Liver hyperplasia

Coni, P, Pichiri-Coni, G, Ledda-Cohunbano, G.M., Rao, P.M.. Rajalakshmi, S., Sarma, D.S.R. Columbano, A. (1990) Liver hyperplasia is not necessarily associated with increased expression of c-fos and c-myc RNA. Carcinogenesis, 11. 835-839... 

Kotsanis, N. and J. Iliopoulou-Georgudaki. Arsenic induced liver hyperplasia and kidney fibrosis in rainbow trout Oncorhynchus mykiss) by microinjection technique a sensitive animal bioassay for environmental metal-toxicity. Bull. Environ. Contam. Toxicol. 62 169—178, 1999. 

Alteration of Cell Proliferation/Apoptosis Balance by PPARa Activators. PPARa activators produce multiple tumor precursor effects including liver hyperplasia, and altered growth in preneoplastic foci. Increased cell replication induced by PPARa activators may increase the frequency of spontaneous mutations... 

M., Moore, D.D., Huang, W., Tian, J. and Locker, J. (2005) Gadd45fS is induced through a CAR-dependent, TNF-independent pathway in murine liver hyperplasia. Hepatology, 42, 1118—1126. 

CHRONIC HEALTH RISKS conjunctivitis may cause defatting of skin severe injury to the liver hyperplasia of hematopoietic tissue reproductive effects toxic effects may be enhanced by use of alcoholic beverages. 

Ear, nose and throat, endocrine and gastrointestinal systems The safety of ginkgo biloba extract was investigated in rats and mice as part of a U.S. National Toxicology Program [9. Animals were administered com oil extract with or without ginkgo biloba, at different doses, for up to 2 years. Ginkgo biloba induced liver and thyroid hypertrophy in rats and mice liver hyperplasia in rats hyperplasia and atrophy of the epithelium in the nose of rats and inflammation, hyperplasia and ulcer in the stomach of mice. Moreover, there was an increased incidence of thyroid cancer in rats and male mice, and liver cancer in mice [9 ]. 

As regards toxicity, pyrazole itself induced hyperplasia of the thyroid, hepatomegaly, atrophy of the testis, anemia and bone marrow depression in rats and mice (72E1198). The 4-methyl derivative is well tolerated and may be more useful than pyrazole for pharmacological and metabolic studies of inhibition of ethanol metabolism. It has been shown (79MI40404) that administration of pyrazole or ethanol to rats had only moderate effects on the liver, but combined treatment resulted in severe hepatotoxic effects with liver necrosis. The fact that pyrazole strongly intensified the toxic effects of ethanol is due to inhibition of the enzymes involved in alcohol oxidation (Section 4.04.4.1.1). 

Dibutyltin dichloride induced acute pancreatitis and bile duct lesions in rats, depending on dose (6 and 8 mg/kg body weight intravenously) and time (1-24 weeks) (Merkord Hennighausen, 1989 Merkord et al., 1997, 1999 Sparmann et al., 2001). The lesions in the pancreas developed into a pancreatic fibrosis, and the lesions in the liver into liver cirrhosis. A single intravenous administration of dibutyltin dichloride at 4 mg/kg body weight induced a mild interstitial pancreatitis after 2 days (Merkord et al., 2001). Repeated administration of dibutyltin dichloride (4 mg/kg body weight intravenously) to rats at intervals of 3 weeks induced acute interstitial pancreatitis and, after 9-12 weeks, a pancreatic fibrosis and liver lesions (intrahepatic bile duct hyperplasia) (Merkord et al, 2001). 

An elevated activity of serum acid 3-glycerophosphatase was not specific for carcinoma, as Marshall and Amdor found it in 8% of patients with uncomplicated prostatic hyperplasia, in some patients with bone fractures, carcinoma involving the liver, and other diseases of bone and liver. This activity has also been reported to be elevated in 3 of 12 patients with Gaucher s disease. 

Hepatic peroxisome proliferation, characterized by liver enlargement due to hyperplasia and hypertrophy, has been proposed as a basis for differences in species susceptibility to trichloroethylene carcinogenicity. Peroxisomes are membrane-bound organelles which contain enzymes generally involved in lipid metabolism. 

Cyclosporine demonstrates immunosuppressive activity by inhibiting the first phase of T-cell activation. It also inhibits release of inflammatory mediators from mast cells, basophils, and polymorphonuclear cells. It is used in the treatment of both cutaneous and arthritis manifestations of severe psoriasis. The usual dose is between 2.5 and 5 mg/kg/day given in two divided doses. Adverse effects include nephrotoxicity, hypertension, hypomagnesemia, hyperkalemia, alterations in liver function tests, elevations of serum lipids, GI intolerance, paresthesias, hypertrichosis, and gingival hyperplasia. Cumulative treatment for more than 2 years may increase the risk of malignancy, including skin cancers and lymphoproliferative disorders. 

Animal data suggest that renal and liver effects may occur in humans exposed to high doses of hexachloroethane. Kidney and liver effects are not specific to hexachloroethane. Lesions of the kidney (nephropathy, linear mineralization, and hyperplasia) were reported at 10 mg/kg/day or greater in male rats (NTP 1989). Urinalysis also revealed granular and cellular casts in rats exposed to hexachloroethane (47 mg/kg/day or greater) for 13 weeks (NTP 1989). Because other compounds cause similar effects and because some of these effects are unique to male rats, they are not valuable as biomarkers for human hexachloroethane exposure. 

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. 

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