A severe syndrome associated with alcoholic liver damage is known as alcoholic hepatitis. It is distinguished by the sudden onset of jaundice, malaise, hepatomegaly, and subtly inflammatory characteristics throughout the body.
If alcohol consumption is prolonged, alcoholic hepatitis typically develops into cirrhosis. Hepatitis reciprocates to normal in individuals who discontinue alcohol within a few months, but the progressed cirrhosis is not irreversible.
Epidemiology
In the United States, over two-thirds of individuals consume alcohol, and 7.2% have an alcohol use disorder. The third most common preventable cause of death in the US is excessive alcohol consumption. A survey of 211 hospitals over ten years, from 2001 to 2011, found that 0.08 to 0.09% of admissions were due to alcoholic hepatitis.
Anatomy
Pathophysiology
In the hepatocytes, alcohol enters an oxidative metabolic route that lowers the proportion of NAD to NADH. Preventing the oxidation of triglycerides and fatty acids encourages lipogenesis. The transfer of endotoxins in lipopolysaccharides from the intestines into the hepatocytes is yet another recognized route of alcohol-induced liver damage.
Lipopolysaccharides bind to CD 14 and toll-like receptor 4 in the hepatic Kupffer cells, which induce a rush of reactive oxygen species to be released (ROS).
The production of cytokines such as platelet-derived growth factor, interleukin-8, tumor necrosis factor-alpha, monocyte chemotactic protein, and the ROS stimulates these cytokines, which cause an increase of macrophages and neutrophils as well as systemic clinical signs of alcohol injury.
Etiology
Although the most significant risk factor for developing the chronic liver disease is the amount of alcohol consumed, neither the course of alcohol-induced chronic liver disease nor the relationship between the amount of alcohol and liver injury is linear. Alcoholic hepatitis may result from alcohol usage for even shorter periods.
A typical patient would be between the ages of 40 and 60, have a history of consuming more than 1 ounce of alcohol per day for ten years, and have had all other potential causes of acute hepatitis excluded.
High body mass index (BMI), female gender, and a genetic variation of patatin-like phospholipase domain-containing protein 3 are risk factors. An unfavorable prognostic indicator is a clinical jaundice. In patients with a history of persistent alcohol misuse, acute binge drinking is most often the cause of alcoholic hepatitis.
Genetics
Prognostic Factors
30-50 % of patients with severe alcoholic hepatitis and Maddrey discriminant factor higher than 32 might collapse within 30 days. Patients with severe alcoholic hepatitis have a mortality rate of 40% within six months of the onset of the clinical condition.
At the presentation time, jaundice and hepatic encephalopathy foresee a worse outcome. With the cessation of alcohol use, mild alcoholic hepatitis typically has a benign course and is curable.
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
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Imaging Studies
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References
https://www.ncbi.nlm.nih.gov/books/NBK470217/
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A severe syndrome associated with alcoholic liver damage is known as alcoholic hepatitis. It is distinguished by the sudden onset of jaundice, malaise, hepatomegaly, and subtly inflammatory characteristics throughout the body.
If alcohol consumption is prolonged, alcoholic hepatitis typically develops into cirrhosis. Hepatitis reciprocates to normal in individuals who discontinue alcohol within a few months, but the progressed cirrhosis is not irreversible.
In the United States, over two-thirds of individuals consume alcohol, and 7.2% have an alcohol use disorder. The third most common preventable cause of death in the US is excessive alcohol consumption. A survey of 211 hospitals over ten years, from 2001 to 2011, found that 0.08 to 0.09% of admissions were due to alcoholic hepatitis.
In the hepatocytes, alcohol enters an oxidative metabolic route that lowers the proportion of NAD to NADH. Preventing the oxidation of triglycerides and fatty acids encourages lipogenesis. The transfer of endotoxins in lipopolysaccharides from the intestines into the hepatocytes is yet another recognized route of alcohol-induced liver damage.
Lipopolysaccharides bind to CD 14 and toll-like receptor 4 in the hepatic Kupffer cells, which induce a rush of reactive oxygen species to be released (ROS).
The production of cytokines such as platelet-derived growth factor, interleukin-8, tumor necrosis factor-alpha, monocyte chemotactic protein, and the ROS stimulates these cytokines, which cause an increase of macrophages and neutrophils as well as systemic clinical signs of alcohol injury.
Although the most significant risk factor for developing the chronic liver disease is the amount of alcohol consumed, neither the course of alcohol-induced chronic liver disease nor the relationship between the amount of alcohol and liver injury is linear. Alcoholic hepatitis may result from alcohol usage for even shorter periods.
A typical patient would be between the ages of 40 and 60, have a history of consuming more than 1 ounce of alcohol per day for ten years, and have had all other potential causes of acute hepatitis excluded.
High body mass index (BMI), female gender, and a genetic variation of patatin-like phospholipase domain-containing protein 3 are risk factors. An unfavorable prognostic indicator is a clinical jaundice. In patients with a history of persistent alcohol misuse, acute binge drinking is most often the cause of alcoholic hepatitis.
30-50 % of patients with severe alcoholic hepatitis and Maddrey discriminant factor higher than 32 might collapse within 30 days. Patients with severe alcoholic hepatitis have a mortality rate of 40% within six months of the onset of the clinical condition.
At the presentation time, jaundice and hepatic encephalopathy foresee a worse outcome. With the cessation of alcohol use, mild alcoholic hepatitis typically has a benign course and is curable.
https://www.ncbi.nlm.nih.gov/books/NBK470217/
medtigo
Alcoholic Hepatitis
Updated :
September 5, 2023
A severe syndrome associated with alcoholic liver damage is known as alcoholic hepatitis. It is distinguished by the sudden onset of jaundice, malaise, hepatomegaly, and subtly inflammatory characteristics throughout the body.
If alcohol consumption is prolonged, alcoholic hepatitis typically develops into cirrhosis. Hepatitis reciprocates to normal in individuals who discontinue alcohol within a few months, but the progressed cirrhosis is not irreversible.
In the United States, over two-thirds of individuals consume alcohol, and 7.2% have an alcohol use disorder. The third most common preventable cause of death in the US is excessive alcohol consumption. A survey of 211 hospitals over ten years, from 2001 to 2011, found that 0.08 to 0.09% of admissions were due to alcoholic hepatitis.
In the hepatocytes, alcohol enters an oxidative metabolic route that lowers the proportion of NAD to NADH. Preventing the oxidation of triglycerides and fatty acids encourages lipogenesis. The transfer of endotoxins in lipopolysaccharides from the intestines into the hepatocytes is yet another recognized route of alcohol-induced liver damage.
Lipopolysaccharides bind to CD 14 and toll-like receptor 4 in the hepatic Kupffer cells, which induce a rush of reactive oxygen species to be released (ROS).
The production of cytokines such as platelet-derived growth factor, interleukin-8, tumor necrosis factor-alpha, monocyte chemotactic protein, and the ROS stimulates these cytokines, which cause an increase of macrophages and neutrophils as well as systemic clinical signs of alcohol injury.
Although the most significant risk factor for developing the chronic liver disease is the amount of alcohol consumed, neither the course of alcohol-induced chronic liver disease nor the relationship between the amount of alcohol and liver injury is linear. Alcoholic hepatitis may result from alcohol usage for even shorter periods.
A typical patient would be between the ages of 40 and 60, have a history of consuming more than 1 ounce of alcohol per day for ten years, and have had all other potential causes of acute hepatitis excluded.
High body mass index (BMI), female gender, and a genetic variation of patatin-like phospholipase domain-containing protein 3 are risk factors. An unfavorable prognostic indicator is a clinical jaundice. In patients with a history of persistent alcohol misuse, acute binge drinking is most often the cause of alcoholic hepatitis.
30-50 % of patients with severe alcoholic hepatitis and Maddrey discriminant factor higher than 32 might collapse within 30 days. Patients with severe alcoholic hepatitis have a mortality rate of 40% within six months of the onset of the clinical condition.
At the presentation time, jaundice and hepatic encephalopathy foresee a worse outcome. With the cessation of alcohol use, mild alcoholic hepatitis typically has a benign course and is curable.
https://www.ncbi.nlm.nih.gov/books/NBK470217/
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