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We examined the human fat-storing cell (Ito cell, lipocyte) in normal and pathologic liver biopsies using toluidine blue staining and transmission electron microscopy. We studied 5 normal patients, 6 non-alcoholic patients with liver steatosis, 8 patients with early alcoholic liver damage, 4 patients with extrahepatic cholestasis, 10 patients with chronic active hepatitis B (N = 2) or C (N = 8) with mild fibrosis, 5 patients with alcoholic cirrhosis and 4 with posthepatitic cirrhosis. We found that fat-storing cells were increased in patients with alcoholic steatofibrosis and extrahepatic cholestasis and decreased in cirrhotic patients. The mean number of lipid droplets per fat-storing cell was significantly increased in patients with alcoholic steatofibrosis. Transmission electron microscopy confirmed the light microscopic findings, especially the accumulation of lipid droplets in fat storing cells in early alcoholic liver disease. Sometimes lipid droplets with different electron density were noted. In cirrhosis there was a more prominent development of intracellular organelles, and cells often changed into a more elongated, myofibroblast-like shape.

The term "microvesicular steatosis of the liver" refers to a variant form of hepatic fat accumulation whose histologic features contrast with the much more common macrovesicular steatosis. Microvesicular steatosis of the liver was originally described in association with conditions who share a number of biochemical and a limited number of clinical features: acute fatty liver of pregnancy, Reye's syndrome, Jamaican vomiting sickness, sodium valproate toxicity, high-dose tetracycline toxicity and certain congenital defects of urea cycle enzymes; they were thought to constitute an entity of "microvesicular fat diseases". In recent years the disease has been described in a wide variety of conditions: alcoholism, toxicity of several medications, delta hepatitis in South America and Central Africa, sudden childhood death, congenital defects of fatty acid beta oxidation, cholesterol ester storage disease, Wolman disease and Alpers syndrome. Not much is known regarding the pathogenesis of microvesicular steatosis but in many instances the primary defect could be a mitochondrial lesion, and inhibition of the mitochondrial beta oxidation of fatty acids has been the most frequently implicated defect. The different conditions associated with microvesicular steatosis are heterogenous in many aspects. Maintaining the concept of "microvesicular fat diseases" as a unique entity seems no longer justified.