Current Clinical Medicine 2010
DOI: 10.1016/b978-1-4160-6643-9.00075-8
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Alcoholic Liver Disease

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Cited by 5 publications
(9 citation statements)
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“…One hypothesis that has been proposed to explain higher mortality rates in patients with more severe disease is a ceiling effect of drug therapy in preventing the inflammatory cascade and ultimate liver damage. 2,5 Mendenhall and colleagues first described this phenomenon after observing that steroid treatment increased mortality in patients with an MDF > 54. 5 This cutoff should be further studied to determine if a true MDF range of treatment benefit exists before reaching a treatment ceiling.…”
Section: Discussionmentioning
confidence: 99%
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“…One hypothesis that has been proposed to explain higher mortality rates in patients with more severe disease is a ceiling effect of drug therapy in preventing the inflammatory cascade and ultimate liver damage. 2,5 Mendenhall and colleagues first described this phenomenon after observing that steroid treatment increased mortality in patients with an MDF > 54. 5 This cutoff should be further studied to determine if a true MDF range of treatment benefit exists before reaching a treatment ceiling.…”
Section: Discussionmentioning
confidence: 99%
“…1 ALD encompasses AH that occurs as a result of prolonged alcohol consumption and ranges in severity from asymptomatic to liver failure. 2 AH is associated with a high mortality burden, up to 15% at 30 days, which is dependent on disease severity at presentation. 1 Per American Association for the Study of Liver Diseases (AASLD) guidelines, disease severity should be initially established upon presentation in all AH patients to aid in therapeutic management.…”
mentioning
confidence: 99%
“…The cytochrome P450 system is also intimately involved in the metabolism of alcohol; more specifically the cytochrome P450 2E1 (CYP2E1) isoenzyme is involved (21). About 10% of ethanol oxidation occurs in the microsomal cytochrome P450 CYP2E1.…”
Section: Cytochrome P450 2e1 Pathwaymentioning
confidence: 99%
“…Both, alcohol dehydrogenase and acetaldehyde dehydrogenase, cause a reduction of NAD + to NADH (21). This leads to an increase in the NADH/NAD + ratio in the hepatocyte, which promotes lipogenesis and decreases gluconeogenesis and fatty acid oxidation (21). Increased lipogenesis in hepatocytes leads to fat accumulation (steatosis) throughout hepatocytes and liver parenchyma.…”
Section: A Increase In the Nadh/nad + Ratiomentioning
confidence: 99%
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