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The liver, gallbladder and pancreas
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Dina G. Tiniakos, Alastair D. Burt
Despite the many diverse causes of liver disease, the liver has a rather limited set of responses to injury. In some conditions, the injury is manifest by the accumulation of lipids within the hepatocytes: this is a central theme in alcohol-related liver disease and in liver injury associated with the so-called ‘metabolic syndrome’ (type 2 diabetes, hypertension, obesity, and dyslipidaemia) – the fatty liver disease. In many disorders, there is irreversible liver cell injury through either necrosis or apoptosis (see Chapter 3). Inflammation is a common feature, particularly in chronic conditions. The predominant inflammatory cell type is the T lymphocyte; these cells may have a key role in liver cell apoptosis. In response to liver cell loss, there is regeneration of surviving epithelial cells as noted above. In some situations, there may be massive liver cell necrosis, where most of the parenchyma is lost; under such circumstances, there may then not be sufficient critical mass of surviving cells to repopulate the liver. When there is persistent injury and inflammation there is stimulation of a repair process involving the hepatic stellate cells; this leads to the development of fibrosis and is discussed more fully in Chapter 3.
Non-viral liver disease
Published in Michael JG Farthing, Anne B Ballinger, Drug Therapy for Gastrointestinal and Liver Diseases, 2019
John ML Christie, Roger WG Chapman
Alcohol is the most common cause of cirrhosis in the Western world. Over 50% of deaths from cirrhosis in the UK are a result of alcohol. The amount of alcohol ingested and the duration of intake correlate with the incidence of alcohol-related liver disease.91 The risk of developing liver disease, however, varies from individual to individual for the same quantity of alcohol ingested: less than 20% of men consuming more than 12 units per day for 10 years will become cirrhotic. Separate factors, other than the quantity of alcohol, influence the development of alcoholic liver disease.92 Women are at greater risk of liver disease from alcohol intake, which cannot be explained solely by differences in body composition or alcohol distribution. One possible theory is that gastric mucosal alcohol dehydrogenase is lower in women, resulting in higher quantities of absorbed alcohol. Genetic variability is thought to be important, although the genes responsible remain to be elucidated. Other predisposing factors include poor nutrition, co-infection with hepatropic viruses and co-exposure to drugs or toxins.
Alcohol-Induced Liver Disease
Published in Timothy R. Billiar, Ronald D. Curran, Hepatocyte and Kupffer Cell Interactions, 2017
The possibility also exists that the decreased phagocytic activity of blood monocytes50 and macrophages51 reported in chronic alcoholics may play some role in the pathogenesis of alcohol-related liver disease.
Utilization of health care resources, long-term survival and causes of death after intensive care unit admission in relation to high-risk alcohol consumption
Published in Journal of Substance Use, 2021
Siiri Hietanen, Johanna Herajärvi, Sanna Lahtinen, Riikka Käkelä, Tero Ala-Kokko, Janne Liisanantti
We have previously reported lower one-year mortality in patients with high-risk alcohol consumption in this patient cohort. (Hietanen et al., 2017). However, the trend seems to even out in longer follow-up and the present study found no significant difference in long-term mortality between the patient groups. Our findings are in agreement with previous studies reporting no difference or even better long-term survival in patients with high-risk alcohol consumption. (Christensen et al., 2012; Lynch et al., 2017). The patients with high-risk alcohol consumption suffered less from severe chronic diseases during the ICU treatment period affecting the mortality rates. The prevalence of alcohol-related liver disease with demonstrated poor prognosis was only 5.7% in our study population and was not significant enough to influence the mortality rates in the alcohol group. Respectively, the prevalence of cardiovascular diseases and malignancies were high in the non-alcohol group associated with higher mortality as discovered earlier among ICU population (Mayr et al., 2006). Alcohol group’s leveling off mortality rate might be explained by evolving complications of alcohol-related diseases over time and this might indicate that patients continue to consume alcohol even after ICU admission.
Increased Risk of Hypertension in Alcohol Use Disorder of alcohol-related Liver disease-A Hospital Based Case Control Study
Published in Alcoholism Treatment Quarterly, 2023
Prabhudas Nelaturi, Sangeetha P Kademani, Vithiavathi Siva Subramanian, Sambandam Ravikumar
Alcohol-related liver disease is a major health concern worldwide and the pathological spectrum consists of alcohol-related fatty liver, alcohol-related steatohepatitis, fibrosis and cirrhosis. Metabolic syndrome, alcohol use disorder, environmental and genetic factors contribute to the pathogenesis of ALD. Alcohol-related cirrhosis accounted for 0.6% of global disability-adjusted life years (DALYs) and 0.9% of all mortalities, and 47.9% of cirrhosis-related deaths were reported(“Alcohol use and burden for 195 countries and territories, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016,” 2018). The MELD score (29.08 ± 1.5in ALD and 27.71 ± 1.6 in NAFLD; F = 22.73, P = .001) was used to evaluate the condition of patients with end-stage liver disease and it is also positively correlated with the increased mortality. The altered expression of collagen isoforms in ventricular heart tissue is positively associated with diastolic dysfunction in progressive liver disease. Inflammatory mediators also play a significant role as the levels are increasing in chronic inflammation-related diseases such as liver fibrosis and cardiovascular diseases(El Hadi, Di Vincenzo, Vettor, & Rossato, 2020). The presence of esophageal varices due to obstructed blood flow via portal veins indicates an elevated transhepatic pressure gradient in liver disease progression. Hepatic stellate cell activation plays a major role in the pathogenesis of portal hypertension(Engelmann, Clària, Szabo, Bosch, & Bernardi, 2021). Over time, the loss of pulsatility in the liver leads to secondary liver cirrhosis, known as cardiac cirrhosis.
N-acetyl cysteine in the treatment of alcohol use disorder in patients with liver disease: Rationale for further research
Published in Expert Opinion on Investigational Drugs, 2018
Kirsten C. Morley, Andrew Baillie, Wim Van Den Brink, Kate E. Chitty, Kathleen Brady, Sudie E. Back, Devanshi Seth, Greg Sutherland, Lorenzo Leggio, Paul S. Haber
Alcohol misuse is linked to over 200 physical and mental conditions [1] and is a leading cause of morbidity and mortality worldwide. The liver is commonly affected by regular or heavy alcohol use and patients with alcohol-related liver disease present a particular clinical challenge [2]. In terms of alcohol-attributable deaths, alcoholic liver disease (ALD) stands as the most common cause [3] and abstinence from alcohol is key to reducing this mortality. In this paper, we present a rationale for studies investigating N-acetyl cysteine (NAC) to increase abstinence in alcohol use disorder (AUD) in the presence of ALD.