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)

Nitric oxide was identified as the relaxing factor derived from the endothelium in 1987. Nitric oxide synthesis allows the vascular system to maintain a state of vasodilation, thereby regulating arterial pressure. Nitric oxide is also found in platelets, where it inhibits adhesion and aggregation; in the immune system, where it is responsible for the cytotoxic action of macrophages; and in the nervous system, where it acts as neurotransmitter. A deficit in endogenous synthesis of nitric oxide contributes to such conditions as essential arterial hypertension, pulmonary hypertension and heart disease. An excess of nitrous oxide induced by endotoxins and cytokinins, meanwhile, is believed to be responsible for hypotension in septic shock and for hyperdynamic circulatory state in cirrhosis of the liver. Nitric oxide has also been implicated in the rejection of transplanted organs and in cell damage after reperfusion. Inhaled nitrous oxide gas reduces pulmonary hypertension without triggering systemic hypotension in both experimental and clinical conditions. It also produces selective vasodilation when used to ventilate specific pulmonary areas, thereby improving the ventilation/perfusion ratio and, hence, oxygenation. Nitric oxide inhalation is effective in pulmonary hypertension-coincident with chronic obstructive lung disease, in persistent neonatal pulmonary hypertension and in pulmonary hypertension with congenital or acquired heart disease. Likewise, it reduces intrapulmonary shunt in acute respiratory failure and improves gas exchange. Under experimental conditions nitric oxide acts as a bronchodilator, although it seems to be less effective for this purpose in clinical use.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Nitric oxide]. 789 26

Among cardiovascular diseases coronary artery disease ranks first as cause of death in the age group that is of importance for life insurance. It is the main cause of death in males age 30 and up. More females die from cerebral hemorrhage than from coronary artery disease. From age 50 upwards coronary artery disease is also the main cause of cardiovascular death in females. Over two thirds of all deaths due to gastrointestinal diseases are caused by liver disease, mainly cirrhosis of the liver. Chronic obstructive pulmonary disease causes two thirds of all respiratory deaths. Accidental deaths seem to be a male privilege, since only 20 per cent females are involved. Especially young males are at risk to get killed in an accident. The particular situation of accidents in the elderly mainly due to falls is discussed. Neurological, psychiatric illnesses, alcohol and drug addiction are discussed briefly. Males in general are more prone to commit suicide than females who account for only one quarter of all suicide deaths. Hanging was the preferred method. Young males especially are in danger of killing themselves. The importance of this new method of compiling vital statistics for life insurance purposes is discussed. These are the conclusions: 1. Main risk for life insurance is death due to cancer, mainly of the alimentary and respiratory tract. This applies to the population at large. In females breast and genital cancer are of crucial importance. 2. In males cardiovascular diseases cause slightly more deaths than tumors. From age 30 on coronary artery disease is the main cause of cardiovascular death.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cause of death statistics (III). Sources for insurance medicine: cardiovascular diseases and selected causes of death]. 797 84

Construction laborers have some of the highest death rates of any occupation in the United States. There has been very little systematic research focused exclusively on "laborers" as opposed to other workers in the construction industry. We reviewed the English language literature and various data bases describing the occupational tasks, exposures, and work-related health risks of construction laborers. The sources of information included 1) occupational mortality surveillance data collected by the states of California and Washington and the National Institute for Occupational Safety and Health (NIOSH); 2) National Occupational Exposure Survey; 3) national fatality data; 4) cancer registry data; and 5) case reports of specific causes of morbidity. While the literature reported that construction laborers have increased risk for mesothelioma, on-the-job trauma, acute lead poisoning, musculoskeletal injury, and dermatitis, the work relatedness of excess risks for all-cause mortality, cirrhosis, cerebrovascular disease, chronic obstructive pulmonary disease, ischemic heart disease, and leukemia is less clear. Furthermore, while laborers are known to be potentially exposed to asbestos, noise, and lead, and the NIOSH Job Exposure Matrix describes other potential hazardous exposures, little research has characterized other possible exposures and no research has been found that describes the exposures associated with specific job tasks. More advanced study designs are needed that include a better understanding of the job tasks and exposures to construction laborers, in order to evaluate specific exposure-disease relationships and to develop intervention programs aimed at reducing the rate of work-related diseases.
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PMID:Job tasks, potential exposures, and health risks of laborers employed in the construction industry. 825 61

This paper reviews the effects of pulmonary artery hypertension on gas exchange by exploring three different issues, namely: 1) how does gas exchange behave in diseases characterized by increased vascular tone (primary pulmonary hypertension (PPH), chronic obstructive pulmonary disease (COPD) and interstitial pulmonary fibrosis (IPF)) or decreased vascular tone ("hepatopulmonary syndrome"); 2) how does exercise, as a non-pharmacological tool of increasing pulmonary blood flow, modify gas exchange in these diseases; and 3) how do several drugs that lower (vasodilators) or increase (almitrine) the active component of pulmonary hypertension interact with gas exchange. Available data show that: 1) in PPH a high pulmonary vascular tone enhances gas exchange and when it is lowered, either by oxygen or vasodilators, ventilation perfusion (VA/Q) distributions deteriorate; 2) in COPD a lowered (vasodilators) or augmented (almitrine) active vascular tone is almost invariably paralleled by a deterioration or enhancement of ventilation-perfusion matching, respectively; 3) in IPF an adequate active response of the pulmonary vasculature is essential to maintain gas exchange, both at rest and during exercise; and 4) in patients with liver cirrhosis a low pulmonary vascular tone induces an abnormal VA/Q distribution. In summary, these data show that any situation and/or therapeutic intervention that lowers the active vascular tone deteriorates VA/Q relationships and vice versa. The final effect of pulmonary vascular tone on arterial oxygen tension (PaO2) is less predictable. The reason for this uncertainty is that the actual PaO2 value depends on the interplay of the intra- and extrapulmonary factors that control gas exchange in humans, and not only on the degree of VA/Q mismatching.
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PMID:Effect of pulmonary hypertension on gas exchange. 828 57

For the period 1979-1991, 54% of the 644,045 deaths in Missouri were attributed to nine chronic diseases--cancers of the breast, uterine cervix, lung, colon/rectum; coronary heart disease; stroke; diabetes; chronic obstructive pulmonary disease; hepatic diseases/cirrhosis. Elimination of risk factors and screening have been shown to reduce the mortality caused by these diseases. To evaluate the range in excess mortality in the state, we calculated excess mortality by county and correlated these rates with three sociodemographic variables. Based on these analyses, an estimated 100,000 deaths may have been prevented through prevention and early detection activities.
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PMID:Preventable mortality in Missouri: excess deaths from nine chronic diseases, 1979-1991. 832 Nov 74

We investigated the association of non-insulin-dependent (Type 2) diabetes mellitus and depression symptoms in a representative community-dwelling elderly population independently of other conditions such as gender, age, status, disability, cognitive impairment and a number of chronic medical conditions such as chronic obstructive lung disease, degenerative joint disease, heart disease, cirrhosis of the liver, cholelithiasis, peptic ulcer and kidney stones. A total of 1339 elderly subjects living in southern Italy were randomly selected from electoral rolls and evaluated. All subjects were tested by the Geriatric Depression Scale to detect depression, the Mini-Mental State Examination to study cognitive function and the Activity Daily Living Index to evaluate disability. Non-insulin-dependent diabetes mellitus affected 14.7% of our sample. Depression was more prevalent in women over 75 years of age than in younger women (15.9 vs 8.1%, p < 0.001). In multiple linear regression analysis, diabetes mellitus was found to be significantly associated with depression independently of age, gender, loneliness, cognitive impairment, chronic obstructive lung disease, degenerative joint disease, heart diseases, cancer, kidney disease, cirrhosis of the liver and cholelithiasis. It is concluded that non-insulin-dependent diabetes mellitus is significantly associated with depression in the elderly, which may have clinical implications for the achievement of sufficient blood glucose control.
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PMID:Non-insulin-dependent diabetes mellitus is associated with a greater prevalence of depression in the elderly. The Osservatorio Geriatrico of Campania Region Group. 889 92

1. Adrenomedullin is a potent vasodilating peptide first isolated from phaeochromocytoma and adrenal medulla but also found in the heart, lungs and kidneys. It may also be a paracrine factor because endothelial and smooth muscle cells synthesize adrenomedullin as well as express the receptors. Adrenomedullin induces vasorelaxation by activating adenylate cyclase and also by stimulating the release of nitric oxide. 2. We have developed a specific radioimmunoassay and measured the immunoreactivity of human adrenomedullin in the plasma of 58 male subjects: eight with essential hypertension, 12 with heart failure, 10 with ascites due to cirrhosis, 12 with chronic renal failure, four with hypoxia due to chronic obstructive pulmonary disease and 12 control subjects. 3. Plasma levels (mean +/- SEM) in patients with essential hypertension (16.3 +/- 1.9 pmol/l), congestive heart failure (17.5 +/- 2.8 pmol/l) and renal failure (17.7 +/- 2.5 pmol/l) were raised compared with control subjects (7.8 +/- 1.4 pmol/l, P < 0.05), confirming previous reports. 4. In addition, we observed that plasma levels of adrenomedullin were significantly raised in patients with ascites due to liver cirrhosis (15.5 +/- 1.9 pmol/l) and chronic obstructive pulmonary disease with hypoxia (20.0 +/- 1.5 pmol/l). 5. We concluded that the plasma level of adrenomedullin is raised in a variety of diseases.
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PMID:Elevated plasma levels of human adrenomedullin in cardiovascular, respiratory, hepatic and renal disorders. 903 92

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

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

alpha 1-Antitrypsin (AAT) deficiency, also known as alpha 1-antiprotease inhibitor deficiency, is a disease caused by genetically determined AAT deficiency. It occurs as a result of inheritance of two protease inhibitor (PI) deficiency alleles from the AAT gene locus (designated PI) on chromosomal segment 14q32.1. The most common deficiency allele is PI*Z and a large majority of individuals with severe AAT deficiency are PI type ZZ. The disease occurs predominantly in white persons of European origin and its frequency in Europe and North America is comparable to that of cystic fibrosis (1 in 2000 to 1 in 7000.) Persons with AAT deficiency may have no clinical manifestations. Chronic obstructive pulmonary disease (COPD) with a high frequency of panacinar emphysema is the most prevalent clinical disorder associated with AAT deficiency and the most frequent cause of disability and death. Tobacco smoking is the major risk factor for developing COPD, which generally begins by the third decade of life, much earlier than "usual" COPD that occurs in AAT-replete individuals. Liver disease, the second most frequent clinical manifestation of AAT deficiency, typically presents as cholestasis in infancy but is usually not severe and generally remits by adolescence. Chronic liver disease develops infrequently, although AAT deficiency is the commonest cause of chronic liver disease in childhood. Cirrhosis and carcinoma of the liver affect at least 25% of AAT-deficient adults over the age of 50 years. AAT deficiency appears to be widely underdiagnosed and based on predicted gene frequencies even in the most intensely studied populations, only a small proportion of those predicted to have AAT deficiency have been diagnosed. Human AAT is available in limited quantity for augmentation therapy. This Memorandum summarizes the discussions and recommendations made by participants at a WHO meeting held in Geneva on 18-20 March 1996 to review existing knowledge about this highly prevalent genetic disorder, develop a strategy for enhancing awareness of it among health-care-givers and the general public, and explore new case-finding and disease-prevention strategies.
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PMID:Alpha 1-antitrypsin deficiency: memorandum from a WHO meeting. 944 74


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