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)

1. The radioimmunoassay (RIA) and the competitive ligand binding assay (CLBA) are convenient routine methods for the precise and reproducible measurement of TBG in large numbers of serum samples. 2. There is an age dependent variation of the TBG-concentration in serum. There is a steady decrease of TBG with increasing age with a minimum between the 20th and 50th year. In higher age TBG increases again significantly. 3. There are significantly negative correlation between TBG-serum levels on the one hand and free T4- and T3- fractions on the other. The low TBG-level in hyperthyroid patients increases gradually to normal during treatment with thyroid blocking drugs, the elevated TBG-concentrations in hypothyroid patients decrease to normal during treatment with thyroid hormones. 4. Estrogen stimulates TBG-synthesis in the liver. During enhanced endogenous estrogen production (pregnancy) as well as during exogenous estrogen application a rise occurs in TBG-concentration in serum, which seems to be dose related. 5. Androgens induces a decrease of the TBG-concentration in serum. 6. During viral hepatitis and in compensated cirrhosis of the liver TBG-concentration is significantly elevated. In cirrhosis of the liver with poor hepatic function the TBG-concentration is decreased. 7. The T4/TBG-quotient is a good parameter to estimate free T4-concentration in serum.
 ...
PMID:[Thyroxine-binding globulin (TBG). Clinical studies on the regulation of TBG concentration in serum and the value of TBG for the evaluation of thyroid function]. 11 50

To study the influence of the adrenal gland on plasma estrogen levels in male patients with hepatic cirrhosis, estrone and estradiol were measured under a variety of experimental conditions. Compared to controls, estradiol levels were moderately elevated by 26% (P is less than 0.05) in patients with hepatic cirrhosis (28.5 +/- 5.4 vs. 36.0 +/- 4.7 pg/ml plasma; n: 12), whereas estrone levels exhibited a two- to threefold increase under basal conditions (32.5 +/- 5.6 vs. 67.8 +/- 20.8 pg/ml; P is less than 0.01). ACTH application resulted in a striking increase in plasma estrone levels in both patients with hepatic cirrhosis and in normal subjects (61.8 +/- 27.5 vs. 27.3 +/- 7.8 pg/ml). During stimulation with ACTH, estradiol levels showed no significant changes. After suppression of the adrenal gland by dexamethasone administered for 5 days, plasma concentrations of estrone and estradiol were found to be reduced. The absolute decrease of estrone was significantly greater in patients with hepatic cirrhosis than in healthy male subjects (35.5 +/- 12.6 vs. 21.3 +/- 6.0 pg/ml; P is less than 0.05; n: 8). Estrogen values, however, were still high in patients with hepatic cirrhosis after 5 days of dexamethasone administration (37.1 +/- 17.6 pg estrone/ml and 23.9 +/- 3.6 pg estradiol/ml plasma). It is suggested that elevated plasma values of estrogens in this disorder may be derived predominantly from adrenal production. Peripheral conversion of androgens to estrone rather than to estradiol appears to be more effective in sustaining plasma levels of estrogens in patients with hepatic cirrhosis.
 ...
PMID:Estrone and estradiol in patients with cirrhosis of the liver: effects of ACTH and dexamethasone. 18 10

Estrogen metabolism was studied in spontaneous hyperthyroidism (Graves disease) and in alcoholic cirrhosis of the liver. The plasma concentration of estradiol-17beta (PCE2) was increased in men with hyperthyroidism. Although the metabolic clearance rate of estradiol-17beta (MCRE2) was reduced, the production rate (PR) of the steroid was increased above normal. The MCRE2 was also decreased in women with hyperthyroidism but the PCE2 and PRE2 was unchanged from normal. The conversion ratio of estradiol-17beta (CRE2E1) was increased in both hyperthyroid men and women. The PCE2 was significantly increased in men with cirrhosis of the liver. The MCRE2 was normal and this resulted in an increase in the PRE2 in this disorder. The CRE2E1 was significantly higher than normal. The plasma concentration of estrone (E1) was elevated in men with both disorders.
 ...
PMID:Estrogen metabolism in hyperthyroidism and in cirrhosis of the liver. 116 83

The pathologic features, clinical presentation and natural history of hepatocellular carcinoma (HCC) developing in the noncirrhotic liver were studied in 61 patients against a background of 63 patients seen concurrently with HCC complicating cirrhosis. Noncirrhotic HCC had a bimodal age distribution, with females predominating the first age-clustering (10-50 years) and males predominating the second age-clustering (50-90 years). Cirrhotic HCC had a unimodal age distribution (40-90 years) with male dominance throughout. Estrogen exposure was noted in 57% of the noncirrhotic HCC women overall and in 80% of those in the younger age-clustering. The majority of noncirrhotic HCC presented with a single hepatic mass or a dominant primary with satellite lesions in contrast to the usual multinodular or diffuse disease seen with cirrhosis. Twenty-nine noncirrhotic patients survived complete resection of disease limited to the liver and exhibited a median survival of 2.7 years with a 5-year survival of 25%. Low histologic grade, minimal necrosis, and the absence of hemoperitoneum, hepatomegaly, and adjacent organ involvement were all favorable prognostic variable. Patients with metastatic or locally unresectable noncirrhotic HCC had a median survival of 9 months, and 24% survived in excess of 2 years. This survival experience is significantly more favorable than cirrhotic HCC patients, who had only a 1.2-month median and a 3% 2-year survival. Low histologic grade, mild mitotic activity and the presence of some fibrosis within the specimen were associated with a favorable outcome in advanced noncirrhotic HCC. The favorable prognosis and heterogeneous composition of the noncirrhotic, when compared to the cirrhotic HCC cohort, may be important considerations in the design and evaluation of future clinical trials.
 ...
PMID:Hepatoma in the noncirrhotic liver. 284 80

Estrogen receptors (ER) were assayed on hepatocellular carcinoma (HCC) and surrounding liver tissue in 30 adult patients. All specimens were obtained at the time of surgery. Cirrhosis of the liver was associated with 28 patients and chronic hepatitis in 2 patients. ERs were detected in 12 of 30 HCCs. The value ranged from 1.4 to 9.2 fmol/mg cytosol protein with the dissociation constant (Kd) value less than 1 nanomol. On the other hand, 13 of 28 cirrhotic livers had measurable amounts of the receptors that ranged from 1.5 to 4.1 fmol/mg cytosol protein. Two livers with chronic hepatitis did not have detectable amounts of ERs. The receptors were not detected in both the tumor and liver in ten patients. The ER titers in HCC did not have any correlation with serum levels of alpha-fetoprotein or carcinoembryonic antigen, hepatitis B virus profiles, and histologic types of the tumor. In the light of the current results, it would be of great interest whether hormone therapy can be used or not as a treatment of naturally occurring HCC in humans.
 ...
PMID:Estrogen receptors in hepatocellular carcinoma. 300 May 73

Idiopathic hemochromatosis in young adults has been increasingly recognized over the last three decades. Younger patients with hemochromatosis frequently have presenting problems other than diabetes, cirrhosis, and hyperpigmentation. A young woman with idiopathic hemochromatosis is described. Arthritis and secondary amenorrhea developed at age 20, and liver biopsy showed hemochromatosis at age 29. Further work-up revealed that the amenorrhea was due to underproduction of pituitary gonadotropins. The patient was treated with phlebotomy. Estrogen and progesterone replacement was begun because of severe osteoporosis. Serum iron studies may be useful in young patients with unexplained amenorrhea and/or arthropathy.
 ...
PMID:Idiopathic hemochromatosis presenting as amenorrhea and arthritis. 357 42

It is well known that females show a greater susceptibility to alcohol-induced liver injury than males. Additionally, females who consume alcohol regularly and have been obese for 10 years or more are at greater risk for both hepatitis and cirrhosis. Female rats on an enteral alcohol protocol exhibit injury more quickly than males, with widespread fatty changes over a larger portion of the liver lobule. Levels of plasma endotoxin, intercellular adhesion molecule-1, free radical adducts, infiltrating neutrophils, and nuclear factor-kappaB are increased about twofold more in livers from female than male rats after enteral alcohol treatment. Estrogen treatment in vivo increases the sensitivity of Kupffer cells to endotoxin. Evidence has been presented that Kupffer cells are pivotal in the development of alcohol-induced liver injury. Destruction of Kupffer cells with gadolinium chloride (GdCl3) or reduction of bacterial endotoxin by sterilization of the gut with antibiotics blocks early inflammation due to alcohol. Similar results have been obtained with anti-tumor necrosis factor-alpha antibody. These findings led to the hypothesis that alcohol-induced liver injury involves increases in circulating endotoxin, leading to activation of Kupffer cells, which causes a hypoxia-reoxygenation injury. This idea has been tested using pimonidazole, a nitroimidazole marker, to quantitate hypoxia in downstream pericentral regions of the liver lobule. After chronic enteral alcohol, pimonidazole binding increases twofold. Enteral alcohol also increases free radicals detected with electron spin resonance. Importantly, hepatic hypoxia and radical production detected in bile are decreased by destruction of Kupffer cells with GdCl3. These data are consistent with the hypothesis that Kupffer cells participate in important gender differences in liver injury caused by alcohol.
 ...
PMID:II. Alcoholic liver injury involves activation of Kupffer cells by endotoxin. 975 87

Phytoestrogens are plant substances that are similar to 17-beta-estradiol and produce estrogenic effects. A protective role in the development of breast and prostate cancer has been hypothesized. Estrogen receptors and their variant forms play a significant role in the pathogenesis of hepatocellular carcinoma (HCC); therefore weak estrogenic substances in the diet may play a role in its development. To investigate the role of phytoestrogens in HCC an investigation of dietary intake of these substances has been performed. Cases, patients at first diagnosis of cirrhosis or HCC were chosen. Questionnaire was built up using indications from previously published papers, extending the registration of details of the diet to reconstruct intake of nutrients for the last year. Interviews were always performed by the same dietician. Quantities determined with the help of photos of servings. Data were analyzed with Winfood database completed with data regarding content in phytoestrogens of food, beverages and seasonings. So far 92 cirrhotic patients and 32 HCCs have been interviewed. No significant difference was registered among the two groups regarding total caloric intake or single nutrients (lipids, carbohydrates, proteins). A significant lower intake of genistein was evidenced in patients at first diagnosis of HCC in comparison with cirrhotics; no significant difference was found in daidzein intake. Lignans intake was strictly related with wine intake; intake was significantly lower in cases only when wine was taken into account otherwise it was similar. Results can be summarized as follows: (1) there are no clear-cut differences (both qualitative or quantitative) between cirrhotics and HCC patients in the overall daily caloric intake while; (2) definite differences exist in the intake of some of the phytoestrogens (genistein, SEC, MAT); (3) differences between cases and controls in SEC and MAT are mainly attributable to lower alcohol intake in cases while; (4) significantly lower genistein intake in HCC only seems due to personal preferences of patients. In conclusion, these differences that we have evidenced in the diet in regard to estrogen-like substances may be relevant in modulating the risk of developing HCC in cirrhotic patients.
 ...
PMID:Phytoestrogens and liver disease. 1216 Oct 5

Unexplained liver test abnormalities are frequent in patients with Turner's syndrome. This cohort study was performed to clarify the histopathologic features, causes, and long-term outcome of liver involvement in these patients. Thirty patients with persistently abnormal liver test results were followed-up for 8.8 +/- 5.2 years. Liver specimens were available in 27 patients. Marked architectural changes were present in 10 patients, including nodular regenerative hyperplasia in six, multiple focal nodular hyperplasia in two, and cirrhosis in two patients. These changes frequently were associated with obliterative portal venopathy lesions and with aortic malformations. There was mild to moderate portal fibrosis in 15 of the 17 other patients, inflammatory infiltrates in nine patients, and nonalcoholic fatty liver disease in 11 patients. Bile duct alterations resembling small duct sclerosing cholangitis were observed in 21 patients (with or without architectural changes). There was no viral, alcoholic, autoimmune, or drug-induced liver damage. Portal hypertension was observed in four patients with marked architectural changes, including three in whom refractory ascites or recurrent variceal bleeding developed, one of whom underwent transplantation. None of the patients without marked architectural changes experienced progressive or decompensated liver disease. There was no evidence of liver toxicity from estrogen replacement therapy. In conclusion, the main causes of liver involvement in Turner's syndrome are vascular disorders, probably of a congenital origin, and nonalcoholic fatty liver disease. In patients with vascular disorders, severe liver disease requiring liver transplantation may develop. Estrogen therapy does not appear to be pathogenically implicated.
 ...
PMID:Vascular involvement of the liver in Turner's syndrome. 1475 43

The potential cytoprotective effects of estrogen in the brain are of special interest in aging, neurodegenerative diseases, exposure to toxins, and trauma. Estrogen effects on neurons have been widely explored, but less is known about estrogen effects on glia. Glial cells are primary targets of ammonia toxicity, which arises from liver disease or failure (such as from cirrhosis in alcoholics), urea cycle disorders, or inborn errors of metabolism. We examined the ability of estrogen to protect glial cells from ammonium chloride toxicity using an in vitro model system. C6-glioma cells in later passage have many astrocytic characteristics and provided a convenient and well established model system for this work. When C6-glioma cells were exposed to 15 mM ammonium chloride, we observed major cell death (only 32% cell survival relative to control) within 72 h. Pretreatment with 17beta-estradiol (10 microM) significantly protected C6-glioma cells from ammonia toxicity (99% cell survival relative to control). In addition to enhancing the viability of C6-glioma cells against ammonia challenge, estrogen pretreatment was also found to protect mitochondrial function as assayed using the MTT reduction assay. Mitochondrial function was reduced to 39% of control levels in ammonia-challenged cultures and was mostly protected by estrogen (72% of control levels). The findings are potentially relevant for the development of therapeutic strategies to protect glial cells against ammonia toxicity resulting from hepatic failure or other causes.
 ...
PMID:Cytoprotective effect of estrogen on ammonium chloride-treated C6-glioma cells. 1520 65


1 2 Next >>