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Alcohol, drugs, toxins and post-mortem toxicology
Published in Helen Whitwell, Christopher Milroy, Daniel du Plessis, Forensic Neuropathology, 2021
Colin Smith, Christopher Milroy
Hepatic failure is commonly due to alcoholic liver disease. This may be accompanied by hepatic encephalopathy (HE). In acute HE, there is swelling and oedema, which has been shown to be due to swelling of perivascular astrocytes ultrastructurally. HE is associated with Alzheimer type II change in astrocytes, the cells having enlarged optically clear nuclei. Chronic HE can be associated with pseudo-laminar spongy degeneration in the deep layers of the cerebral cortex (Victor et al. 1965).
Medical Problems in Alcoholics
Published in Frank Lynn Iber, Alcohol and Drug Abuse as Encountered in Office Practice, 2020
Mental changes as a complication of cirrhosis apart from hepatic encephalopathy are not usually thought about. A recent study by Van Thiel and Tarter17 compared 18 neuropsychological tests assessing visuospacial, memory, language, and perceptual capacities in normals, cirrhotics, and alcoholics without cirrhosis. They found the most severe impairment in liver disease and found moderate improvement with treatment of the cirrhosis. The ultimate treatment of alcoholic liver disease and its complications is transplantation. The Pittsburgh group have had the most experience with this form of therapy and discuss the pros and cons of its use.18
Liver Diseases
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Milder forms of alcoholic liver disease are characterized by the accumulation of excess fat in hepatocytes, representing the so-called fatty liver.74 Lipid deposition originates from three major sources: (1) dietary lipids transported in the blood stream as chylomicrons, (2) adipose tissue lipids transferred from adipocytes to the liver as free fatty acids, and (3) lipids produced in the liver from basic precursors. Fats derived from these sources can accumulate in the liver as a consequence of various metabolic disturbances such as (1) decreased hepatic metabolism with decreased oxidative processes, (2) increased hepatic synthesis of lipids, (3) decreased synthesis of lipid carrier proteins, (4) decreased elimination of lipids by decreased hepatic release of lipoproteins due to reduced receptor synthesis, (5) increased mobilization of peripheral fat depots, and (6) increased uptake of circulating lipids into the liver. The mechanism of fatty liver production is illustrated in Figure 33. A case illustrating fatty change of the liver is shown on Plate 3.
Efficacy of bile acid profiles in diagnosing and staging of alcoholic liver disease
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2023
Gaixia Zhang, Haizhen Chen, Wenbo Ren, Jing Huang
Prolonged excessive alcohol consumption leads to alcoholic liver disease (ALD), which is characterized by several histopathological changes, from simple steatosis to alcoholic steatohepatitis, progressive liver fibrosis and even cirrhosis. One of the features of alcoholic liver injury is the presence of oxidative stress, which leads to lipid peroxidation, steatosis, liver cell damage and death that in turn leads to the release of damage-related molecular patterns. Moreover, alcohol consumption promotes changes in the composition of the microbiota, increases intestinal permeability as well as the displacement of bacterial products. All these aspects activate Kupffer cells and promote the release of inflammatory cytokines, further exacerbating the inflammatory and fibrotic processes in the liver [3,4]. Patients with ALD may also suffer from cholestasis, mainly due to the accumulation of bile acids (BAs) due to the abnormal intestinal and hepatic circulation of BAs, which accelerates the progression of ALD [5]. Current studies found that ALD is rarely detected in the early stages compared with other liver diseases, leading to a poor prognosis in advanced patients, and alcohol consumption is also one of the causes of the progression of other liver diseases [6,7]. Therefore, accurate and noninvasive diagnostic indicators are urgently needed for the diagnosis of ALD and the evaluation of ALD staging.
Bone disease in patients with cirrhosis of different etiology and severity; are Klotho protein and osteoprotegerin potential biomarkers?
Published in Scandinavian Journal of Gastroenterology, 2023
Panagiotis V. Katsaounis, Emilia S. Hadjiyannis, Teressa Skaltsi, Vassiliki A. Anargyrou, Alexandra A. Alexopoulou, Spyridon P. Dourakis, John S. Koskinas
A total of 74 patients and 25 matched healthy controls were enrolled in this study with a ratio 3:1. The median age of patients group was 59.2 years (range 37–82) and their mean body mass index was 26.25, whereas the median age of the control group was 57 years (range 33–78) and the body mass index was 27.7. Patients with cirrhosis had diverse underlying etiologies with the majority of patients (n = 39) diagnosed with alcoholic cirrhosis (n = 28) and cirrhosis due to nonalcoholic fatty liver disease (NAFLD) (n = 11). Patients with alcoholic liver disease were abstained from alcohol the last 6 months. Thirty patients had viral infection (15 with HBV infection and 15 with HCV infection), four autoimmune diseases (three with primary biliary cirrhosis and one with primary sclerosing cholangitis) and one with Wilson’s disease.
Taxifolin, a novel food, attenuates acute alcohol-induced liver injury in mice through regulating the NF-κB-mediated inflammation and PI3K/Akt signalling pathways
Published in Pharmaceutical Biology, 2021
Chuanbo Ding, Yingchun Zhao, Xueyan Chen, Yinan Zheng, Wencong Liu, Xinglong Liu
Regular heavy drinking is harmful to health, and alcohol affects various body systems. Although its harmful effects vary with individual differences, long-term heavy drinking can lead to many chronic diseases and other serious health problems, which has become a serious public health problem. When the body’s intake of alcohol exceeds the metabolic rate, the excess will accumulate in the blood, leading to changes in normal body functions, and even a binge drinking can cause obvious body damage. Most acute alcoholic liver injury refers to toxic pathological damage to the liver caused by short-term heavy drinking; its incidence and the mortality rate are increasing year by year, and the research has attracted increasing attention (Yang et al. 2020). Alcoholic liver disease (ALD) may develop from hepatic steatosis to alcoholic hepatitis without intervention, and eventually lead to liver fibrosis, alcoholic cirrhosis and even liver cancer (Baghy et al. 2012). However, effective treatments can reverse the symptoms of early alcoholic liver toxicity, so finding effective treatment options is essential.