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Liver Disease—Alcoholic Hepatitis/Cirrhosis
Published in Charles Theisler, Adjuvant Medical Care, 2023
Cirrhosis can result from any cause of chronic liver inflammation, but is primarily due to alcoholic hepatitis, NASH, or the hepatitis C virus.3 The spectrum of alcoholic liver disease encompasses several conditions so that a single patient may be affected by fatty liver, and/or alcoholic hepatitis, and/or alcoholic cirrhosis. Symptoms of liver toxicity are right upper abdominal pain, jaundice (yellowing of the skin and whites of the eyes), itching, fatigue, loss of appetite, weight loss, and dark or tea-colored urine. Alcoholic hepatitis can lead to scarring, or cirrhosis, of the liver and ultimately liver failure.
Crises in Treatment
Published in Frank Lynn Iber, Alcohol and Drug Abuse as Encountered in Office Practice, 2020
Therapists vary in their methods of intensifying support of the client under such circumstances. Some intensify interpersonal input, some work to diminish the stress (often impractical), and some use pharmacological support with sedatives or benzodiazepine drugs. A recent evaluation of the suitability of alcoholic cirrhosis patients for liver transplantation indicated that standard support by a therapist was sufficient to get the majority of patients through this complex and stressful situation.
Liver Diseases
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
The major action of ethanol manifests in the liver cell which exerts an essential role in ethanol metabolism.358,549 These effects include alcoholic hepatitis, alcoholic fatty liver, and alcoholic cirrhosis (Figure 33). There are, however, other organs which are involved in alcohol-induced disease and the onset and prognosis of many nonhepatic conditions such as gastritis, peptic ulcer, heart and arterial diseases, cancer of the larynx, stomach, mouth, and throat, are greatly influenced by the excessive consumption of alcoholic drinks. Alcoholic beverages contain ethyl alcohol and many other congeners. Some of the additional beverage congeners may be inherently toxic and other constituents are beneficial such as essential minerals, nutrients, and vitamins, as in wine and beer.329,330,602
Multifactorial jaundice and pigmented choledocholithiasis secondary to warm autoimmune hemolytic anemia and alcoholic cirrhosis
Published in Baylor University Medical Center Proceedings, 2022
Colten Watson, Mazen Hassan, Grant Breeland
In warm autoimmune hemolytic anemia (w-AIHA), the body creates the autoantibodies IgG1 and IgG3 that can bind and lyse red blood cells, causing anemia.1 These autoantibodies, called hemolysins, can be detected with a Coombs test and confirmed with a direct antiglobulin test. Alcoholic cirrhosis presents with several of the same features, such as extreme jaundice and constitutional symptoms. It usually presents in the fifth to sixth decade of life in the setting of excessive chronic ethanol ingestion. Most evidence supporting ethanol consumption as an etiology for cirrhosis has come from epidemiological studies. The overwhelming cause of acute jaundice in patients with alcohol abuse is acute alcoholic hepatitis. The pathogenesis of alcoholic hepatitis is attributed mainly to the expression of cytokines, oxidative stress, reactive oxygen species, and SREBPs and SREBP-1, which impair fatty acid oxidation. Abstinence remains the most effective treatment method.2 The combination of alcoholic cirrhosis with w-AIHA in patients is not well documented in the medical literature.
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.
Changes in the fecal bacterial microbiota associated with disease severity in alcoholic hepatitis patients
Published in Gut Microbes, 2020
Sonja Lang, Bradley Fairfied, Bei Gao, Yi Duan, Xinlian Zhang, Derrick E. Fouts, Bernd Schnabl
Alcohol-associated liver disease includes a wide spectrum of hepatic clinical syndromes and pathologic findings associated with heavy alcohol consumption1. Approximately 1 in 20 deaths worldwide is attributed to alcohol abuse, and alcohol-associated liver disease resulted in over 22,000 deaths in the US alone in 2017.2 Alcohol-associated liver disease includes steatosis, fibrosis, cirrhosis, and alcoholic hepatitis. These clinical entities, despite discrete definition, have substantial overlap and are closely interrelated. Simple steatosis involves fatty infiltration of the liver and is typically asymptomatic with normal or mild elevation in liver transaminases. A subset of these patients will go on to develop liver fibrosis, and ultimately, alcoholic cirrhosis. Alcoholic hepatitis is its own separate entity, which is related to but does not lie within the linear spectrum of steatosis, fibrosis, and cirrhosis in any predictable way. Thirty to 40% of chronic heavy drinkers will develop alcoholic hepatitis, but there is no clear identifiable trigger.3 Within alcoholic hepatitis, there is a wide range of disease severity, ranging from chronic and clinically silent to a fulminant syndrome of inflammation and cholestasis. Prognosis in alcoholic hepatitis varies widely, but is generally poor, with 30-day mortality reaching up to 50%.4