Liver cell hyperplasia

A classical example is alcoholic cirrhosis, which in the case of chronic alcohol abuse, leads to multiple, polyclonal areas of liver cell hyperplasia and an increased risk for development of hepatocellular neoplasia. In both preneoplasia and certain forms of hyperplasia, the antecedent lesions typically have a higher rate of cell proliferation than the surrounding normal cells and, thus, these cells are at increased risk to sustain additional genetic damage and progress to the next stage in the carcinogenic process. 

A wide spectrum of hepatic lesions has been reported in AIDS (H4), but it is not known whether the changes are related to the presence of HIV-1. Therefore, sections from livers of autopsied patients with AIDS were examined for the presence of HIV-1 antigen p 24 (core) and gp 41 (envelope) by the avidin-biotin-peroxidase complex methods using monoclonal antibodies. The most common histologic abnormalities were steatosis, portal inflammation, Kupffer cell hyperplasia, and focal hepatocellular and bile duct damage. Immunoreactivity for HIV-1 antigens was demonstrated in 80% of cases. 

In two-year studies, lesions attributed to administration of the sulfate salt in rats included liver cystic degeneration in males and hepatocyte cytoplasmic vacuolization in animals of each sex. No lesion was reported in treated mice. When treated with the chloride salt, mice and rats showed hepatocyte cytoplasmic vacuolization. Moreover, male rats showed liver cystic degeneration, female mice displayed thyroid follicular-cell hyperplasia and female rats spleen haematopoeisis (lARC, 1990). 

Other Species. The discussion of hepatic effects in the above subsections is based on effects in rats and mice. Not all animal species are equally susceptible to the hepatic effects of DEHP. Differences in responsiveness are particularly evident with respect to the increases in peroxisomal content of liver cells, induction of peroxisomal enzymes, and increased liver weight (hypertrophy and hyperplasia). Although these responses clearly occur in rats and mice, hamsters are only partially responsive and guinea pigs, and monkeys are refractory. 

The following lesions may be hypoechoic (7.) metas-tases, (2.) liver cell carcinoma, (3.) adenomas, (4.) focal nodular hyperplasia, (5.) abscesses, (6.) haematomas, (7.) early liver infarction, (S.) foci showing reduced fatty infiltration, (9.) lymphomas, and (10.) lipomas. In individual cases, differentiation between a benign and a malignant structural defect may cause considerable difficulties. (59) (s. fig. 9.4)... 

Mast cell hyperplasia can affect several organ systems. Regarding the liver, 50% of cases present as hepatomegaly. Mast cell infiltrates are found in the portal fields. They can lead to occlusion of the small vessels with subsequent fibrosis or cirrhosis. (112) Moreover, there is evidence of marked lymphadenopathy and skin lesions. Polygonal cells with eosinophilic granules are... 

Bioulac-Sage P, Balabaud C, Bedossa P, et al. Pathological diagnosis of liver cell adenoma and focal nodular hyperplasia Bordeaux update. J Hepatol. 2007 46 521-527. 

After chronic exposure to hydroquinone, nephropathy occurred in 80% of male rats, 27% of female rats, and not at all in mice. Mice developed squamous cell hyperplasia in the stomach 67% of male mice developed hypertrophy of the liver and 47% developed hepatocellular adenoma. No differences in survival, however, were noted between treated animals and controls (Hoffman-Bohm and Simon 1992). 

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