Excess Weight Risk Factor for Alcoholic Liver Disease

Background: Alcoholic hepatitis (AH) is a severe manifestation of alcohol-related liver disease characterised by jaundice and liver failure. It is not known what might trigger an episode of AH. We interviewed patients to investigate changes in behaviour before the onset of AH. Methods: Structured interviews were performed with patients with AH to examine their alcohol use, diet, drug use and smoking habit. Clinical and laboratory results were noted. Patients were followed up for 12 months after interview. Results: Data from 39 patients was analysed. No single behavioural change occurred before the onset of jaundice, although reductions in alcohol and/or dietary intake were common. Reduction in alcohol use was seen to occur approximately 14 days before the onset of jaundice. Increased alcohol intake was not common. Clinical and laboratory data varied between types of behaviour changes, although these were not statistically significant. No changes in drug use or tobacco were reported before AH. Those who had not reduced alcohol intake or had increased their drinking had better survival. Conclusions: No single type of behaviour change is associated with AH. Contrary to previous assertions, increased alcohol intake was not common; in fact, participants were much more likely to have reduced their alcohol intake.

Section: Discussioncontrasting

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Alcohol, Diet and Drug Use Preceding Alcoholic Hepatitis

Parker

Neuberger

2018

“…This amount is based on epidemiological studies showing that alcohol-induced steatosis occurs above this threshold [4,5]. Owing to its increasing prevalence and strong association with the metabolic syndrome [6], it is now recognized that NAFLD/NASH can occur in association with other CLD [2], and that in some circumstances (chronic hepatitis C [7], hemochromatosis [8], alcoholic liver disease [9]) this association can increase liver damage [10]. …”

Section: Definition Epidemiology and Natural Historymentioning

confidence: 99%

ASH and NASH

Scaglioni

Ciccia

Marino

et al. 2011

Non-alcoholic steatohepatitis (NASH) and alcoholic steatohepatitis (ASH) have a similar pathogenesis and histopathology but a different etiology and epidemiology. NASH and ASH are advanced stages of non-alcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease (AFLD). NAFLD is characterized by excessive fat accumulation in the liver (steatosis), without any other evident causes of chronic liver diseases (viral, autoimmune, genetic, etc.), and with an alcohol consumption ≤20–30 g/day. On the contrary, AFLD is defined as the presence of steatosis and alcohol consumption >20–30 g/day. The most common phenotypic manifestations of primary NAFLD/NASH are overweight/obesity, visceral adiposity, type 2 diabetes, hypertriglyceridemia and hypertension. The prevalence of NAFLD in the general population in Western countries is estimated to be 25–30%. The prevalence and incidence of NASH and ASH are not known because of the impossibility of performing liver biopsy in the general population. Up to 90% of alcoholics have fatty liver, and 5–15% of these subjects will develop cirrhosis over 20 years. The risk of cirrhosis increases to 30–40% in those who continue to drink alcohol. About 10–35% of alcoholics exhibit changes on liver biopsy consistent with alcoholic hepatitis. Natural histories of NASH and ASH are not completely defined, even if patients with NASH have a reduced life expectancy due to liver-related death and cardiovascular diseases. The best treatment of AFLD/ASH is to stop drinking, and the most effective first-line therapeutic option for NAFLD/NASH is non-pharmacologic lifestyle interventions through a multidisciplinary approach including weight loss, dietary changes, physical exercise, and cognitive-behavior therapy.

“…Actually, several clinical studies suggest a strong causative link between the consumption of alcohol and progressive liver disease in individuals with high fat intake and/or diabetes [2,10,11]. In subjects with heavy alcohol consumption, obesity is an independent risk factor for the development of both acute alcohol-induced hepatitis and cirrhosis [10,12].…”

Section: Combined Effects Of Alcohol and Excessive Calorie Intake On mentioning

confidence: 99%

“…In subjects with heavy alcohol consumption, obesity is an independent risk factor for the development of both acute alcohol-induced hepatitis and cirrhosis [10,12]. Combined effects appear to affect all pathophysiological steps of disease development and progression, starting with hepatic steatosis [13].…”

Section: Combined Effects Of Alcohol and Excessive Calorie Intake On mentioning

confidence: 99%

Pathophysiological Similarities and Synergisms in Alcoholic and Non-Alcoholic Steatohepatitis

Hellerbrand¹

2010

Chronic alcohol consumption is one of the main etiological factors for liver disease worldwide, however only a fraction of drinkers develop significant hepatic inflammation (alcoholic steatohepatitis), and even less progress to significant hepatic fibrosis and cirrhosis. The pathophysiological significance of hepatic lipid accumulation in the absence of significant alcohol consumption is also increasingly recognized. Non-alcoholic fatty liver disease (NAFLD) is regarded as the hepatic manifestation of the metabolic syndrome, and it is the most common cause of liver enzyme elevations in Western countries. Similarly to alcoholic liver disease, NAFLD encompasses mild hepatic steatosis to non-alcoholic steatohepatitis with significant necroinflammation and progressive fibrosis. Several clinical studies suggest a strong causative link between the consumption of alcohol and progressive liver disease in individuals with high fat intake and/or diabetes. However, it is incompletely understood how alcohol and obesity interact and whether the combined effects on the progression of liver injury are additive or synergistic. This review describes single as well as combined effects of alcohol and (components of) the metabolic syndrome on hepatic steatosis, inflammation and fibrosis. In addition to direct effects on the liver, the view is expanded to other organs affected by chronic alcohol consumption or the metabolic syndrome, to understand also extrahepatic pathophysiological mechanisms involved in hepatocellular injury. Undoubtedly, alcohol and the metabolic syndrome appear as a dangerous mix, and there are important synergistic effects of either condition with regard to crucial triggers of liver injury.