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)

Alcoholism may lead to a great many physical and mental problems in individuals of any age. Elderly alcoholics often have additional problems resulting from the interaction of age related changes in physiology and "heavy" alcohol intake. Some of the more important problems are: Impairment of the immune system with decreased ability to deal with infection or cancer. Increased incidence of hypertension, cardiac arrhythmia, myocardial infarction, and cardiomyopathy. Increased incidence of stroke. Alcohol dementia. Increased incidence of esophageal and other cancers. Cirrhosis and other liver disease. Malnutrition. There seems to be no area in which even moderate alcohol intake is of definite benefit, and some areas in which even small amounts are detrimental.
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PMID:Medical manifestations of alcoholism in the elderly. 875 18

This article summarizes the results of a recent study of atomic bomb radiation and non-cancer diseases in the AHS (Adult Health Study) population by the RERF (Radiation Effects Research Foundation) along with a general discussion of previous studies. The association of atomic bomb radiation and CVD was examined by incidence studies and prevalence studies of various endpoints of atherosclerosis, such as MI, stroke, aortic arch calcification, isolated systolic hypertension, and pulse wave velocity, and, although the excess was small, all endpoints indicated an increase of CVD in the heavily exposed group. Because of the consistency of the results, it is almost certain that CVD is higher among atomic bomb survivors. However, all CVD risk factors associated with lifestyle had not necessarily been adjusted for in studies to date, and it is difficult at present to conclude that the increase in CVD among survivors was a direct effect of radiation. Recent studies have demonstrated almost certainly that uterine myoma is more frequent among atomic bomb survivors. It cannot, at present, be concluded that uterine myoma is caused by radiation, because there are no reported studies of other exposed populations. Further analyses including the role of confounding factors as well as molecular approaches are needed to verify this radiation effect. The relationship between atomic bomb radiation exposure and hyperparathyroidism can now be said to have been established in view of the strong dose response, the agreement with results of studies of other populations, the high risk in the younger survivors, and the biological plausibility. Future studies by molecular approaches, etc., are needed to determine the pathogenic mechanism. Among other benign tumours, a dose response has been demonstrated for tumours of the thyroid, stomach and ovary. Although fewer studies have been conducted than for cancer, a clear association between radiation and various benign tumours is emerging. Concerning the association between atomic bomb radiation exposure and chronic liver diseases, the recent incidence study of members of the AHS population demonstrated a significant dose response. Both chronic hepatitis and cirrhosis were suggested as being associated with exposure. The possibility that the increased occurrence of chronic liver diseases among the survivors may be due to hepatitis virus infection cannot be excluded, and the results of the ongoing hepatitis C virus antibody titre studies are awaited.
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PMID:Profiles of non-cancer diseases in atomic bomb survivors. 889 51

4.1 CURRENT STATUS. While an extensive clinical literature of MRS of muscle, brain, heart and liver has been achieved, the MRS technique is not considered essential for routine diagnosis because it is inherently insensitive and metabolic changes tend to be small. However, MRS techniques have proven to be of considerable value for prognosis in some circumstances, notably for predicting outcome following hypoxic-ischaemic injury in the newborn and also in predicting graft viability following organ transplantation. The chemical specificity of MRS has been illustrated, and exploiting the non-invasive nature of the technique, metabolic fingerprinting of pathophysiological processes throughout the natural history of a wide variety of diseases is now being accomplished. Particularly exciting are the applications of 13C MRS for measuring hepatic and muscle glycogen levels, for example in diabetics, and the use of hepatic 31P MRS for assessing liver function in cirrhosis. Other areas of excitement are the applications of 1H MRS in assessing neuronal function in epilepsy and stroke, and for measuring the evolution of lactate in stroke and hypoxic-ischaemic encephalopathy. Emphasis on technique development continues, and applications still tend to be technology-led. The availability of routine clinical MRI systems with spectroscopy capabilities has given MRS studies wider applicability. The recent improvements in spatial resolution have been impressive and the technique is slowly becoming more quantitative. 4.2. FUTURE PERSPECTIVES. Given the flexibility of clinical magnetic resonance techniques, particularly magnetic resonance imaging, it is likely that MRI will be the diagnostic tool of choice in a wider range of diseases, such as multiple sclerosis, stroke, neurodegenerative conditions, sports injuries and in staging malignancies. Since proton magnetic resonance spectroscopy packages have become a routine addition to many MRI systems, it is feasible to select the MRI sequences of most value in highlighting anatomical and pathological abnormalities and to incorporate specifically selected MRS sequences to emphasize biochemical differences. Improvements in technical methodologies are central to further developments. For example, use of internal coils, such as implantable or endoscopic coils, will enable small regions of tissue to be studied in considerable detail, which may otherwise be inaccessible to measurement. Chemical MRS studies have benefited from the use of higher magnetic fields, and the same may be expected for clinical MRS studies. Whole-body magnets up to 4 T have been used in a few centres, and certainly 3 T systems are becoming more widely available with the recent tremendous interest in functional imaging. Certainly, better control of artefacts can be expected; for example, improved definition of spectral changes due to voluntary or involuntary movements. Wider use of proton decoupling methods will improve the specificity of the spectra, by allowing definitive assignments of overlapping resonances, as well as the sensitivity. Comparing PET and MRS studies, it is becoming increasingly obvious that both will be required in parallel to explore parameters of brain metabolism and function. The ability to measure 13C MR signals in the brain has been demonstrated, which allows measurements of glutamate and glucose turnover. MRS measurements have the advantage of not requiring a radioactive isotope, as well as being insensitive to activity-related changes in regional cerebral blood flow. Also the study of cerebral glucose metabolism by MRS is very promising, allowing a resolution and sensitivity comparable to PET. A combination of MRS and PET studies will allow the pathogenesis of neuropsychiatric disorders to be better understood. (ABSTRACT TRUNCATED)
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PMID:Development and applications of in vivo clinical magnetic resonance spectroscopy. 902 41

Premature chronic disease mortality continues to be a problem among American Indian populations. To document the chronic disease burden in the Wisconsin American Indian population, age- and sex-specific incidence-density mortality rates for ten chronic diseases (ischemic heart disease, stroke, diabetes, chronic obstructive pulmonary disease, cirrhosis, and cancer of the breast, cervix, lung, colorectum and prostate) were estimated for a 10-year period (1984-1993) and compared with the Wisconsin non-Hispanic white population. Compared with whites, American Indians had markedly higher mortality rates from diabetes and cirrhosis in all age- and sex-specific groups. Ischemic heart disease mortality was significantly greater in both American Indian men and women 45-64 years of age (Rate Ratio [RR] = 1.7 and 2.1, respectively) compared to whites of the same age, but was lower in American Indians 65 years of age or older (RR = 0.9 for both sexes). Overall, these ten chronic diseases were responsible for a significant excess number of deaths in middle-aged American Indian men and women (i.e., 45-64 years of age), whereas the chronic disease mortality experience of older American Indian men and women (i.e., > or = 65 years of age) was similar to that of the older white population. Diabetes and cirrhosis were the most important causes of increased mortality overall; however, ischemic heart disease was responsible for a large number of excess deaths in middle-aged American Indian men and women.
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PMID:Chronic disease mortality among Wisconsin Native American Indians, 1984-1993. 904 31

It seems that hypervolemia and vasodilatation coincide in compensated cirrhosis, but neither rank nor importance of these factors has been fully clarified in adaptive response to postural change. We studied, with gated equilibrium radionuclide angiography and thoracic electrical bioimpedance the hemodynamic status of 19 patients with compensated cirrhosis and 18 healthy subjects in upright and supine positions. In the upright position, the cirrhotic patients were hypotensive and had decreased peripheral vascular resistance despite increased cardiac output. The transition to the supine position was accompanied by a significant fall in the heart rate and an increase in the stroke volume in both controls (92 +/- 22 to 63 +/- 10 beats/min, and 38 +/- 9 to 62 +/- 19 ml/m2, respectively) and cirrhotic patients (101 +/- 20 to 79 +/- 13 beats/min, and 44 +/- 15 to 63 +/- 19 ml/m2, respectively). Besides, the diastolic arterial pressure fell in controls from 89 +/- 9 mmHg to 81 +/- 11 mmHg; p < 0.01, while it remained unchanged in cirrhotic patients (77 +/- 17 vs 82 +/- 13 mmHg). In the supine position, the cirrhotic patients presented tachycardia and left ventricular hyperkinesy (increased velocity of left ventricular filling and emptying). In conclusion, these results show that in compensated cirrhosis the decreased arterial tone and peripheral blood pooling are important factors of adaptive hemodynamic reaction to postural change.
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PMID:Cardiovascular status after postural change in compensated cirrhosis: an argument for vasodilatory concept. 906 72

Cigarette smoking has been clearly and unambiguously identified as a direct cause of cancers of the oral cavity, oesophagus, stomach, pancreas, larynx, lung, bladder, kidney and leukaemia, especially acute myeloid leukaemia. Additionally, cigarette smoking is a direct cause of ischaemic heart disease (the commonest cause of death in western countries), respiratory heart disease, aortic aneurysm, chronic obstructive lung disease, stroke, pneumonia and cirrhosis and cancer of the liver. Cigarette smoking can kill in 24 different ways and, although smoking protects against several fatal and non-fatal conditions, the adverse effect of smoking on health is largely negative. In developed countries as a whole, tobacco is responsible for 24% of all male deaths and 7% of all female deaths: these figures rise to over 40% in men in some countries of central and eastern Europe and to 17% in women in the United States. The average loss of life of smokers is 8 years. Among United Kingdom doctors followed for 40 years, overall death rates in middle age were about three times higher among doctors who smoked cigarettes as among doctors who had never smoked regularly. About half of all regular cigarette smokers will eventually be killed by their habit. The important information is that it is never too late to stop smoking: among United Kingdom doctors who stopped smoking, even in middle age, there was a substantial improvement in life expectancy. World-wide, smoking is killing three million people each year and this figure is increasing. In most countries the worst is yet to come, since by the time the young smokers of today reach middle or old age there will be about 10 million deaths/year from tobacco. Approximately 500 million individuals alive today can expect to be killed by tobacco, 250 million of these deaths will occur in middle age. Tobacco is already the biggest cause of adult death in developed countries. Over the next few decades tobacco could well become the biggest cause of adult death in the world. For men in developed countries, the full effects of smoking can already be seen. Tobacco now causes one-third of all male deaths in middle age (plus one fifth in old age). Tobacco is a cause of about half of all male cancer deaths in middle age (plus one-third in old age). Of those who start smoking in their teenage years and keep on smoking, about half will be killed by tobacco. Half of these deaths will be in middle age (35-69) and each will lose an average of 20-25 years of non-smoker life expectancy. In non-smokers in many countries, cancer mortality is decreasing slowly and total mortality rapidly. The war against cancer is being won slowly: the effects of cigarette smoking are holding back this victory. Lung cancer now kills more women in the United States each year than breast cancer. For women in developed countries, the peak of the tobacco epidemic has not yet arrived. Tobacco now causes almost one-third of all deaths in women in middle age in the United States. Although it has only 5% of the world's female population, the United States has 50% of the world's deaths from smoking in women. Tobacco smoking is a major cause of premature death. Throughout Europe, in 1990 tobacco smoking caused three quarters of a million deaths in middle age (between 35 and 69). In the Member States of the European Union in 1990 there were over one quarter of a million deaths in middle age directly caused by tobacco smoking: there were 219700 in men and 31900 in women. There were many more deaths caused by tobacco at older ages. In countries of central and eastern Europe, including the former USSR, there were 441200 deaths in middle age in men and 42100 deaths in women. There is a need for urgent action to help contain this important and unnecessary loss of life. In formulating Recommendations, the European Cancer Experts Consensus Committee recognised that Tobacco Control depends on various parts of society and not only on the individual.
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PMID:Cancer, cigarette smoking and premature death in Europe: a review including the Recommendations of European Cancer Experts Consensus Meeting, Helsinki, October 1996. 919 26

Tumor necrosis factor-alpha (TNF) causes vasodilatation and a hyperdynamic state by activating nitric oxide (NO) synthesis. Tyrphostins, specific inhibitors of protein tyrosine kinase (PTK), block the signaling events induced by TNF and NO production. A hyperdynamic circulatory syndrome (HCS) is often observed in portal hypertension (PHT). TNF and NO seem to mediate these hemodynamic changes. The aim of this work was to study the effect of PTK inhibition on the systemic and portal hemodynamics, TNF and NO production, in cirrhotic rats with portal hypertension. Rats with liver cirrhosis induced by chronic inhalation of carbon tetrachloride were used. Animals were treated daily with tyrphostin AG 126 (alpha-cyano-(3-hydroxy-4-nitro) cinnamonitrile) or placebo for 5 d. Mean arterial pressure (MAP), heart rate (HR), and portal pressure (PP) were measured by indwelling catheters. Cardiac output (CI) and stroke volume (SV) were estimated by thermodilution, systemic vascular resistance (SVR) was calculated (MAP/CI), and portal systemic shunting (PSS) was quantitated using radioactive microspheres. Serum and mesenteric lymph node (MLN) TNF levels were measured using an immunoassay kit, and serum NOx was determined photometrically by its oxidation products. The AG 126-treated group showed a statistically significant increase in MAP and SVR, and decreases in CI, SV, MLN TNF, and serum NO oxidation products nitrite and nitrate (NOx) in comparison with the placebo-treated rats. No significant differences were noticed in HR, PP, PSS, or serum TNF. Significant correlations were observed between MAP and NOx, MAP and MLN TNF, PSS and NOx, and serum TNF and serum NOx. The HCS observed in PHT seems to be mediated, at least in part, by TNF and NO by the activation of PTKs and their signaling pathways. PTK activity inhibition ameliorates the hyperdynamic abnormalities that characterize animals with cirrhosis and PHT.
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PMID:Tyrosine kinase inhibition ameliorates the hyperdynamic state and decreases nitric oxide production in cirrhotic rats with portal hypertension and ascites. 923 14

To determine the mortality experience of Hispanic residents of New York City and the influence of birthplace on their mortality rates, NYC Department of Health mortality records for 1988 to 1992 were linked for analysis with 1990 United States census data for New York City. Age-specific death rates for all Hispanics were compared by birthplace with those of non-Hispanic whites. Age-adjusted death rates were also compared. Overall, Hispanics had death rates lower than non-Hispanic blacks, and death rates similar to those of non-Hispanic whites. Hispanics had higher rates of death from HIV-infection, diabetes, stroke/hypertensive disease, cirrhosis and homicide, and fewer deaths from cancer and coronary heart disease than did non-Hispanic whites. Moreover, there were substantial differences in mortality between Hispanic subgroups categorized by birthplace. Migrants from Puerto Rico had the highest, and those from Central and South America the lowest mortality rates. United States-born Hispanics, although younger, had age-adjusted mortality rates higher than New York City non-Hispanic whites. In summary, the mortality of Hispanics generally approximated that of non-Hispanic whites, and was lower than that of non-Hispanic blacks. However, stratification of Hispanics by birthplace revealed substantial variation within the Hispanic population of New York City.
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PMID:The influence of birthplace on mortality among Hispanic residents of New York City. 925 56

In this article, as part of an evaluation of the future of medical education in California, we characterize the distribution of disease and injury in California; identify major factors that affect the epidemiology of disease and injury in California, and project the burden of disease and injury for California's population to the year 2007. Our goal is to elucidate the major causes of illness and disability at present and in the near future in order to focus state resources on the interventions likely to have the greatest impact. Data from various governmental agencies were utilized; the base year, 1993, is the most recent year with sufficient information available when this report was prepared. Several major risk factors have decreased, including smoking (30% decline from 1984 to 1993) and drinking and driving. However, hypertension prevalence has not changed, and overweight has increased dramatically. Poverty continues to burden about 15% of Californians, with poverty highest among children. During 1993, 220,271 Californians died, with 3 major causes accounting for 61% of these deaths: coronary heart disease (31%), cancer (23%), and stroke (7%). In terms of potential years of life lost (years lost before age 65), the most important causes of death in 1993 were unintentional injury (756 years lost/100,000 population), cancer (632 years), and the acquired immunodeficiency syndrome (AIDS; 491 years). Mortality rates were highest among blacks and lowest among Asians. Overall mortality in California has been declining for decades; in just 1 decade, from 1980 to 1991, mortality declined from 780 to 680 deaths per 100,000 population. Several major causes of death have declined, including coronary heart disease, stroke, unintentional injury, cirrhosis, and suicide, while others have increased, for example, chronic obstructive lung disease and diabetes mellitus. Death from AIDS increased dramatically in the past decade, but is leveling off, and death from cancer is beginning to decline. Rates for overall mortality and morbidity, and for most specific conditions, should continue to decline. A projected 28% population increase by 2007 will yield a corresponding increase in the absolute level of disease cases and death; a disproportionate increase in younger and older groups will yield increased conditions affecting young (unintentional injury, AIDS) and older (heart disease, cancer, stroke, diabetes mellitus) people. Californians should experience overall improved health in coming years, reaping benefits of reduced environmental and behavioral risk factors as well as improved medical treatment and rehabilitation. Coordinated strategies for health promotion, disease prevention, delivery of medical treatment, and rehabilitation are needed to maintain and improve present levels of health across the life span.
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PMID:Disease and injury in California with projections to the year 2007. Implications for medical education. 961 96

Many epidemiological studies have shown that moderate alcohol intake, from 10 to 30 g of ethanol a day, decreases cardiovascular mortality from atherosclerotic ischaemic heart disease and ischaemic stroke as compared to non-drinkers. This beneficial effect outweighs the risks of alcohol consumption in subgroups of people with a higher risk of atherosclerosis: the elderly, people with coronary risk factors and patients with previous coronary events. It has not been demonstrated that alcohol intake, even in moderate amounts, is beneficial for the general population, in particular, men under the age of 40 and women under 50, because it raises mortality due to other causes, especially injury, cirrhosis of the liver and some types of cancer, thereby outweighing the benefits for coronary artery disease. Thus, alcohol consumption should not be recommended as a prophylaxis for the general population. Guidelines on alcohol drinking habits--whether to continue, to start, to modify or to stop--must be given on an individual basis, taking into account the relative risks and benefits for each patient. The benefits of moderate alcohol consumption on the cardiovascular system seem to be exerted fundamentally through its effects on plasma lipoproteins, principally by raising high density lipoprotein (HDL) cholesterol and to a lesser degree, by decreasing low density lipoprotein (LDL) cholesterol. It appears to exert additional beneficial effects on the heart by decreasing platelet aggregability and by bringing about changes in the clotting-fibrinolysis system. Although there has been some debate about the relative superiority of different types of alcoholic beverages (wine, beer or hard liquor), and to a greater extent, about different types of wine, there is no current evidence of any kind of beneficial effect from other components of the beverage besides ethanol. Thus, it does not seem appropriate to recommend any particular type of alcoholic drink, except for sociocultural reasons. The added benefits from some components of different types of wine with a high antioxidant activity on plasma lipoproteins remain only an interesting hypothesis. Meanwhile, encouraging a healthy diet, flavonoid rich and with a predominance of natural ingredients (fruit, legumes, cereals and seeds), in the general population should stop the current tendency of Southern European countries from abandoning the Mediterranean diet. Because of the multifactorial nature of coronary heart disease, it is necessary to remember that atherosclerotic risk reduction is achieved by behavior modification of multiple risk factors present in individual patients and in the general population. Therefore, guidelines regarding alcohol intake should always be linked to pertinent recommendations about other atherosclerotic risk factors.
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PMID:[Wine and heart]. 1021 74


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