Marsano et al., 2003, reported that Alcoholic liver disease (ALD) is a serious and potentially fatal outcome caused due to alcohol usage. ALD encompasses three conditions mainly fatty liver, alcoholic hepatitis and cirrhosis. The diagnosis and management of this disease is important for decreasing the mortality. For accurate diagnosis of ALD new bio marker or idenififier proteins are being investigated. There is no specific therapy for ALD hence lifestyle changes, nutritional support and other therapies to improve the outcome are only there. The new therapies are mainly aimed to improve the quality of life and to reduce the mortality rates.
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Maher Jacquelyn J 1997 found that most of the alcoholic liver damage is caused due to the direct toxicity of the metabolic by-products formed during alcohol metabolism. These by-products leads to inflammation, expose liver cells to bacterial toxins and cause liver diseases. This can contribute to fibrosis and ultimately cirrhosis. Increased understanding of the mechanism of tissue injury has led to new treatments like corticosteroids, antioxidants, antibiotics. By understanding the biological mechanisms underlying liver injury it is possible to find new treatment approaches for alcoholic liver disease.
Wu D et al., 2003 alcohol promotes generation of ROS and thereby interferes with the normal defense mechanism of the body through various processes. It stimulates the activity of various enzymes (Cytochrome P450) and leads to the increased production of ROS. Alcohol reduces the level of antioxidants that can eliminate the ROS which leads to increase the oxidative stress in cell and causes cell injury
Mann et al., 2003 alcohol induced liver disease is a main cause of mortality worldwide. It was estimated that 10-15% of alcoholics will develop cirrhosis; it is mainly depending upon the duration and the amount of heavy drinking. Study also suggests that alcohol and hepatitis C may increase the incidence of cirrhosis and liver disease.
Szabo et al., 2010 Reported the concepts of kupffer cell activation and their role of these cells in liver inflammation, oxidative stress related injury, stellate cell activation and fibrosis. He also demonstrates the role of free radicals in alcoholic liver injury. It was also found that steatosis may occur in 90% of individuals who consume more than 60g/d of alcohol.
Brenner et al., 2004 A wide spectrum of functional and morphological alterations are caused by alcohol in the liver. The earlier change in that is the progressive accumulation of fat leading to the development of steatosis (fatty liver) followed by ASH that may progress to fibrosis. The end stage of alcoholic liver disease is micro nodular alcoholic cirrhosis. All the stages prior to liver cirrhosis are potentially reversible. The important mechanism of alcoholic liver disease is the pronounced inflammatory response of kupffer cells and other leukocytes (macrophages, neutrophils, lymphocytes) and due to elevated gut derived endotoxin plasma levels. Alcoholic liver cirrhosis is mostly micronodular because of the inhibitory action of ethanol on hepatocyte growth.
Purohit et al., 2002 Alcohol intake is the major cause of hepatitis that can lead to alcoholic cirrhosis. One third of the heavy drinkers develop alcoholic hepatitis, which is characterized by liver cell death and infiltration of leukocytes in hepatic parenchyma.
Osna ., 2007 Alcohol-induced fatty liver (steatosis) is caused as a result of excessive generation of reducing equivalents from ethanol metabolism, thereby enhancing fat accumulation. Transcription factors are also involved in this, which include the sterol regulatory element binding protein 1 (SREBP-1) which is also having important role in hepatic steatosis. Steatosis is a significant factor for advanced liver pathology, so understanding the molecular mechanism in its etiology is needed for developing new therapies. Ethanol consumption results in activation of SREBP-1 this induces genes involved in lipid biosynthesis. Ethanol consumption also down-regulates the PPAR-a transcription factor, which regulates the enzymes involved in fatty acid oxidation.
O’ Shea et al., 2009 Alcohol is a major cause of liver disease worldwide. The dose, duration, type of alcohol consumption, drinking patterns, gender, and ethnicity, associated risk factors like obesity, iron over load, liver infections and genetic factors can effect in the development of the liver injury. There is no single biochemical marker that identifies the exact etiology of alcoholic liver disease, because alcohol may be one of the factors that contribute to liver damage and specific role of alcohol alone is difficult to assess in a patient with multifactorial liver disease. There is no proper treatment for ALD or AH, until further evidence of efficacy has been obtained.
Gramenzi et al., 2006 Alcoholic liver disease causes significant mortality and morbidity rates with a complex and incompletely known pathogenesis. The mechanisms of alcohol hepatoxicity are complex and multifactorial. It’s because several primary and secondary factors interact to initiate the alcoholic liver injury. Primary factors include genetic factors and complex interrelationship with liver toxicity and secondary factors include nutritional and hepatotoxic conditions that can lead to liver damage. Ethanol induces altered redox state associated with free radical generation, resulting in lipid peroxidisation, cell membrane damage and depletion of mitochondrial antioxidants, and reduced GSH
Caughan et al., 2000 chronic inflammation, cellular damage, regeneration and fibrosis are the hallmarks of chronic liver damage. Serum DPPIV levels are elevated in liver diseases as it is located on the bile canaliculus, still the sources of DPPIV is unknown. In human cirrhosis intense expression of DPPIV was observed on proliferating bile ductules, neovascular structures and infiltrating leucocytes.
Sanchez et al., 2005 alcoholic liver disease had a wide clinical spectrum. It may progress from cirrhosis to end stage liver disease which requires liver transplantation. The histological manifestations of liver damage ranges from steatosis without inflammation to liver cell injury. There are no specific tests to establish a diagnosis of steatohepatits. Liver biopsy is useful in confirming the suspected diagnosis of the disease.
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Petrasek et al., 2010 inflammatory cascade activation plays an important role in pathophysiology of alcoholic liver disease. The contribution of Toll like receptor signaling in induction of liver fibrosis and hepatocellular cancer is discussed here. The ethanol intake increases the gut permeability because of this there is increased permeability of normally nonabsorbable substances. Increased gram negative bacteria as well as blood endotoxin are increased in acute and chronic alcoholic liver models. LPS a component of Gram Negative bacteria is a potent activator of innate immunity response through binding with TLR receptors. Greater this leads to accumulation of lipids, opening of mitochondrial permeability transition pores and depletion of glutathione.
Lakatos et al., 2000 DPP IV is an enzyme whose expression has been seen in hepatocyte-extracellular matrix interactions, fibroblast activation and proliferation and in T-cell activation. Aberrant DPP IV expression was found in human liver cirrhosis and elevated serum DPP IV activity was reported in patients with primary biliary cirrhosis and chronic hepatitis C virus infection. So elevated DPP IV levels can be a indicator for liver cirrhosis.
Madhotra et al., 2003 The exact mechanism of liver injury in alcoholic hepatitis is not properly understood, this has hampered in developing effective treatment. The recent advaces in understanding the pathogenesis of the disease, including the role of cytokines and apoptosis has lead to the development of new treatment options. Now there are specific therapies for challenging and serious condition.
Shen et al., 2010 The role of sirutin 1(SIRT1) and AMPK activity in alcoholic fatty liver has already been known. The PPAR-γ plays an important role in the regulation of adiponectin in adipose tissues. In alcoholics the adiponectin levels are decreased and this also can contribute to liver damage. Rosiglitazone a PPAR-γ agonist is having the ability to attenuate the alcoholic steatosis in mice by increasing the adiponectin levels.
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