Publications
701 results found
Ndow G, Ceesay A, Shimakawa Y, et al., 2022, Concordance of the Xpert hepatitis B viral load test and conventional quantitative PCR in detecting and quantifying viremia using stored plasma and dried blood spot samples in West Africa, Publisher: ELSEVIER, Pages: S258-S259, ISSN: 0168-8278
Tebeka NN, Atkinson S, Tyson LD, et al., 2022, Loss of solute carrier family 38 member 4 (SLC38A4) as a driver for the pathogenesis of severe alcoholic hepatitis, Publisher: ELSEVIER, Pages: S140-S141, ISSN: 0168-8278
Vergis N, Hall I, Arthurs C, et al., 2022, In severe alcohol-related hepatitis, hepatocyte ballooning correlates with expression of p16 and components of a secretory phenotype that has been associated with cellular senescence, International Liver Congress, Publisher: ELSEVIER, Pages: S132-S132, ISSN: 0168-8278
Phillips S, Mistry S, Harris N, et al., 2022, Predictive immune biomarkers to safely discontinue nucleos (t)ide analogue treatment in HBeAg negative chronic hepatitis B (NUC-B study), International Liver Congress, Publisher: ELSEVIER, Pages: S188-S189, ISSN: 0168-8278
Artru F, Atkinson S, Trovato F, et al., 2022, Untargeted lipidomics unveils a specific plasma signature of severe alcoholic hepatitis, International Liver Congress, Publisher: ELSEVIER, Pages: S135-S135, ISSN: 0168-8278
Artru F, Atkinson S, Forrest E, et al., 2022, Untargeted lipidomics differentiate ACLF precipitated by severe alcoholic hepatitis, Publisher: ELSEVIER, Pages: S352-S353, ISSN: 0168-8278
Vergis N, Patel VC, Bogdanowicz K, et al., 2022, Il-1beta Signal Inhibition in acute alcoholic hepatitis: a multicentre, randomised, double-blind, placebo-controlled phase 2 trial of canakinumab therapy (ISAIAH), Publisher: ELSEVIER, Pages: S34-S35, ISSN: 0168-8278
- Author Web Link
- Cite
- Citations: 4
Liu T, Wu G, Gudd C, et al., 2022, Proximity labelling reveals potential cis interactions of CD52 glycoprotein counter-receptors on circulating CD4+HLA-G+ regulatory T cells in acute decompensation of cirrhosis, Publisher: ELSEVIER, Pages: S185-S186, ISSN: 0168-8278
Forlano R, Mullish BH, Martinez-Gili L, et al., 2022, Factors associated with increased gut permeability and severity of liver disease in diabetic patients with NAFLD, The International Liver CongressTM 2022, Publisher: Elsevier, Pages: S674-S675, ISSN: 0168-8278
Skinner C, Marchesi J, Mullish BH, et al., 2022, Tight junction damage and increased gut permeability in alcohol-related liver disease may be mediated by gut proteases, JOURNAL OF HEPATOLOGY, Vol: 77, Pages: S121-S122, ISSN: 0168-8278
Habboub N, Manousou P, Forlano R, et al., 2022, Designing a polymetabolic risk score for non-alcoholic steatohepatitis patients by differentiating their metabolic profiles from healthy controls, JOURNAL OF HEPATOLOGY, Vol: 77, Pages: S179-S179, ISSN: 0168-8278
Szabo G, Thursz M, Shah VH, 2022, Therapeutic advances in alcohol-associated hepatitis, JOURNAL OF HEPATOLOGY, Vol: 76, Pages: 1279-1290, ISSN: 0168-8278
- Author Web Link
- Cite
- Citations: 7
Whitfield JB, Schwantes-An T-H, Darlay R, et al., 2022, A genetic risk score and diabetes predict development of alcohol-related cirrhosis in drinkers (vol 76, pg 275, 2022), JOURNAL OF HEPATOLOGY, Vol: 76, Pages: 1244-1245, ISSN: 0168-8278
Morales-Arraez D, Ventura-Cots M, Altamirano J, et al., 2022, The MELD Score Is Superior to the Maddrey Discriminant Function Score to Predict Short-Term Mortality in Alcohol-Associated Hepatitis: A Global Study (vol 117, pg 301, 2022), AMERICAN JOURNAL OF GASTROENTEROLOGY, Vol: 117, Pages: 818-818, ISSN: 0002-9270
Atkinson SR, Aly M, Remih K, et al., 2022, Serum keratin 19 (CYFRA21-1) is a prognostic biomarker in severe alcoholic hepatitis, LIVER INTERNATIONAL, Vol: 42, Pages: 1049-1057, ISSN: 1478-3223
- Author Web Link
- Cite
- Citations: 3
Singal AK, Kwo P, Kwong A, et al., 2022, Research methodologies to address clinical unmet needs and challenges in alcohol-associated liver disease, HEPATOLOGY, Vol: 75, Pages: 1026-1037, ISSN: 0270-9139
- Author Web Link
- Cite
- Citations: 16
Kaura A, Hartley A, Panoulas V, et al., 2022, Mortality risk prediction of high-sensitivity C-reactive protein in suspected acute coronary syndrome: a cohort study, PLoS Medicine, Vol: 19, ISSN: 1549-1277
BACKGROUND: There is limited evidence on the use of high-sensitivity C-reactive protein (hsCRP) as a biomarker for selecting patients for advanced cardiovascular (CV) therapies in the modern era. The prognostic value of mildly elevated hsCRP beyond troponin in a large real-world cohort of unselected patients presenting with suspected acute coronary syndrome (ACS) is unknown. We evaluated whether a mildly elevated hsCRP (up to 15 mg/L) was associated with mortality risk, beyond troponin level, in patients with suspected ACS. METHODS AND FINDINGS: We conducted a retrospective cohort study based on the National Institute for Health Research Health Informatics Collaborative data of 257,948 patients with suspected ACS who had a troponin measured at 5 cardiac centres in the United Kingdom between 2010 and 2017. Patients were divided into 4 hsCRP groups (<2, 2 to 4.9, 5 to 9.9, and 10 to 15 mg/L). The main outcome measure was mortality within 3 years of index presentation. The association between hsCRP levels and all-cause mortality was assessed using multivariable Cox regression analysis adjusted for age, sex, haemoglobin, white cell count (WCC), platelet count, creatinine, and troponin. Following the exclusion criteria, there were 102,337 patients included in the analysis (hsCRP <2 mg/L (n = 38,390), 2 to 4.9 mg/L (n = 27,397), 5 to 9.9 mg/L (n = 26,957), and 10 to 15 mg/L (n = 9,593)). On multivariable Cox regression analysis, there was a positive and graded relationship between hsCRP level and mortality at baseline, which remained at 3 years (hazard ratio (HR) (95% CI) of 1.32 (1.18 to 1.48) for those with hsCRP 2.0 to 4.9 mg/L and 1.40 (1.26 to 1.57) and 2.00 (1.75 to 2.28) for those with hsCRP 5 to 9.9 mg/L and 10 to 15 mg/L, respectively. This relationship was independent of troponin in all suspected ACS patients and was further verified in those who were confirmed to have an ACS diagnosis by clinical coding. The main limitation of our study is that we did not
Whitfield JB, Schwantes-An T-H, Darlay R, et al., 2022, A genetic risk score and diabetes predict development of alcohol-related cirrhosis in drinkers, JOURNAL OF HEPATOLOGY, Vol: 76, Pages: 275-282, ISSN: 0168-8278
- Author Web Link
- Cite
- Citations: 20
Morales-Arraez D, Ventura-Cots M, Altamirano J, et al., 2022, The MELD Score Is Superior to the Maddrey Discriminant Function Score to Predict Short-Term Mortality in Alcohol-Associated Hepatitis: A Global Study, AMERICAN JOURNAL OF GASTROENTEROLOGY, Vol: 117, Pages: 301-310, ISSN: 0002-9270
- Author Web Link
- Cite
- Citations: 28
Forlano R, Mullish BH, Roberts LA, et al., 2022, The intestinal barrier and its dysfunction in patients with metabolic diseases and non-alcoholic fatty liver disease, International Journal of Molecular Sciences, Vol: 23, ISSN: 1422-0067
Non-alcoholic fatty liver disease (NAFLD) represents an increasing cause of liver disease worldwide, mirroring the epidemics of obesity and metabolic syndrome. As there are still no licensed medications for treating the disease, there is an ongoing effort to elucidate the pathophysiology and to discover new treatment pathways. An increasing body of evidence has demonstrated a crosstalk between the gut and the liver, which plays a crucial role in the development and progression of liver disease. Among other intestinal factors, gut permeability represents an interesting factor at the interface of the gut–liver axis. In this narrative review, we summarise the evidence from human studies showing the association between increased gut permeability and NAFLD, as well as with type-2 diabetes and obesity. We also discuss the manipulation of the gut permeability as a potential therapeutical target in patients with NAFLD.
Mohamed Z, Scott N, Nayagam S, et al., 2022, Cost effectiveness of simplified HCV screening-and-treatment interventions for people who inject drugs in Dar-es-Salaam, Tanzania, International Journal of Drug Policy, Vol: 99, ISSN: 0955-3959
Staudacher JJ, Bauer J, Atkinson SR, et al., 2022, Systemic Activin Is Elevated in Patients With Severe Alcoholic Hepatitis., Gastro Hep Adv, Vol: 1, Pages: 147-149
Vincent JP, Ndow G, Ogawa S, et al., 2022, Mac-2 binding protein glycosylation isomer (M2BPGi) to evaluate liver fibrosis and cancer in HBV-infected in West Africa, JOURNAL OF GLOBAL HEALTH, Vol: 12, ISSN: 2047-2978
Forlano R, Mullish BH, Dhar A, et al., 2021, Liver function tests and metabolic-associated fatty liver disease: Changes in upper normal limits, does it really matter?, World Journal of Hepatology, Vol: 13, Pages: 2104-2112, ISSN: 1948-5182
BACKGROUND: Metabolic-associated fatty liver disease (MAFLD) is the commonest cause of abnormal liver function tests (LFTs). Current upper normal of limit (UNL) of LFTs was derived from a “healthy” population, where undiagnosed MAFLD and viral hepatitis might be suspected.AIM :To evaluated potential implications of changes in UNL of alanine aminotrans-ferase (ALT) in MAFLD.METHODS:We retrospectively assessed consecutive first referrals with a diagnosis of MAFLD from 2010 to 2017. The conventional UNL of ALT was 45 IU/L for men and 34 IU/L for women, while a low UNL of ALT was 30 IU/L for men and 19 IU/L for women. The UNL of aspartate aminotransferase (AST) was 40 IU/L.RESULTS:Total 436 patients were enrolled; of these, 288 underwent liver biopsy. Setting a lower UNL reduced the percentage of those with significant disease despite normal ALT; specifically, patients with advanced fibrosis (F ≥ F3) or definite “metabolic-associated steato-hepatitis (MASH)” (NAS ≥ 5) within normal ALT decreased from 10% to 1% and from 28% to 4% respectively. However, the proportion of those with elevated ALT and no evidence of advanced fibrosis or “definite MASH” increased from 39% to 47% and from 3% to 19%. Overall, LFTs performed poorly in distinguishing “definite MASH” from simple steatosis (receiver operating characteristic areas under the curves 0.59 for ALT and 0.55 for AST).CONCLUSION:Liver function tests might both under- and overestimate MASH-related liver disease. Reducing the UNL might not be beneficial and imply an increase in healthcare burden. Risk stratification in MAFLD should rely on a combination of risk factors, not on LFTs alone.
Charania AS, Vergis N, Phillips R, et al., 2021, Multi-Arm Trial of Inflammatory Signal Inhibitors (MATIS) for hospitalised patients with mild or moderate Covid-19 pneumonia: a structured summary of a study protocol for a randomised controlled trial, 63rd ASH Annual Meeting and Exposition, Publisher: American Society of Hematology, Pages: 4200-4200, ISSN: 0006-4971
Vergis N, Patel V, Bogdanowicz K, et al., 2021, IL-1 Signal Inhibition In Alcoholic Hepatitis (ISAIAH): a study protocol for a multicentre, randomised, placebo controlled trial to explore the potential benefits of canakinumab in the treatment of alcoholic hepatitis, Trials, Vol: 22, Pages: 1-16, ISSN: 1745-6215
Background: Alcohol consumption causes a spectrum of liver abnormalities and leads to over 3 million deaths per year. Alcoholic hepatitis (AH) is a florid presentation of alcoholic liver disease characterized by liver failure in the context of recent and heavy alcohol consumption. The aim of this study is to explore the potential benefits of the IL-1β antibody, Canakinumab, in the treatment of AH.Methods: This is multicentre, double-blind, randomised placebo-controlled trial. Participants will be diagnosed with AH using clinical criteria. Liver biopsy will then confirm that all histological features of AH are present. Up to 58 participants will be recruited into two groups from 15 centres in the United Kingdom. Patients will receive an infusion of Canakinumab or matched placebo by random 1:1 allocation. The primary outcome is reduction in lobular inflammation, comparing histological appearances at baseline with appearances at 28 days. Patients with evidence of ongoing disease activity will receive a second infusion of Canakinumab or placebo. Participants will be followed up for 90 days. Secondary outcomes include mortality and change in MELD score at 90 days. Discussion: This phase II study will explore the benefits of the IL-1β antibody, canakinumab, in the treatment of AH to provide proof of concept that inhibition of IL-1β signaling may improve histology and survival for patients with AH. Trial registration: Prospectively registered with EudraCT 2017-003724-79.
Ingiliz P, Maurice J, Shimakawa Y, et al., 2021, Impact of an add-on strategy of the C-C chemokine receptor 5 (CCR5) antagonist maraviroc on hepatic inflammation in HIV-infected individuals with non-alcoholic steatohepatitis: a paired-liver biopsy proof-of-concept study, 18th European AIDS Conference (EACS 2021), Publisher: Wiley, Pages: 191-191, ISSN: 1464-2662
Introduction. Non-alcoholic steatohepatitis (NASH) is of concern in an agingand antiretroviral therapy (ART)-pretreated HIV-infected population. Notherapeutic agent has yet been licensed for the treatment of NASH in orderto reduce hepatic inflammation, steatosis, or liver fibrosis. The CCR5receptor antagonist maraviroc is an approved HIV drug, but hepatic CCR5inhibition has also been suggested to reduce hepatic inflammation andfibrogenesis in animal models. This study aimed to investigate the impact ofa maraviroc add-on strategy on hepatic inflammation in ART-treated HIVmono-infected individuals with NASH.Methods. The MASH study (Maraviroc-Add on for Steatohepatitis in HIVinfected patients) was a single-arm, open-label trial conducted across 5sites in Germany and the United Kingdom. HIV-infected individuals withbiopsy proven NASH were invited to add maraviroc BID to their existing,suppressive ART regimen for 48 weeks, and undergo a second liver biopsythereafter. Patients had immunologic, cytokine, metabolic, and histologicassessment at baseline and end of treatment (EOT).Results. Overall, 24 subjects were screened, and 13 completed the study and were analyzed. All participants were male,median age 50.5 years [45.5-55.5], baseline BMI 30.66 kg/m2 [27.92-33.63]; 83.3% (10/12) had insulin resistance. Atbaseline, 11/13 patients (85%) had fibrosis >1 (Metavir). At EOT no significant changes in the hepatic immune cell infiltrate(CD4/CD8/CD68) were observed, however, the NAS score decreased non significantly from 4.077 ± 0.76 at baseline to 3.64 ±0.51 at EOT (p = 0.125). At week 48, 7/11 patients (63%) showed significant fibrosis> stage 1, EOT BMI was similar comparedto baseline. Add-on MVC had no significant impact on inflammatory markers or lipid metabolism.
Innes AJ, Mullish BH, Ghani R, et al., 2021, Fecal microbiota transplant mitigates adverse outcomes in patients colonized with multidrug-resistant organisms undergoing allogeneic hematopoietic cell transplantation, Frontiers in Cellular and Infection Microbiology, Vol: 11, Pages: 1-8, ISSN: 2235-2988
The gut microbiome can be adversely affected by chemotherapy and antibiotics prior to hematopoietic cell transplantation (HCT).This affects graft success and increases susceptibility to multidrug-resistant organism (MDRO) colonization and infection. Weperformed an initial retrospective analysis of our use of fecal microbiota transplantation (FMT) from healthy donors as therapy forMDRO-colonized patients with hematological malignancy. FMT was performed on eight MDRO-colonized patients pre-HCT (FMT-MDROgroup), and outcomes compared with 11 MDRO colonized HCT patients from the same period. At 12 months, survival wassignificantly higher in the FMT-MDRO group (70% versus 36% p = 0.044). Post-HCT, fewer FMT-MDRO patients required intensivecare (0% versus 46%, P = 0.045) or experienced fever (0.29 versus 0.11 days, P = 0.027). Intestinal MDRO decolonization occurred in25% of FMT-MDRO patients versus 11% non-FMT MDRO patients. Despite the significant difference and statistically comparablepatient/transplant characteristics, as the sample size was small, a matched-pair analysis to non-MDRO colonized control cohorts(2:1 matching) was performed. At 12 months, the MDRO group who did not have an FMT had significantly lower survival (36.4%versus 61.9% respectively, p=0.012), and higher non relapse mortality (NRM; 60.2% versus 16.7% respectively, p=0.009) than theirpaired non-colonized cohort. There was no difference in survival (70% versus 43.4%, p=0.14) or NRM (12.5% versus 31.2%respectively, p=0.24) between the FMT-MDRO group and their paired cohort. Negative outcomes, including mortality associatedwith MDRO colonization, may be ameliorated by pre-HCT FMT, despite lack of intestinal decolonization. Further work is needed toexplore the observed benefit.
Khamri W, Gudd C, Liu T, et al., 2021, Suppressor CD4+ T cells expressing HLA-G are expanded in the peripheral blood from patients with acute decompensation of cirrhosis, Gut, Vol: 71, Pages: 1192-1202, ISSN: 0017-5749
Objective Identifying components of immuneparesis, a hallmark of chronic liver failure, is crucial for our understanding of complications in cirrhosis. Various suppressor CD4+ T cells have been established as potent inhibitors of systemic immune activation. Here, we establish the presence, regulation and mechanism of action of a suppressive CD4+ T cell subset expressing human leucocyte antigen G (HLA-G) in patients with acute decompensation of cirrhosis (AD).Design Flow cytometry was used to determine the proportion and immunophenotype of CD4+HLA-G+ T cells from peripheral blood of 20 healthy controls (HCs) and 98 patients with cirrhosis (28 with stable cirrhosis (SC), 20 with chronic decompensated cirrhosis (CD) and 50 with AD). Transcriptional and functional signatures of cell-sorted CD4+HLA-G+ cells were delineated by NanoString technology and suppression assays, respectively. The role of immunosuppressive cytokine interleukin (IL)-35 in inducing this population was investigated through in vitro blockade experiments. Immunohistochemistry (IHC) and cultures of primary human Kupffer cells (KCs) were performed to assess cellular sources of IL-35. HLA-G-mediated T cell suppression was explored using neutralising antibodies targeting co-inhibitory pathways.Results Patients with AD were distinguished by an expansion of a CD4+HLA-G+CTLA-4+IL-35+ immunosuppressive population associated with disease severity, clinical course of AD, infectious complications and poor outcome. Transcriptomic analyses excluded the possibility that these were thymic-derived regulatory T cells. IHC analyses and in vitro cultures demonstrate that KCs represent a potent source of IL-35 which can induce the observed HLA-G+ phenotype. These exert cytotoxic T lymphocyte antigen-4-mediated impaired responses in T cells paralleled by an HLA-G-driven downregulation of T helper 17-related cytokines.Conclusion We have identified a cytokine-driven peripherally derived suppressive population that may contr
Forlano R, Harlow C, Mullish BH, et al., 2021, Binge-eating disorder is associated with an unfavourable body mass composition in patients with Non-alcoholic fatty liver disease, International Journal of Eating Disorders, Vol: 54, Pages: 2025-2030, ISSN: 0276-3478
The interaction between eating disorders and non-alcoholic fatty liver disease (NAFLD) remains unexplored, especially with regards to binge-eating disorder (BED). Our team conducted a service evaluation project in order to assess risk factors for the presence of BED among patients with NAFLD and the impact of BED on body mass composition. The overall prevalence of patients screening positive to BED Screener-7 (BEDS-7) was 28.4%, while a previous diagnosis of depression and marital status (as single or separated) were independently associated with positive BED. Furthermore, patients with positive BEDS-7 had higher BMI, with greater visceral component and overall lower muscle mass. There was no difference in terms of liver disease severity as assessed by noninvasive markers of fibrosis. However, as body mass composition and sarcopenia have been shown to be associated to disease progression in patients with NAFLD, further studies are required to ascertain the long-term impact of BED in these patients. Moreover, further work is warranted to identify to implement multidisciplinary approach within clinical psychology for the management of patients with BED, who may be particularly challenging in terms of achieving lifestyle modifications. As a hepatology community, we should address NAFLD with a more holistic approach.
This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.