Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An unusual case of adenomatous hyperplasia of the liver arose spontaneously in an 82-year-old woman. Massive fatal ascites developed during an eight-week period in the absence of cirrhosis. No drug, chemical, or hormone could be identified as the causative agent. Estrogens may play a role as possible promoters in the growth of hepatic tumors. Identifying liver tumors in women that are not associated with oral contraceptive use is valuable.
 ...
PMID:Adenomatous hyperplasia of the liver. 21 2

Estrogens are known to have mitogenic activities and to influence hematic crasis. A wide literature on this subject allows us to re-evaluate the results of research performed in 1950. Estrogens injected into the peritoneum (estradiol propionate 2.5-5 mg, twice weekly) or into tibial bone marrow (estradiol propionate 1.5 mg weekly) of guinea pigs, after carbon tetrachloride induced cirrhosis (CCI4 inhalation for 7-15 min twice weekly), caused hyperchromic anemia, with erythroblastosis and leucocytosis; hyperplasia of reticulo-hystiocitary cells of bone marrow and lymphoid organs; splenic hemosiderosis; hyperplasia of immature bone marrow cells, with maturative inhibition; and terminal bone marrow hypoplasia. Our results agree with recent literature data concerning the role played by natural estrogens and environmental xenoestrogens that are capable of stimulating bone marrow progenitor cell proliferation and delaying their maturation, by the secretion of growth factors, especially from hyperplastic stromal cells, in solid and hematological tumors.
 ...
PMID:Hematological modifications induced by estrogens in cirrhotic animals. 941 24

There is considerable evidence that reactive oxygen species (ROS) have a causative role in chronic hepatic injury and cancer development via direct and indirect mechanisms. Estrogens produce free oxygen radicals through redox cycling and affect cell proliferation, also in the liver. We are presently involved in evaluating the possible relationship between estrogens receptor expression, type of receptor, oxidative DNA damage and c-myc in chronic liver disease. The data on DNA adducts, c-myc mRNA and variant estrogen receptor in patients with HCV- or HBV-related chronic liver disease are suggesting that those positive for variant liver estrogen receptor present higher genomic oxidative damage, as reflected in 8-OHdG levels. We are also observing that patients with chronic hepatitis and cirrhosis, when positive for variant estrogen receptor, present higher c-myc m-RNA expression, a factor reportedly associated with increased genomic instability, augmented cytoproliferation and carcinogenesis. Our own and other author's data are shedding new light on estrogen pathophysiology, liver damage and hepatic cancer.
 ...
PMID:Estrogens receptors and oxidative damage in the liver. 1216 Oct 6

The effects of dose and duration of estrogen treatment on cholestasis, hepatic regeneration, and the genesis of liver tumors are evaluated in this work. Estrogens, especially at high doses during pregnancy or after long use of oral contraceptives (OCs), cause a constant diminution of bile secretion which remains subclinical in the great majority of cases. Ethinyl estradiol causes a constant but reversible cholestasis in the rat. 2 categories of cholestasis related to estrogens are distinguished in clinical practice; cholestasis induced by estrogens in pregnancy or in OCs, and cholestasis aggravated or revealed by estrogens, such as primitive biliary cirrhosis. Cholestasis induced by estrogens is dose-dependent, but few clinical data are available on this point. Experience has shown that a woman predisposed to cholestasis due to condition even with low-dose combined OCs. OCs are contraindicated for women genetically predisposed to cholestasis. Evidence has been found of an interaction between estrogen and DNA in the initiation of regenerative processes after experimental hepatectomy. 2 benign liver tumors, hepatic adenomas and focal nodular hyperplasias, have become more common with widespread diffusion of OCs. The role of estrogens in the genesis of hepatic adenomas is well established, but is more controversial with focul nodular hyperplasia. The appearance of low- dose OCs does not seem to have decreased the incidence of benign liver tumors. On the other hand, 2 series totalling 113 cases have demonstrated that the risk of adenoma increases significantly with the duration of treatment, and another study of 32 cases of focal nodular hyperplasia and 12 adenomas showed that most of the women had used OCs for more than 5 years. Both types of tumor carry risks of hemorrhagic accidents, and adenomas at least also carry carcinoma appears more significant in a country like Great Britain with a very low prevalence of such cancers. Benign liver tumors are very rare and should not affect prescription of OCs. A hepatobiliary sonogram should be obtained for women seeking OCs. A sonographic image of a tumor less than 5 cm in diameter with the characteristics of a benign tumor should prompt termination of OCs and reexamination in 4 weeks. If the tumor is over 5 cm in diameter the diagnosis should be confirmed by another technique. The nodular hyperplasias that are large, painful, and easily accessible. Recent epidemiologic studies suggest that the prevalence of asymptomatic lithiases is not very different in OC users and nonusers, but the frequency of complications leading to cholecystectomy is greater in women receiving longterm estrogen treatment. An asymptomatic lithiasis in a young OC user does not necessarily require termination of OCs.
 ...
PMID:[Hepatic and biliary repercussions of estrogens: dose or duration of treatment effect]. 1231 61

Estrogens play important roles in the cell proliferation and invasion of estrogen-dependent human neoplasms. Aromatase overexpression has been also reported in hepatitis and hepatocellular carcinoma (HCC) compared with normal liver but its details in these hepatic disorders have remained unclear. Therefore, in this study, we first immunolocalized aromatase using immunohistochemistry in patients with liver cirrhosis, steatosis, hepatitis, HCC, and metastasis liver carcinoma (MLC) in order to study the detailed status of intrahepatic aromatase. Aromatase immunoreactivity was predominantly detected in nonneoplastic hepatocytes around tumor cells. We then evaluated the effects of an interaction between hepatocytes and carcinoma cells upon aromatase mRNA expression, using HepG2 as a substitute model of hepatocytes by coculture systems. Aromatase mRNA levels in HepG2 were significantly increased by coculture with all carcinoma cell lines examined. We also evaluated alternative splicing of aromatase exon 1 but the same splicing variant was used in HepG2 cells regardless of carcinoma cell lines employed in the coculture system. These findings obtained in HepG2 indicated that carcinoma cells, whether metastatic or primary, induced aromatase expression in adjacent normal hepatocytes possibly through the soluble aromatase inducible factors in human hepatic microenvironments.
...
PMID:Aromatase in human liver and its diseases. 2393 Feb 7