risk of septic shock and potentially prolong management with fluids, vasopressors, and other therapies. Due to limited available guidance, this study aimed to characterize vasopressor use in patients with cirrhosis in relation to patients without cirrhosis in septic shock. This was a retrospective matched cohort analysis of 122 patients admitted to the intensive care unit (ICU) at an academic medical center from January 2015 to November 2017. Patients were grouped based on the presence or absence of cirrhosis and matched based on severity of illness scoring. The primary outcome was vasopressor duration. Secondary comparisons included total vasopressor requirement, length of hospital and ICU stay, in-hospital mortality, change in organ function, and discharge disposition. The group with cirrhosis had significantly longer median (interquartile range [IQR]) durations of vasopressor therapy compared with the group without cirrhosis (86.0 [42.0-164.5] vs 39.0 [14.5-82.0] hours; P = 0.003) leading to increased median (IQR) vasopressor exposure (71.7 [15.5-239.5] vs 24.7 [5.3-77.9] mg norepinephrine [NE] equivalents; P = 0.003). No difference was found in in-hospital mortality between groups. However, regression analysis showed vasopressor exposure was associated with in-hospital mortality. Patients with cirrhosis in septic shock have increased vasopressor durations and overall requirements compared with patients without cirrhosis. Increased durations and requirements is associated with poorer outcomes independent of presence of cirrhosis. Future studies are needed to improve vasopressor treatment strategies and end points utilized in cirrhosis.

Brief Report: Accuracy of FIB-4 for Cirrhosis in People Living With HIV and Hepatocellular Carcinoma.

Hepatocellular carcinoma (HCC) may develop in the absence of cirrhosis in HIV, and determining how often this occurs can provide insights into mechanisms of carcinogenesis. Studies evaluating the prevalence of cirrhosis in the setting of HCC among people living with HIV (PLWH) often rely on noninvasive markers, such as the Fibrosis-4 Index for Hepatic Fibrosis (FIB-4). However, the accuracy of FIB-4 for cirrhosis in the setting of HCC has not been determined among PLWH. We conducted a cross-sectional study among PLWH in the Veterans Aging Cohort Study with VA cancer registry-confirmed HCC diagnosed between 1999 and 2015. FIB-4 was calculated using the age, alanine aminotransferase, aspartate aminotransferase, and platelet count obtained closest to, but within 1 year before, HCC diagnosis. Medical records were reviewed within 1 year before HCC diagnosis to determine the cirrhosis status. We evaluated the area under the receiver-operating characteristic curve and performance characteristics of FIB-4 for confirmed cirrhosis. Incident HCC was diagnosed in 302 PLWH. After medical record review, 203 (67.2%, 95% confidence interval: 61.6% to 72.5%) had evidence of cirrhosis. FIB-4 identified patients with cirrhosis with an area under the receiver-operating characteristic curve of 0.67 (95% confidence interval: 0.60 to 0.73). FIB-4 scores >5.0 had a positive predictive value >80% and specificity of >77%, negative predictive value of <41%, and sensitivity of <45%. The accuracy of FIB-4 for cirrhosis in the setting of HIV and HCC is modest and may result in misclassification of cirrhosis in this population.

Long-Term Efficacy of α-Interferon in β-Thalassemics With Chronic Hepatitis C

AbstractHepatitis C virus (HCV) infection is a common cause of liver disease among polytransfused thalassemics. We treated a cohort of subjects with β-thalassemia major and chronic hepatitis C with α-interferon. The aims of the study were to assess the long-term biochemical and virologic efficacy of α-interferon and to evaluate the influence of HCV type and liver siderosis on the outcome of therapy. Seventy subjects (mean age, 14.1 years) with chronic HCV infection and abnormal aminotransferases received recombinant α-interferon for 12 months and were observed after therapy for at least 24 months. Sixty-three subjects (90%) were HCV-RNA positive at the start of therapy. HCV type 1b was found in 41 subjects (65.1%), non-1b types in 13 (20.6%), and mixed HCV types in 9 (14.3%). Liver biopsy showed cirrhosis in 11 subjects (15.7%) and siderosis grade 3-4 in 24 patients (34.2%). Three patients stopped therapy due to adverse events. Twenty-eight subjects (40%) had normal aminotransferases and had cleared HCV-RNA when last observed (mean follow-up, 36.5 months; range, 25 to 49 months). Of 41 patients who did not normalize aminotransferases, 9 had become HCV-RNA negative at the end of follow-up. The absence of cirrhosis, low liver iron content, and infection with non-1b HCV type were independently associated to complete sustained response upon multivariable analysis. In conclusion, α-interferon may induce a sustained virologic and biochemical remission of hepatitis in β-thalassemic patients with chronic HCV infection and nonadvanced liver disease.

Hepatocellular carcinoma after Fontan surgery: A systematic review

Fontan surgery is often the procedure of choice for patients with congenital single effective ventricle. In the long term, elevated systemic venous pressure and chronic ischemia following this procedure could lead to advanced chronic liver disease and there is also a risk of hepatocellular carcinoma (HCC). This review systematically summarizes the characteristics and outcomes of this rare condition. PubMed and Embase databases were searched from inception to January 2020 for studies reporting on HCC after Fontan surgery. The factors analyzed were clinical presentation, histology, imaging findings, treatments, and survival. Our primary analysis was based on biopsy-proven HCC. The records selected were 26 observational studies (19 case reports/case series and seven cohort studies) including 65 biopsy-proven HCC. Age at the time of HCC diagnosis ranged from 12 to 52years, and 62% of the patients were female. Only one case occurred earlier than 10 years after Fontan surgery. Twenty patients had no imaging or histological evidence of liver cirrhosis and 78.3% had elevated α-fetoprotein levels. Advanced stage was the most common at diagnosis. The most frequent treatments were transarterial chemoembolization (n = 18) and surgery (n = 12). One-year survival was 50% and only four patients (6.2%) were under liver imaging surveillance. We also analyzed 17 patients with non-biopsy-proven HCC. After Fontan surgery, HCC usually occurs at least 10 years later and can develop in the absence of cirrhosis. Biopsy is mandatory to confirm the diagnosis. Patients were diagnosed at a late stage and survival outcomes were poor, highlighting a need for liver surveillance.

Hepatocellular Carcinoma in Acute Hepatic Porphyrias: Results from the Longitudinal Study of the U.S. Porphyrias Consortium

The risk for hepatocellular carcinoma (HCC) is increased in acute hepatic porphyrias (AHP). The aim of this study was to explore the clinicopathologic characteristics, outcomes, and frequency of HCC in patients with AHP in the United States. This cross-sectional analysis evaluated patients with HCC in a multicenter, longitudinal study of AHP. Among 327 patients with AHP, 5 (1.5%) were diagnosed with HCC. Of the 5 HCC cases, 4 had acute intermittent porphyria and 1 had variegate porphyria, confirmed by biochemical and/or genetic testing. All patients were white females, with a median age of 27years (range 21-75) at diagnosis. The median age at HCC diagnosis was 69years (range 61-74). AHP was asymptomatic in 2 patients; 2 reported sporadic attacks; and 1 reported recurrent attacks (>4 attacks/year). All patients had a single HCC lesion on liver imaging that was 1.8-6.5 centimeters in diameter. Serum alpha fetoprotein levels were below 10ng/mL in all 4 patients with available results. Four patients underwent liver resection, and 1 was treated with radioembolization. No significant inflammation or fibrosis was found in adjacent liver tissues of 3 patients who underwent liver resection. Two patients developed recurrence of HCC at 22 and 26months following liver resection. All patients are alive with survival times from HCC diagnosis ranging from 26-153months. In this U.S. study, 1.5% of patients with AHP had HCC. HCC in AHP occurred in the absence of cirrhosis, which contrasts with other chronic liver diseases. Patients with AHP, regardless of clinical attacks, should be screened for HCC, beginning at age 50. The pathogenesis of hepatocarcinogenesis in AHP is unknown and needs further investigation.

Clinical Course of Porto-Sinusoidal Vascular Disease Is Distinct From Idiopathic Noncirrhotic Portal Hypertension

Porto-sinusoidal vascular disease (PSVD) was recently proposed as novel clinical entity characterized by typical histological changes with or without portal hypertension (PH) in the absence of cirrhosis. Thus, we aimed to describe clinical characteristics and the outcome of PSVD patients and to compare these to patients meeting traditional idiopathic non-cirrhotic portal hypertension (INCPH) criteria.Patients undergoing liver biopsy (baseline) ±hepatic venous pressure gradient (HVPG) measurement at the Vienna General Hospital between 2000-2019 were screened for PSVD and INCPH criteria.91 patients were diagnosed with PSVD of which 28 (30.8%) also fulfilled INCPH criteria (INCPH+/PSVD+). Specific histological and specific clinical PH signs were found in 72 (79.1%) and 54 (59.3%) patients, respectively. INCPH+/PSVD+ showed higher Child-Pugh-scores (7±2 vs 6±1 points; P = .002) and a higher prevalence of decompensation (57.1% vs 28.6%; P = .009) than INCPH-/PSVD+ patients. Importantly, hepatic decompensation after three years (3Y) occurred in 11.2% of PSVD patients with specific clinical signs of PH, while no decompensation occurred in patients with only specific histological or with unspecific clinical/histological signs (P = .002). When categorizing by INCPH definition, 3Y decompensation was 13.4% in INCPH+/PSVD+ and 3.8% in INCPH-/PSVD+ (P = .120). While overall mortality was similar in INCPH+/PSVD+ (n = 6; 21.4%) and INCPH-/PSVD+ (n = 10; 15.9%) patients (P = .558), liver-related mortality tended to be higher in INCPH+/PSVD+ (6.9%) than in INCPH-/PSVD+ (0%; P = .078).Novel PSVD criteria facilitate diagnosis. Compared to INCPH, clinical course of PSVD patients is more favorable. Importantly, specific signs of PH including varices and collaterals are associated with hepatic decompensation and mortality.

Direct antiviral drugs in the treatment of hepatitis C-infected rheumatoid arthritis Egyptian cohort: safety and clinical impact.

Data about the safety and efficacy of direct-acting antivirals (DAAs) in the treatment of hepatitis C virus (HCV) patients with concomitant rheumatoid arthritis (RA) are scarce. We assessed the impact and safety of DAAs treatment of hepatitis C on rheumatoid arthritis disease activity. Prospectively, we enrolled 65 patients with RA and HCV. A clinico-laboratory evaluation was done at baseline, including liver assessment and RA disease activity score-28 (DAS28). At 12 weeks of post-DAAs treatment, sustained virologic response (SVR12) and DAS28 were reevaluated. The SVR12 was achieved in 59 (90.8%) patients. RA control was achieved in 47 (79.9%) patients. The post SVR12 DAS28 score was significantly lower than the baseline (3.32 ± 0.93 vs. 4.37 ± 0.90; P < 0.001). There was a significant decline in the mean values of serum anticyclic citrullinated peptide, rheumatoid factor, erythrocyte sedimentation rate and C-reactive protein after achieving an SVR12 (30.47 ± 12.37 vs. 57.61 ± 15.91 U/ml; 29.78 ± 19.58 vs. 55.14 ± 16.89 IU/ml; 17.13 ± 10.84 vs. 29.68 ± 14.32 mm/h and 5.76 ± 1.57 vs. 11.44 ± 4.13 mg/l, respectively; P < 0.05). RA activity and antirheumatic drugs were stepped-down [12 (20.3%) and 35 (59.3%) patients showed good and moderate RA response, respectively]. The baseline viral load, absence of cirrhosis and SVR12 were the only predictors of disease control (P < 0.05). No drug-related adverse events or drug-related discontinuation. Unlike interferon, HCV elimination by DAAs significantly improves RA activity and treatment outcome with high safety and efficacy.

Predictive factors of severe abdominal pain during and after transarterial chemoembolization for hepatocellular carcinoma.

To prospectively assess the frequency of severe abdominal pain during and after transarterial chemoembolization (TACE) for hepatocellular carcinoma (HCC) using the visual analog scale (VAS), and to identify predictive factors. Ninety-eight TACE performed in 80 patients (mean 65 ± 12years old, 60 men) were consecutively and prospectively included. Abdominal pain was considered severe if the VAS ≥ 30/100 after treatment administration, or if opioid analgesic (grades 2-3) intake was required during hospitalization. Patient and tumor characteristics as well as technical factors associated with severe pain were identified by binary logistic regression. The criterion for severe pain was met in 41/98 (42%) of procedures (peri-procedural pain 30/98 [31%] and opioid consumption during hospitalization 24/98 [25%]). Multivariate analysis identified age (odds ratio [OR] = 0.943 (95% confidence interval 0.895-0.994), p = 0.029), cirrhosis (OR = 0.284 (0.083-0.971), p = 0.045), and alcoholic liver disease (OR = 0.081 (0.010-0.659), p = 0.019) as negative predictive factors of severe abdominal pain. Severe abdominal pain occurred in or after 1/13 (8%), 8/34 (24%), 22/41 (54%), and 10/10 (100%) TACE sessions when none, one, two, and three of the protective factors were absent, respectively (p < 0.001). The area under the ROC curve of the combination of factors for the prediction of severe abdominal pain was 0.779 (CI 0.687-0.871). Severe abdominal pain was frequent during and after TACE revealing a clinically relevant and underestimated problem. A predictive model based on three readily available clinical variables suggests that young patients without alcoholic liver disease or cirrhosis could benefit from reinforced analgesia. • Severe abdominal pain occurs in 43% of TACE for HCC. • Younger age, absence of cirrhosis, and absence of alcoholic liver disease were identified as independent predictive factors of severe abdominal pain. • A simple combination of the three abovementioned features helped predict the occurrence of severe abdominal pain.