This 54-year-old man with a long history of alcohol abuse had been admitted to the hospital numerous times for abdominal pain thought to be due to gastritis or a peptic ulcer. On several occasions his serum amylase level was elevated into the range of 300-500 u/L indicating relapsing or recurrent pancreatitisdisorder. Three weeks prior to his demise, the patient began an alcoholic binge. The binge continued until three Three days prior to admission the patient's death at which time he developed fever and malaise, prompting him to cease drinking. He and when he was brought to the hospital he was semi-comatose and with had a fever of 105104.4°F5°F. Shortly after arriving at the hospital, the patient died from massive pneumonia.

== Autopsy Findings ==At autopsy, a necrotizing lobar pneumonia was present which contained organisms consistent with Klebsiella pneumoniae. The liver was enlarged--weighing 2700 grams--and had a yellow-orange color. The liver was firm to palpation and the cut surface had a slightly granular appearance suggestive of early cirrhosis. The pancreas showed multiple areas of fibrosis.

File:IPLab2FattyChange3IPLab2FattyChange3b.jpg|Another low-power photomicrograph illustrates again the pale, washed-out appearance of this tissue. Notice the numerous holes throughout the tissue. There are accumulations of inflammatory cells (arrowsarrow) around portal tracts.File:IPLab2FattyChange4IPLab2FattyChange4b.jpg|A higher-power photomicrograph illustrates more clearly the inflammatory cells (arrowsarrow) around the portal areas.File:IPLab2FattyChange5IPLab2FattyChange5b.jpg|This higher-High power photomicrograph view of the centrilobular area gives the appearance of fatty tissue, as indicated by many empty spaces. Very few normal liver cells can be seen in this slide. A few more normal-appearing hepatocytes are present at the left portion of the slide (arrows)with lipid vacuoles.File:IPLab2FattyChange6.jpg|Another view at In many cases the same power illustrates nucleus is displaced to the proliferation periphery of bile ducts in the interlobular cell and perichordal regions (arrows).File:IPLab2FattyChange7.jpg|A high-power photomicrograph of the liver parenchyma shows that each individual liver cell entire cytoplasm is filled with a large, clear droplet which represents taken up by the space remaining after giant lipid was dissolved by the dehydration procedure used to embed the tissue. Note that each empty space is surrounded by a thin rim of eosinophilic cytoplasm; in many instances, the hepatocyte nucleus can be seen as well. The red body (arrow) seen within a cell in the center of the slide is an acidophilic body associated with alcoholic hepatitisvacuole.

File:IPLab2FattyChange9.jpg|This photomicrograph of the liver is from another patient with a history of alcohol use. There are some clear vacuoles indicating fat droplets (1) and there are numerous red-staining granular deposits within the cytoplasm of hepatocytes (23)this is alcoholic hyalin. Alcoholic hyalin is easily distinguished from red blood cells (32) that are also present in this section.File:IPLab2FattyChange10IPLab2FattyChange10b.jpg|This is a low-power photomicrograph of liver stained with a trichrome stain. In this section, connective tissue stains green blue (arrows) and hepatic parenchymal cells are red. Note that many of the parenchymal cells have clear spaces indicating fatty degeneration. The proliferation of scar tissue between the liver lobules is the result of cirrhosis.

== Virtual Microscopy ===== Liver: Fatty Change and Cirrhosis ===<peir-vm>IPLab2FattyChange</peir-vm> === Normal Liver ===<peir-vm>UAB-Histology-00149</gallerypeir-vm>

* <spoiler text=" What causes hepatocellular steatosis in an alcoholic?"> Alcohol induces hepatic steatosis primarily by: * the shunting of normal substrates away from catabolism and toward biosynthesis due to generation of excess NADH by alcohol dehydrogenase,* impaired assembly and secretions of lipoproteins,* and increased peripheral catabolism of fat. Many other factors also come into play.</spoiler>* <spoiler text=" Is the accumulation of fat in this liver a reversible or an irreversible change?"> Reversible</spoiler> == Additional Resources == === Reference === * [http://emedicine.medscape.com/article/185856-overview eMedicine Medical Library: Cirrhosis]* [http://emedicine.medscape.com/article/170539-overview eMedicine Medical Library: Alcoholic Hepatitis]* [http://www.merckmanuals.com/professional/hepatic_and_biliary_disorders/alcoholic_liver_disease/alcoholic_liver_disease.html Merck Manual: Alcoholic Liver Disease]* [http://www.merckmanuals.com/professional/hepatic_and_biliary_disorders/fibrosis_and_cirrhosis/cirrhosis.html Merck Manual: Cirrhosis] === Journal Articles ===* Satapathy SK, Narayan S, Varma N, Dhiman RK, Varma S, Chawla Y. [http://www.ncbi.nlm.nih.gov/pubmed/11595070 Hyposplenism in alcoholic cirrhosis, facts or artifacts? A comparative analysis with non-alcoholic cirrhosis and extrahepatic portal venous obstruction]. ''J Gastroenterol Hepatol'' 2001 Sep;16(9):1038-43. === Images ===* [{{SERVER}}/library/index.php?/tags/128-cirrhosis PEIR Digital Library: Cirrhosis Images]* [{{SERVER}}/library/index.php?/tags/231-fatty_change PEIR Digital Library: Fatty Change Images]* [http://library.med.utah.edu/WebPath/LIVEHTML/LIVERIDX.html#2 WebPath: Cirrhosis] == Related IPLab Cases ==* [[IPLab:Lab 5:&alpha;1 Antitrypsin Deficiency|Lab 5: Lung: &alpha;1-Antitrypsin Deficiency]]* [[IPLab:Lab 11:Schistosomiasis|Lab 11: Schistosomiasis]]* [[IPLab:Lab 12:Alcoholic Cirrhosis|Lab 12: Liver: Alcoholic Cirrhosis]]