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

Breast cancer in men is a rare cancer manifestation, accounting for less then 1% of all breast cancers in both genders. The incidence in Germany during the last years has been approximately 1.0 per year/100,000. In the US, only 0.2% of all malignancies in men. Predisposing risk factors seem to include radiation exposure, hereditary factors, estrogen administration, and diseases associated with hyperestrogenism, such as cirrhosis of the liver or genetic syndromes (i.e. Klinefelter disease). The incidence of male breast cancer is increased in families with a number of first degree relatives affected with breast or prostate cancer. An increased risk of male breast cancer has been reported in families with a mutation of the breast cancer susceptibility gene BRCA-2. For a period of decades, prognosis of breast cancer in males was thought to be worse than that of female patients. Data and cases being published demonstrate that prognosis and strategies of treatment in male breast cancer do not differ from those in females. The cases presented clearly demonstrate that diagnostic work-up, staging procedures and treatment options for primary treatment and advanced stages are identical compared to the recommendation for female breast cancer.
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PMID:Clinical management of breast cancer in males: a report of four cases. 1203 93

Recently, several epidemiologic observations have suggested that obesity might be an independent risk factor for certain malignancies such as breast cancer, colon cancer, renal cell carcinoma, and esophageal adenocarcinoma. However, there are no studies examining the risk of hepatocellular carcinoma (HCC) in obesity. The aim of the present study was to determine whether obesity is an independent risk factor for HCC in patients with cirrhosis. Explanted liver specimens from a national database on patients undergoing liver transplantation were examined for HCC, and the incidence was compared among patients with varying body mass indices according to the etiology of cirrhosis. A multivariate analysis was used for controlling other potentially confounding variables such as age and sex. Among 19,271 evaluable patients, the overall incidence of HCC was 3.4% (n = 659) with a slightly higher prevalence among obese patients compared with lean patients. Obesity was an independent predictor for HCC in patients with alcoholic cirrhosis (odds ratio [OR], 3.2; 95% CI, 1.5-6.6; P =.002) and cryptogenic cirrhosis (OR, 11.1; 95% CI, 1.5-87.4; P =.02). Obesity was not an independent predictor in patients with hepatitis C, hepatitis B, primary biliary cirrhosis, and autoimmune hepatitis. The higher risk of HCC in obese patients is confined to alcoholic liver disease and cryptogenic cirrhosis. In conclusion, more frequent surveillance for HCC may be warranted in obese patients with alcoholic and cryptogenic cirrhosis. However, as this study is based on patients with advanced cirrhosis, our findings need to be confirmed in a broader population of individuals with cirrhosis.
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PMID:Is obesity an independent risk factor for hepatocellular carcinoma in cirrhosis? 1208 59

A 48-year-old woman with Zollinger-Ellison syndrome (ZES), but no evidence of multiple endocrine neoplasia (MEN)-1 syndrome, developed an unusually florid evolution of enterochromaffin-like (ECL) cell hyperplasia, which led to extensive replacement of oxyntic glands by endocrine tissue and resulted in the disappearance of the patient's gastric acid hypersecretion with antisecretory treatment no longer required. The patient's previous history included breast cancer, treated with surgery and 5 years of antiestrogen therapy, and bilateral granulosathecal cell tumor of the ovary. In addition, increased circulating levels of 17 B-estradiol (17BE) and progesterone, possibly depending on concomitant development of liver cirrhosis, were also found. On the basis of these associations, it is suggested that abnormalities in the domain of female sex hormones, with a potential synergistic role of liver dysfunction, may be involved in the florid evolution of hypergastrinemia-driven proliferation of ECL cells observed in the present case.
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PMID:Endocrine Cell Replacement of Oxyntic Glands in Zollinger-Ellison Syndrome: A Role for Female Sex Hormones? 1211 16

Alcohol abuse ranks among the most common and severe environmental hazards to human health. Alcohol is a dependence producing drug and this dependence is associated with an increased risk of morbidity and mortality. While the social and behavioural consequences of alcoholism including psychiatric disorders are staggering, the manifestation of alcohol-related diseases is the most widespread somatic effect. In research conducted both at the social and individual level, alcohol was found to increase the risk of death from a number of specific causes, including injury from traffic accidents and other trauma, violence, suicide, liver cirrhosis, cancer of the liver, breast cancer, haemorrhagic stroke, alcoholic psychosis, alcohol dependence and chronic pancreatitis. The apparent beneficial effect of modest alcohol consumption (one to three drinks per day) on mortality and morbidity rates particularly relating to cardiovascular disease on the other side are of recent interest. Public health policy should aim at reducing the harm done by alcohol use, whilst recognizing its perceived and possible real benefits. The aim of this review is to introduce the reader to the definition of alcohol dependence and alcoholism, and summarize our knowledge about the effects of alcohol consumption on the gastrointestinal tract.
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PMID:Effect of ethanol and alcoholic beverages on the gastrointestinal tract in humans. 1236 39

Alcohol and tobacco consumption are closely correlated and published results on their association with breast cancer have not always allowed adequately for confounding between these exposures. Over 80% of the relevant information worldwide on alcohol and tobacco consumption and breast cancer were collated, checked and analysed centrally. Analyses included 58,515 women with invasive breast cancer and 95,067 controls from 53 studies. Relative risks of breast cancer were estimated, after stratifying by study, age, parity and, where appropriate, women's age when their first child was born and consumption of alcohol and tobacco. The average consumption of alcohol reported by controls from developed countries was 6.0 g per day, i.e. about half a unit/drink of alcohol per day, and was greater in ever-smokers than never-smokers, (8.4 g per day and 5.0 g per day, respectively). Compared with women who reported drinking no alcohol, the relative risk of breast cancer was 1.32 (1.19-1.45, P<0.00001) for an intake of 35-44 g per day alcohol, and 1.46 (1.33-1.61, P<0.00001) for >/=45 g per day alcohol. The relative risk of breast cancer increased by 7.1% (95% CI 5.5-8.7%; P<0.00001) for each additional 10 g per day intake of alcohol, i.e. for each extra unit or drink of alcohol consumed on a daily basis. This increase was the same in ever-smokers and never-smokers (7.1% per 10 g per day, P<0.00001, in each group). By contrast, the relationship between smoking and breast cancer was substantially confounded by the effect of alcohol. When analyses were restricted to 22 255 women with breast cancer and 40 832 controls who reported drinking no alcohol, smoking was not associated with breast cancer (compared to never-smokers, relative risk for ever-smokers=1.03, 95% CI 0.98-1.07, and for current smokers=0.99, 0.92-1.05). The results for alcohol and for tobacco did not vary substantially across studies, study designs, or according to 15 personal characteristics of the women; nor were the findings materially confounded by any of these factors. If the observed relationship for alcohol is causal, these results suggest that about 4% of the breast cancers in developed countries are attributable to alcohol. In developing countries, where alcohol consumption among controls averaged only 0.4 g per day, alcohol would have a negligible effect on the incidence of breast cancer. In conclusion, smoking has little or no independent effect on the risk of developing breast cancer; the effect of alcohol on breast cancer needs to be interpreted in the context of its beneficial effects, in moderation, on cardiovascular disease and its harmful effects on cirrhosis and cancers of the mouth, larynx, oesophagus and liver.
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PMID:Alcohol, tobacco and breast cancer--collaborative reanalysis of individual data from 53 epidemiological studies, including 58,515 women with breast cancer and 95,067 women without the disease. 1294 34

One-third of the breast cancer patients who underwent tamoxifen intake showed less than 0.9 of their liver/spleen CT (computed tomography) ratio on their annual CT study, and were diagnosed as having fatty liver (hepatic steatosis). Among them, patients who showed a lower liver/spleen CT ratio of less than 0.5 were recommended to undergo needle biopsy of the liver in order to obtain histopathological confirmation of non-alcoholic steatohepatitis (NASH), with 15 patients undergoing needle biopsy of the liver. As a result, 14 out of the 15 patients were diagnosed as having NASH, and these patients were additionally administered bezafibrate in order to prevent possible progressive changes of NASH into liver cirrhosis. In this study, we show the changes of follow-up CT findings of 6 patients with histopathologically-proven NASH who continued to undergo bezafibrate intake after the diagnosis of NASH. Two patients showed almost complete improvement as indicated by the liver/spleen CT ratio several months after completion of a tamoxifen intake of 5 years, and another 3 showed partial improvement on their liver/spleen CT ratio by bezafibrate intake in spite of continuing tamoxifen intake. Another patient with diabetes mellitus (type II) showed a continually decreasing liver/spleen CT ratio during adjuvant tamoxifen in spite of bezafibrate intake. Therefore, we concluded that the progression of NASH could be prevented by bezafibrate without any interruption of adjuvant tamoxifen treatment. For patients with diabetes mellitus, critical follow-up using CT study and laboratory tests is considered essential.
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PMID:Follow-up CT findings of tamoxifen-induced non-alcoholic steatohepatitis (NASH) of breast cancer patients treated with bezafibrate. 1288 26

Macrophage inflammatory peptide-1 (MIC-1)/growth/differentiation factor-15 (GDF-15) is a divergent member of the transforming growth factor-beta superfamily cloned by others and us. MIC-1/GDF-15 is expressed in the liver, breast, and colon. Studies have demonstrated a growth-inhibiting effect of MIC-1/GDF-15 on colon and breast cancer cell lines in vitro and on tumor growth in vivo. We previously reported that MIC-1 expression is rapidly induced after a wide variety of murine acute and chronic liver injuries including aniline dye administration. I hypothesized, therefore, that MIC-1/GDF-15 may be a mediator of biliary tract injury and could play a role in regulation of bile duct proliferation. C57BL/6 mice underwent surgical ligation of the common bile duct. Northern blot analysis revealed a time-dependent induction of MIC-1/GDF-15 mRNA in the liver. In situ hybridization of liver sections for MIC-1/GDF-15 expression after bile duct ligation demonstrated a zone 1 or periportal expression pattern, consistent with expression of MIC-1 in periductular hepatocytes. Northern blot analysis of liver mRNA from patients with sclerosing cholangitis or cirrhosis also demonstrated enhanced expression of MIC-1/GDF-15. MIC-1/GDF-15 is expressed after bile duct injury in mice and humans. Taken together with the previously demonstrated growth inhibitory effects of MIC-1/GDF-15 on normal and transformed cells, MIC-1/GDF-15 may play a role in regulation of bile duct proliferation and biliary tumor formation.
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PMID:Induction of MIC-1/growth differentiation factor-15 following bile duct injury. 1459 65

The impact of alcohol intake on mortality from all causes has been described in a large number of prospective population studies from many countries. Most have shown a J-shaped relation between alcohol intake and subsequent mortality, indicating that there are both beneficial and harmful effects of ethanol on health. The risk of death from ischemic heart disease is seen to be significantly increased, and highest among abstainers, but not significantly increased among heavy drinkers. Some studies have found plausible mechanisms for the beneficial effect of light to moderate drinking. Subjects with a moderate alcohol intake have a higher level of high density lipoprotein than abstainers. Further, moderate drinkers are seen to have a lower low density lipoprotein. Also, alcohol has a beneficial effect on platelet aggregation, and thrombin level in blood is higher among drinkers than among non-drinkers. In the other end of the range of intake, the ascending leg of the U-shaped curve has been explained by the increased risk of cirrhosis, pancreatitis, and development oropharynx, oesophagus, and breast cancer. In exploring the French paradox, it has been suggested that wine may have beneficial effects additional to that of ethanol. Recently, several prospective population studies have supported this idea. It is, however, also likely that the apparent additional beneficial effect of wine on health in addition to the effect of ethanol itself is a consequence of confounding.
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PMID:Epidemiologic evidence for the cardioprotective effects associated with consumption of alcoholic beverages. 1500 14

Epidemiological data have identified chronic alcohol consumption as a significant risk factor for upper alimentary tract cancer, including cancer of the oropharynx, larynx and the oesophagus and of the liver. The increased risk attributable to alcohol consumption of cancer in the large intestine and in the breast is much smaller. However, although the risk is lower, carcinogenesis can be enhanced with relatively low daily doses of ethanol. Considering the high prevalence of these tumours, even a small increase in cancer risk is of great importance, especially in those individuals who exhibit a higher risk for other reasons. The epidemiological data on alcohol and other organ cancers is controversial and there is at present not enough evidence for a significant association. Although the exact mechanisms by which chronic alcohol ingestion stimulates carcinogenesis are not known, experimental studies in animals support the concept that ethanol is not a carcinogen but under certain experimental conditions is a cocarcinogen and/or tumour promoter. The metabolism of ethanol leads to the generation of acetaldehyde (AA) and free radicals. Evidence has accumulated that acetaldehyde is predominantly responsible for alcohol associated carcinogenesis. Acetaldehyde is carcinogenic and mutagenic, binds to DNA and proteins, destructs folate and results in secondary hyperproliferation. Acetaldehyde is produced by tissue alcohol hydrogenases, cytochrome P 4502E1 and through bacterial oxidative metabolism in the upper and lower gastrointestinal tract. Its generation or its degradation is modulated due to functional polymorphisms of the genes coding for the enzymes. Acetaldehyde can also be produced by oral and faecal bacteria. Smoking, which changes the oral bacterial flora, and poor oral hygiene also increase acetaldehyde. In addition, cigarette smoking and some alcoholic beverages such as calvados contain acetaldehyde. Other mechanisms by which alcohol stimulates carcinogenesis include the induction of cytochrome P-4502E1, which is associated with an enhanced production of free radicals and enhanced activation of various procarcinogens present in alcoholic beverages; in association with tobacco smoke and in diets, a change in the metabolism and distribution of carcinogens; alterations in cell cycle behaviour such as cell cycle duration leading to hyperproliferation; nutritional deficiencies, such as methyl-, vitamin E-, folate-, pyridoxal phosphate-, zinc- and selenium deficiencies and alterations of the immune system eventually resulting in an increased susceptibility to certain virus infections such as hepatitis B virus and hepatitis C virus. In addition, local mechanisms may be of particular importance. Such mechanisms lead to tissue injury such as cirrhosis of the liver, a major prerequisite for hepatocellular carcinoma. Also, an alcohol-mediated increase in oestradiols may be at least in part responsible for breast cancer risk. Thus, all these mechanisms functioning in concert actively modulate carcinogenesis leading to its stimulation.
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PMID:Alcohol and cancer. 1508 51

It is well known that there are social inequalities in health. Following the ecological approach, unemployment has been one of the most used indicators to study social inequalities. The aim of the present study was to investigate the relationships between indicators of extreme poverty and social unrest, along with unemployment, and mortality in Barcelona, during the years 1989 to 1993. A cross-sectional ecological study was carried out using Primary Health Care Areas (PHCAs) as the unit of analysis. The study population consisted of residents in Barcelona City. The indicators studied as dependent variables were the age-standardized mortality rates of the following causes of death: total mortality; lung cancer; bronchitis, emphysema, and asthma; cirrhosis; cerebrovascular disease; ischemic heart disease; breast cancer; traffic accidents; acquired immunodeficiency syndrome (AIDS); and drug overdose. Independent variables were male unemployment rate of the primary health care areas and indicators of extreme poverty and social conflict. A descriptive analysis, a bivariate analysis using Spearman correlation coefficients, and a multivariate analysis fitting Poisson regression models were carried out. For the main results, one group of causes of death was associated only with unemployment: bronchitis, emphysema and asthma, cerebrovascular disease, and ischemic heart disease (both men and women); lung cancer (only among men); total mortality and cirrhosis (only among women). Among men, another group of causes of death was associated with extreme poverty and/or social unrest, as well as unemployment: total mortality, cirrhosis, and drug overdose. AIDS in men was only associated with extreme poverty and social unrest. We concluded that we see different types of relationships between deprivation and mortality. Unemployment has been related to mortality because of pathologies with socially accepted risk factors (tobacco and alcohol). Causes of death with risk factors not socially accepted (illegal drug use) have been related to indicators of marginality as well as unemployment.
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PMID:Weighing social and economic determinants related to inequalities in mortality. 1527 61


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