scholarly journals Letter: Confounders and outcomes in studies of beta‐blockers in liver disease—role of PPIs? Authors' reply

2021 ◽  
Vol 54 (1) ◽  
pp. 91-91
Author(s):  
Roula Sasso ◽  
Don C. Rockey
Keyword(s):  
Liver Disease ◽  
Beta Blockers

Semi-Quantitative Ultrasonographic Evaluation of NAFLD

2020 ◽  
Vol 26 (32) ◽  
pp. 3915-3927 ◽  
Author(s):  
Stefano Ballestri ◽  
Claudio Tana ◽  
Maria Di Girolamo ◽  
Maria Cristina Fontana ◽  
Mariano Capitelli ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Imaging Techniques ◽  
Metabolic Complications ◽  
Nonalcoholic Fatty Liver ◽  
Non Invasive ◽  
Increased Risk ◽  
Risk Of Progression ◽  
Progressive Liver Disease

: Nonalcoholic fatty liver disease (NAFLD) embraces histopathological entities ranging from the relatively benign simple steatosis to the progressive form nonalcoholic steatohepatitis (NASH), which is associated with fibrosis and an increased risk of progression to cirrhosis and hepatocellular carcinoma. NAFLD is the most common liver disease and is associated with extrahepatic comorbidities including a major cardiovascular disease burden. : The non-invasive diagnosis of NAFLD and the identification of subjects at risk of progressive liver disease and cardio-metabolic complications are key in implementing personalized treatment schedules and follow-up strategies. : In this review, we highlight the potential role of ultrasound semiquantitative scores for detecting and assessing steatosis severity, progression of NAFLD, and cardio-metabolic risk. : Ultrasonographic scores of fatty liver severity act as sensors of cardio-metabolic health and may assist in selecting patients to submit to second-line non-invasive imaging techniques and/or liver biopsy.

scholarly journals The Role of the Transsulfuration Pathway in Non-Alcoholic Fatty Liver Disease

2021 ◽  
Vol 10 (5) ◽  
pp. 1081
Author(s):  
Mikkel Parsberg Werge ◽  
Adrian McCann ◽  
Elisabeth Douglas Galsgaard ◽  
Dorte Holst ◽  
Anne Bugge ◽  
...  
Keyword(s):  
Liver Disease ◽  
Animal Models ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Precise Control ◽  
Transsulfuration Pathway ◽  
Global Population ◽  
Alcoholic Fatty Liver Disease

The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing and approximately 25% of the global population may have NAFLD. NAFLD is associated with obesity and metabolic syndrome, but its pathophysiology is complex and only partly understood. The transsulfuration pathway (TSP) is a metabolic pathway regulating homocysteine and cysteine metabolism and is vital in controlling sulfur balance in the organism. Precise control of this pathway is critical for maintenance of optimal cellular function. The TSP is closely linked to other pathways such as the folate and methionine cycles, hydrogen sulfide (H2S) and glutathione (GSH) production. Impaired activity of the TSP will cause an increase in homocysteine and a decrease in cysteine levels. Homocysteine will also be increased due to impairment of the folate and methionine cycles. The key enzymes of the TSP, cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE), are highly expressed in the liver and deficient CBS and CSE expression causes hepatic steatosis, inflammation, and fibrosis in animal models. A causative link between the TSP and NAFLD has not been established. However, dysfunctions in the TSP and related pathways, in terms of enzyme expression and the plasma levels of the metabolites (e.g., homocysteine, cystathionine, and cysteine), have been reported in NAFLD and liver cirrhosis in both animal models and humans. Further investigation of the TSP in relation to NAFLD may reveal mechanisms involved in the development and progression of NAFLD.

Evaluation of the role of bile acids and serotonin as markers of pruritus in children with chronic cholestatic liver disease

2021 ◽  
Author(s):  
Nehal El Koofy ◽  
Noha Yassin ◽  
Sawsan Okasha ◽  
Hany William ◽  
Wafaa Elakel ◽  
...  
Keyword(s):  
Liver Disease ◽  
Bile Acids ◽  
Cholestatic Liver Disease

scholarly journals Role of Insulin Resistance in MAFLD

2021 ◽  
Vol 22 (8) ◽  
pp. 4156
Author(s):  
Yoshitaka Sakurai ◽  
Naoto Kubota ◽  
Toshimasa Yamauchi ◽  
Takashi Kadowaki
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
De Novo Lipogenesis ◽  
Hepatic Insulin Resistance ◽  
Metabolic Dysfunction ◽  
Alcoholic Fatty Liver ◽  
Fat Accumulation

Many studies have reported that metabolic dysfunction is closely involved in the complex mechanism underlying the development of non-alcoholic fatty liver disease (NAFLD), which has prompted a movement to consider renaming NAFLD as metabolic dysfunction-associated fatty liver disease (MAFLD). Metabolic dysfunction in this context encompasses obesity, type 2 diabetes mellitus, hypertension, dyslipidemia, and metabolic syndrome, with insulin resistance as the common underlying pathophysiology. Imbalance between energy intake and expenditure results in insulin resistance in various tissues and alteration of the gut microbiota, resulting in fat accumulation in the liver. The role of genetics has also been revealed in hepatic fat accumulation and fibrosis. In the process of fat accumulation in the liver, intracellular damage as well as hepatic insulin resistance further potentiates inflammation, fibrosis, and carcinogenesis. Increased lipogenic substrate supply from other tissues, hepatic zonation of Irs1, and other factors, including ER stress, play crucial roles in increased hepatic de novo lipogenesis in MAFLD with hepatic insulin resistance. Herein, we provide an overview of the factors contributing to and the role of systemic and local insulin resistance in the development and progression of MAFLD.

scholarly journals P88 Paroxysmal sympathetic storm and the role of beta-blockers in traumatic brain injury: a scoping review protocol

BJS Open ◽  
2021 ◽  
Vol 5 (Supplement_1) ◽  
Author(s):  
Stéphane Nguembu ◽  
Marco Meloni ◽  
Geneviève Endalle ◽  
Hugues Dokponou ◽  
Olaoluwa Ezekiel Dada ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Length Of Stay ◽  
Glasgow Coma Scale ◽  
Scoping Review ◽  
Beta Blockers ◽  
Clinical Signs ◽  
Sympathetic Hyperactivity ◽  
Paroxysmal Sympathetic Hyperactivity

Abstract Introduction Most cases of paroxysmal sympathetic hyperactivity (PSH) result from traumatic brain injury (TBI). Little is known about its pathophysiology and treatment, and several neuroprotective drugs are used including beta-blockers. The aim of our study is to collate existing evidence of the role of beta-blockers in the treatment of PSH. Method We will search MEDLINE, Web of Science, EMBASE, Cochrane, and Google Scholar. The search terms used will cover the following terms: “paroxysmal sympathetic hyperactivity”, “traumatic brain injury” and “beta-blockers.”: No language or geographical restrictions will be applied. Two independent co-authors will screen the titles and abstracts of each article following predefined inclusion and exclusion criteria. If there is a conflict the two reviewers will find a consensus and if they cannot a third co-author will decide. Using a pre-designed and pre-piloted data extraction form, data from each included citation will be collected (authors identification, study type, TBI severity, type of beta-blockers used, dosage of the drug, clinical signs of PSH, Glasgow Coma Scale, Glasgow Outcome Scale, mortality, morbidity and length of stay). Simple descriptive data analyses will be performed and the results will be presented both in a narrative and tabular form. Results The effectiveness of beta-blockers in post-TBI PHS will be evaluated through clinical signs of PHS(increased heart rate, respiratory rate, temperature, blood pressure, and sweating), Glasgow Coma Scale, and Glasgow Outcome Scale. mortality, morbidity and length of stay. Conclusion At the end of this scoping review we will design a systematic review with metaanalysis if there are a reasonable number of studies otherwise we will design a randomized controlled trial.

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