Alcoholic liver disease: Information in search of knowledge?

Orrego, H; Israel, Yedy; Blendis, Laurence M.

doi:10.1002/hep.1840010313

Cited by 79 publications

(12 citation statements)

References 220 publications

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“…Hepatomegaly associated with alcohol consumption has traditionally been attributed to fat accumulation (19). However, the increase in liver size involves considerably more than the accumulation of fat over time.…”

Section: Discussionmentioning

confidence: 99%

Identification of Factors Contributing to Hepatomegaly in Severely Burned Children

Barrow

Hawkins

Aarsland

et al. 2005

Shock

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Hepatomegaly is a common postmortem observation in severely burned children, with the liver often tripling in size when compared with normal livers for age, weight, and sex. Lesions identified at autopsy include deposition of large and small fat droplets in the hepatocyte, congestion, centrilobular necrosis, and cholestasis. The present study was designed to identify the primary causes of hepatomegaly in severely burned children postmortem. For this purpose, 41 autopsies were reviewed and, when available, blood and tissue samples were studied. Histopathologic findings showed that large intrahepatocytic fat droplets within hepatocytes and cholestasis were important contributors to hepatomegaly. Liver density and wet/dry weight ratios significantly decreased with increasing liver size. Hepatocyte volume increased with increasing liver size (P < 0.001) as did total fat content (P < 0.001). The liver enzymes, alanine aminotransferase and aspartate aminotransferase, remained normal except within 5 to 10 days of injury and 5 to 10 days of death. Triglycerides made up 4% to 70% of the total fat, with the percentage of triglycerides increasing with the severity of hepatomegaly. Saturated fatty acids represented about 85% of the total fatty acids in normal-sized livers, whereas in the largest livers (400% of predicted), only 25% of the fatty acids were saturated. This study provides evidence that 85% to 90% of the hepatomegaly observed in severely burned children postmortem is associated with hepatocyte enlargement, which includes up to 19% intracellular fat. Increases in extracellular protein, intracellular glycogen, and fluid accumulation may make a minor contribution to postburn hepatomegaly.

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Section: Discussionmentioning

confidence: 99%

Identification of Factors Contributing to Hepatomegaly in Severely Burned Children

Barrow

Hawkins

Aarsland

et al. 2005

Shock

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“…Despite improvements in sanitation and the strict attention paid to infection control in most neonatal intensive care units (NICUs) several large outbreaks of HAV infection have occurred in these settings during the last decade (2)(3)(4)(5). Although HAV infection is usually spread by way of a fecal-oral route, the index case in this report and others (3,4) was not an infected health care worker or parent but an infant who received a blood transfusion contaminated with HAV.…”

Section: Commentsmentioning

confidence: 78%

Statistics and Clinical Trials: the Case of Prednisolone in Alcoholic Hepatitis

Henley

Normolle

1992

Hepatology

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HEPATITIS A-NEW INFORMATION ON AN OLD VTRUS Rosenblum LS, Villarino ME, Nainan OV, Melish ME, Hadler SC, Pinsky PP, Jarvis WR, et al. Hepatitis A outbreak in a neonatal intensive care unit: risk factors for transmission and evidence of prolonged viral excretion among preterm infants. J Infect Dis 1991;164: 476-482. ABSTRACT An outbreak of hepatitis A virus (HAW infection in a neonatal intensive care unit (NICU) provided the opportunity to examine the duration of HAV excretion in infants and the mechanisms by which HAV epi-

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“…The first metabolic product of ethanol metabolism, is acetaldehyde (68). Unlike ethanol, acetaldehyde is metabolically active and toxic (68,(69)(70)(71)(72)(73)(74) and binds nonenzymatically to phospholipids, amino acids and sulfhydryl groups, is capable of adversely effecting membrane function, depolymerizing and denaturing protein and exposing or altering surface antigens. By damaging mitochondria and reducing aldehyde dehydrogenase activity, acetaldehyde may initiate a cycle of ongoing tissue injury (64, 75, 76).…”

Section: Galvad-teles Et Almentioning

confidence: 99%