Alcoholic Hepatitis: A Review

Abstract

Alcoholic liver disease (ALD) represents a spectrum of injury, ranging from simple steatosis to alcoholic hepatitis to cirrhosis. Regular alcohol use results in fatty changes in the liver which can develop into inflammation, fibrosis and ultimately cirrhosis with continued, excessive drinking. Alcoholic hepatitis (AH) is an acute hepatic inflammation associated with significant morbidity and mortality that can occur in patients with steatosis or underlying cirrhosis. The pathogenesis of ALD is multifactorial and in addition to genetic factors, alcohol-induced hepatocyte damage, reactive oxygen species, gut-derived microbial components result in steatosis and inflammatory cell (macrophage and neutrophil leukocyte) recruitment and activation in the liver. Continued alcohol and pro-inflammatory cytokines induce stellate cell activation and result in progressive fibrosis. Other than cessation of alcohol use, medical therapy of AH is limited to prednisolone in a subset of patients. Given the high mortality of AH and the progressive nature of ALD, there is a major need for new therapeutic intervention for this underserved patient population.

Mulberry leaves extract ameliorates alcohol-induced liver damages through reduction of acetaldehyde toxicity and inhibition of apoptosis caused by oxidative stress signals

“…Metabolism of alcohol in liver produced damage-associated danger signals and then triggered pro-inflammatory cytokines, such as TNF-α and IL-6 production 22 . These pro-inflammation cytokines recruited immune cells, such as monocyte, macrophage, and neutrophil leukocyte accumulation, in liver and then produced additional pro-inflammation cytokines 23 . Reports have shown that elevation of TNF-α and IL-6 was found in serum of ALD patients 24 .…”

Experimental models of metabolic and alcoholic fatty liver disease

“…However, CD45+ leukocytes and CD163+ Kupffer cells are also increased in pediatric NAFLD patients[ 50 ]. Meanwhile, hepatocyte damage in ALD increases lipopolysaccharide (LPS) leakage into the liver by enhancing intestinal permeability, resulting in TNFα and IL-10 secretion by Kupffer cells[ 51 , 52 ]. The two-state model of macrophage polarization may thus be insufficient to describe immune response under concomitant NAFLD and ALD risk factors.…”

Features of clinical and laboratory indicators in alcoholic liver disease in combination with arterial hypertension depending on T786C polymorphism of the eNOS gene

“…Визначенню генетичних маркерів ризику алкогольної хвороби печінки (АХП) присвячено ряд робіт упродовж останнього десятиріччя. Розвиток та перебіг АХП зумовлюється та модифікується генетичним поліморфізмом і взаємодією генів із численними чинниками, серед яких важливе місце посідають кількість споживаного алкоголю, наявність вірусного ураження печінки та супутні захворювання пацієнтів [1].…”