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)

To investigate whether specific cancers are associated with the occupation of butcher, as has been reported from other countries, a historical prospective cohort study was undertaken. The cohort consisted of all self employed butchers (n = 552) and pork butchers (n = 310) born since 1880 who set up a shop in the canton of Geneva from 1901 to 1969, and of their wives (n = 887). The study group was followed up from 1901 to 1990 for general mortality, from 1942 to 1990 for cause specific mortality, and from 1970 to 1989 for incidence of cancer. There was no trace of 45 men (5%) and 52 women (6%). Compared with the general population of the canton of Geneva, butchers and pork butchers experienced a significant increase, taking into account 15 years of latency, in mortality from all causes (observed deaths (Obs) 540, expected deaths (Exp) 445.5, standardised mortality ratio (SMR) 121, 90% confidence interval (90% Cl) 113-130). There were significant excesses in incidence and mortality from colorectal cancer, cancer of the prostate, and all malignant neoplasms, and in incidence of cancer of the liver. The risk of lung cancer was significantly increased among pork butchers (SMR 176, 90% Cl 114-262; standardised incidence ratio (SIR) 231, 90% Cl 137-368) but not among butchers (SMR 92, 90% Cl 59-138; SIR 113, 90% Cl 67-179). There was also a significant increase in mortality from cancer of the larynx among butchers. For non-malignant causes of death significant excesses were found among all men for ischaemic heart disease, motor vehicle accidents, and cirrhosis of the liver. Analysis of subgroups showed a cluster of deaths from leukaemia among older butchers born between 1880 and 1899 (Obs 5, Exp 0.6, p < 0.0001). Exposure of pork butchers to polycyclic aromatic hydrocarbons during meat smoking, which was assessed in a contemporary study, might have contributed to their increased risk of lung cancer. The possible role of other factors, especially cigarette smoking, nitrosamines, and oncogenic viruses was discussed. Moreover, there was evidence from another contemporary study that butchers and pork butchers ate more animal fat, and probably more animal protein, than the average male population of Geneva. These results suggest that dietary factors could be implicated in the excesses of colorectal cancer, cancer of the prostate, and ischaemic heart disease. An increased risk for alcohol abuse might explain the excesses of liver cirrhosis, cancer of the liver, cancer of the larynx and motor vehicle accidents. Among all wives overall mortality was similar to that expected (SMR 100, 90% Cl 93-108) and there was no significant excess risk for any specific cancer nor for any non-malignant cause of death. Results for cancer of the cervix uteri, especially among subgroups, suggest an increased risk consistent with previous findings from other countries.
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PMID:Mortality and incidence of cancer among a cohort of self employed butchers from Geneva and their wives. 828 Jun 26

Toxic manifestations of digitalis are one of the most prevalent adverse drug reactions encountered in clinical practice. The estimated incidence is about 20% in hospitalized patients in the USA. The authors describe a rare case of myocardial "catecholamine necrosis" (anteroseptal myocardial infarction) during accidental digitalis intoxication. A male patient, 75 years old, suffering from cirrhosis and ascites, take on by mistake a tablet of digoxin 0.25 mg. four times at day for eleven days. He hadn't heart disease in the past. At the eleventh day the patient showed a deep tiredness and so he was submitted to a clinical examination and electrocardiogram. The ECG demonstrated an anteroseptal myocardial infarction in the second-third electrical stage. The patient was hospitalized. The successive examination revealed: very high plasma digitalis concentrations; an increase of the serum levels of CPK and LDH; a significant increase of plasmatic and urinary catecholamine levels which return to normal values after fifteen days; apical akinesia at the echocardiographic examination; no signs of residual myocardial ischemia to the echo-dypiridamole stress test; normal coronary artery to the coronary arteriography and absence of coronary artery spasm to the ergonovine test. Furthermore the abdominal echography and the abdominal computerized tomography didn't reveal surrenal disease but showed an important liver disease. The patient was free from other cardiac events in the follow-up. Generally, during the digitalis intoxication we observe various rhythm and conduction disturbances. Instead in this case no serious arrhythmias were registered and the main expression of the drug toxicity was an anteroseptal myocardial infarction with undamaged coronary artery. Also the usual extracardiac symptoms and signs of the digitalis intoxication were absent in this case. All these observations can be explained with the pathological increase of the cathecholamine levels, indirectly induced by digitalis; with the direct toxic effect of the drug at the myocardic level; with the contemporary absence of ionic disturbances; with the concomitant liver disease. The direct toxic effect of the digitalis produced an increase in calcium ions availability for the electromechanical coupling and an increase of the intramyocardial pressure; the increase of the adrenergic activity determined contemporary an increase in the oxygen consumption of the myocardial cells, a rise of vascular tone and coronary artery tone and a reduction of the duration of the diastole. All these factors provoked a "primary and secondary" ischemia which evolved toward a real "cathecholamine necrosis" and produced a myocardial infarction. This hypothesis explains the myocardial infarction in absence of injury at the coronary arteriography and without coronary spasm at the ergonovine test; moreover it explains the transient increase in cathecholamine plasma levels observed in the acute phases an normalized after fifteen days. The "cathecholamine necrosis" is an anatomical definition, nevertheless in our opinion it gives account of the rare clinical situation observed.
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PMID:[An unusual case of "catecholamine necrosis" caused by accidental digitalis poisoning]. 855 67

The life expectancy of women in the posttotalitarian Central and Eastern European countries varies at present round 75 years, in Western and Northern Europe it is between 78 and 82 years. Linear extrapolation of these data to the year 2000 indicates that at the onset of the next century the life expectancy of women in Western Europe will be round 83 years, in the posttotalitarian countries round 76 years. In Western Europe the premature mortality of women due to cardiovascular diseases (ischaemic heart disease, cerebrovascular diseases), of the respiratory, digestive, nervous, urogenital system is steadily declining. The mortality rate from neoplasms declines only slightly and in some types of cancer (lungs, mammary glands) it is even rising. Round the year 2000 the cause of premature deaths of 60% of women in Western Europe will be neoplasms, while premature deaths caused by cardiovascular diseases will not amount to more than 20%. In the totalitarian part of Europe since 1970 the premature mortality of women due to cardiovascular diseases (mainly ischaemic heart disease), neoplasms (mainly cancer of the lungs and breast) and cirrhosis of the liver rose steadily. It is likely that in this part of Europe also after the year 2000 premature deaths from cardiovascular diseases and neoplasms will remain the main causes of early deaths and together will account for almost 70% female deaths.
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PMID:[Health status in Europe and its projection up to the year 2000. 2. The female population]. 859 29

Historically, alcohol use by the diabetic patient has been controversial. Recent studies in the general population have shown an improvement in mortality with moderate alcohol intake (one to three drinks per day). This improved mortality is greatest in those individuals who have a higher risk of ischemic heart disease. The mechanisms of the beneficial effects of alcohol include positive effects on insulin resistance, HDL cholesterol, platelet aggregation, and fibrinolysis. Since the diabetic patient has an especially high risk of ischemic heart disease because of these factors, the use of a moderate amount of alcohol should not be discouraged. The short-term risks of heavy or continuous alcohol intake include hypoglycemia, glucose intolerance, and ketone and lactate accumulation. In the long term, heavy alcohol intake is associated with an increased prevalence of cancer, hypertension, cirrhosis of the liver, and symptomatic neuropathy. Moderate alcohol intake taken with a meal has been shown to have little or no effect on postprandial glycemic excursions.
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PMID:Alcohol and the NIDDM patient. 873 20

Alcohol is one of the most widely used addictive substances. It can be assumed that everybody encounters alcohol--ethanol in various forms and concentrations in the course of their lives. A global and social problem of our civilization is alcohol consumption which has a rising trend. Since 1989 the consumption of alcoholic beverages is rising and the mean annual consumption of concentrated ethanol per head is cea 10 litres. In ethanol abuse the organism is damaged not only by ethanol alone but in particular by substances formed during its metabolism. Its detailed knowledge is essential for the knowledge and investigations of the metabolic and toxic effect of ethanol on the organism. Ingested alcohol is in 90-98% eliminated from the organism by three known metabolic pathways: 1-alcohol dehydrogenase, 2-the microsomal ethanol oxidizing system and 3-catalase. Alcohol is a frequent important risk factor of serious "diseases of civilization" such as IHD, hypertension, osteoporosis, neoplastic diseases. Cirrhosis of the liver and chronic pancreatitis are the well known diseases associated with alcohol ingestion and also their most frequent cause. It is impossible to list all organs and diseases which develop as a result of alcohol consumption. It is important to realize that regular and "relatively" small amounts in the long run damage the organism and may be even fatal.
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PMID:[Alcohol]. 892 47

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

Patients with homozygous beta-thalassemia show an abnormal lipoprotein profile. In asymptomatic heterozygotes the lipid pattern is less markedly affected but interestingly related to a diminished cardiovascular risk. The extent and significance of these findings are still a matter of debate and no data are available on lipoprotein(a) plasma levels. Seventy patients with homozygous beta-thalassemia (HT-P), 70 beta-thalassemia trait carriers (TT-C) and 70 sex and age-matched controls were investigated and their plasma lipoprotein profile and apo(a) phenotypes determined. In a subgroup of these same subjects (12 HT-P, 12 TT-C and 24 controls) and in 12 bone marrow-transplanted homozygous beta-thalassemic patients (BMT-P) plasma lipoprotein composition was assessed. HT-P disclosed significantly lower total-cholesterol, LDL-cholesterol, HDL-cholesterol, apo A-I, apo B plasma levels and higher triglyceride concentration than TT-C (-7, -11, -8, -8, -13 and +11%, respectively) or controls (-39, -50, -46, -32, -30 and + 35%, respectively). All lipoprotein subclasses were triglyceride-enriched, while LDLs were also protein-enriched and HDLs protein-depleted. TT-C disclosed a small but significant reduction in apo A-I and apo B plasma levels but only minor lipoprotein abnormalities with respect to the controls. BMT-P lipoprotein composition was intermediate between HT-P and normal subjects. Apo(a) plasma levels did not differ among the groups. A higher prevalence of 'small' apo(a) isoforms was present in HT-P. Within the same 'isoform group', apo(a) plasma levels were significantly lower in HT-P than in TT-C or controls. Since liver cirrhosis is almost always present in HT-P, it is conceivable that an altered hepatic apo(a) synthesis or catabolism due perhaps to diminished apolipoprotein glycation may be involved. In TT-C a partially improved cardiovascular risk profile was apparent (low hematocrit, low LDL-cholesterol and apo B), thus justifying the claim for a low prevalence of ischemic heart disease, but no Lp(a) plasma level modification could be detected.
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PMID:Plasma lipoprotein composition, apolipoprotein(a) concentration and isoforms in beta-thalassemia. 918 Feb 53

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

The objective of this study was to test the hypothesis of a lower mortality from cancer and cardiovascular diseases among men expressing glucose-6-phosphate dehydrogenase (G6PD) deficiency. We designed a mortality study based on death certificates from January 1, 1982 through December 31, 1992 in a cohort of G6PD-deficient men. Cohort members were 1,756 men, identified as expressing the G6PD-deficient phenotype during a 1981 population screening of the G6PD polymorphism. The setting was the island of Sardinia, Italy. Outcome measures were cause-specific standardized mortality ratios (SMRs), which were computed as 100 times the observed/expected ratio, with the general Sardinian male population as the reference. Deaths from all causes were significantly less than expected due to decreased SMRs for ischemic heart disease (SMR, 28; 95% confidence interval [CI], 10 to 62), cerebrovascular disease (SMR, 22; 95% CI, 6 to 55), and liver cirrhosis (SMR, 12; 95% CI, 0 to 66), which explained 95.6% of the deficit in total mortality. All cancer mortality was close to the expectation, with a significant increase in the SMR for non-Hodgkin's lymphoma (SMR, 545; 95% CI, 147 to 1,395). A decrease in mortality from cardiovascular diseases was one of the study hypotheses, based on an earlier human report and experimental evidence. However, selection bias is also a likely explanation. Further analytic studies are warranted to confirm whether subjects expressing the G6PD-deficient phenotype are protected against ischemic heart disease and cerebrovascular disease. This cohort study is consistent with more recent case-control studies in rejecting the hypothesis of a decreased cancer risk among G6PD-deficient subjects. The observed increase in mortality from non-Hodgkin's lymphoma and decrease in mortality from liver cirrhosis were not previously reported.
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PMID:Mortality in a cohort of men expressing the glucose-6-phosphate dehydrogenase deficiency. 942 29

In the period 1989-94, mortality rates for the most important causes of death in people migrated to the Tuscany from other Italian regions were analysed. The area of birth was assessed according to the information on province of birth recorded on death certificates. For this analysis we classified Italy into Tuscany and five broad areas, each including a number of political regions: North-West, North-East, Centre, South and Islands. The number of person-years for calculation of the mortality risks was based on 1991 census data, which also included information on place of birth and on current residence. The risks of death of subjects born in other Italian areas and resident in Tuscany ("migrated populations") in comparison to Tuscany born population were assessed by means of Poisson multivariate regression models. For most sites (particularly for lung and breast), cancer mortality rates were higher among North-West and North-East born people and lower among Centre, South and Islands born people. Gastric cancer mortality was higher in Tuscany born subjects. Cardiovascular diseases mortality was generally lower among people born outside of the Tuscany, with the exception of ischaemic heart disease (higher in North-West and Islands born people). Liver cirrhosis mortality was generally higher in North-West, North-East, South and Islands born subjects (with some differences between males and females). Diabetes mellitus mortality was higher in South and Islands born people. AIDS and opioids overdose mortality was higher in North-West born subjects. Mortality for external causes was higher in people born outside of the Tuscany. Both in males and females, overall mortality was higher in North-West and lower in South born people and lower in Centre and Islands born males.
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PMID:[Mortality in population migrated from other Italian regions to the Tuscany region in 1989-94]. 962 2


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