Even though the distinction is actually predicated on presence or lack of a past history of significant alcohol intake, certain histologic features favour one or the other diagnosis

Even though the distinction is actually predicated on presence or lack of a past history of significant alcohol intake, certain histologic features favour one or the other diagnosis. of alcoholic beverages on the liver organ has been known since hundreds of years. A PubMed search shows descriptions of the pathology and ultra-structure in the 1950-1960s[1,2]. Non-alcoholic fatty liver disease (NAFLD) was first explained by Ludwig in 1980 for a set of histological features much like those of alcoholic hepatitis, which he mentioned in liver biopsies of individuals without a significant history of alcohol intake or any medical evidence of alcohol abuse[3]. Therefore the close similarity of histologic findings in the two entities is obvious, however the variations in histology if any, are not well explained. This review intends to describe in detail the histology of alcoholic liver disease (ALD) while highlighting the variations from NAFLD. == ALCOHOLIC LIVER DISEASE == Analysis of alcoholic liver disease can be made in individuals with excessive alcohol intake (20-40 g/d for males and 20 g/d for ladies) and evidence of liver injury[4]. Histologically the spectrum of liver injury in both ALD and NAFLD can vary from simple steatosis to cirrhosis. == HISTOLOGY OF ALCOHOLIC LIVER DISEASE == The liver involvement in ALD classically ranges from alcoholic steatosis, alcoholic hepatitis or steatohepatitis (ASH), and alcoholic cirrhosis. == Alcoholic steatosis == Steatosis is definitely defined as the WS3 build up of lipid droplets in the Rabbit Polyclonal to GSK3beta WS3 hepatocyte cytoplasm. The term fatty degeneration has been used when > 5% of hepatocytes show steatosis while fatty liver is the term explained when > 50% of hepatocytes show steatosis[5]. Presence of steatosis however is not essential for the analysis of ALD as it may actually decrease despite continuing alcohol intake and progression of disease[6]. Steatosis can be macrovesicular or microvesicular, depending not only on the size of the lipid droplet accumulated, but also within the pathogenesis and etiology of disease. In ALD the steatosis is usually macrovesicular or combined microvesicular and macrovesicular. The steatosis begins in the centrilobular Zone 3 and progresses for the periportal Zone 1. It may begin with small droplets of extra fat in the cytoplasm (microvesicular), which later on enlarge to large extra fat droplets (macrovesicular), which drive the nucleus to the periphery. Macrovesicular extra fat droplets can coalesce to form extra fat cysts (large irregular extracellular extra fat vacuole). Continuing build up of extra fat may lead to rupture of extra fat cyst having a histiocytic reaction or lipogranuloma. The macrovesicular extra fat droplets have a high surface/volume ratio and are less susceptible to action of lipases. This allows macrovesicular extra fat to persist for any few months actually after alcohol intake is definitely halted[7]. Microvesicular steatosis is seen as multiple extra fat droplets having WS3 a central nucleus. Pure microvesicular steatosis may be seen in Alcoholic foamy degeneration. This has not been explained in non-ASH (NASH). == Alcoholic steatohepatitis == Steatohepatitis shows evidence of hepatic injury accompanying the steatosis. The injury may be seen in the form of hepatocyte ballooning, neutrophil rich swelling in the lobular parenchyma (Number1), apoptosis or Mallory Denk body. Ballooning degeneration of hepatocytes is the predominant mode of cellular injury in alcoholic hepatitis. The hepatocytes are markedly inflamed with rarified cytoplasm, clumping of intermediate filaments and loss of staining for cytokeratins 8 and 18. The oncotic swelling as a result of severe ATP depletion and increase in intracellular calcium results in loss of plasma membrane volume control, disruption of intermediate filament network, cell swelling and oncotic necrosis[7]. Lytic necrosis following ballooning degeneration is the commoner form of injury in ASH, however apoptosis can also be seen and shows either.