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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

Helicobacter pylori (H. pylori) is the most common cause of peptic ulcers, and is considered as carcinogenic with respect to gastric cancer and MALT lymphoma. The role of H. pylori in other gastroduodenal diseases like atrophic gastritis and functional dyspepsia has been investigated in hundreds of works, but little is done about what role H. pylori may play in non gastric diseases. Gastro-esophageal reflux disease does not seem to be related to H. pylori but Barrett's esophagus might be. Inflammatory bowel diseases tend to be reverse correlated with H. pylori. In coronary heart disease some studies have shown a connection, others not. Diabetes is not likely to be H. pylori-associated and nor do liver diseases with exception for cirrhosis, where a correlation is possible. Respiratory diseases are little examined but bronchiectasis might have a correlation with H. pylori. A small series of children, who had died in sudden infant death, showed a high rate of H. pylori infection.
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PMID:Non-gastric effects of H. pylori infection: a literature review with respect to non gastric diseases which might be associated with H. pylori infection. 1002 62

Fluvastatin, the first fully synthetic HMG-CoA reductase inhibitor, has been shown to reduce cholesterol in patients with hyperlipidaemia, to prevent subsequent coronary events in patients with established coronary heart disease, and to alter endothelial function and plaque stability in animal models. Fluvastatin is relatively hydrophilic, compared with the semisynthetic HMG-CoA reductase inhibitors, and, therefore, it is extensively absorbed from the gastrointestinal tract. After absorption, it is nearly completely extracted and metabolised in the liver to 2 hydroxylated metabolites and an N-desisopropyl metabolite, which are excreted in the bile. Approximately 95% of a dose is recovered in the faeces, with 60% of a dose recovered as the 3 metabolites. The 6-hydroxy and N-desisopropyl fluvastatin metabolites are exclusively generated by cytochrome P450 (CYP) 2C9 and do not accumulate in the blood. CYP2C9, CYP3A4, CYP2C8 and CYP2D6 form the 5-hydroxy fluvastatin metabolite. Because of its hydrophilic nature and extensive plasma protein binding, fluvastatin has a small volume of distribution with minimal concentrations in extrahepatic tissues. The pharmacokinetics of fluvastatin are not influenced by renal function, due to its extensive metabolism and biliary excretion; limited data in patients with cirrhosis suggest a 30% reduction in oral clearance. Age and gender do not appear to affect the disposition of fluvastatin. CYP3A4 inhibitors (erythromycin, ketoconazole and itraconazole) have no effect on fluvastatin pharmacokinetics, in contrast to other HMG-CoA reductase inhibitors which are primarily metabolised by CYP3A and are subject to potential drug interactions with CYP3A inhibitors. Coadministration of fluvastatin with gastrointestinal agents such as cholestyramine, and gastric acid regulating agents (H2 receptor antagonists and proton pump inhibitors), significantly alters fluvastatin disposition by decreasing and increasing bioavailability, respectively. The nonspecific CYP inducer rifampicin (rifampin) significantly increases fluvastatin oral clearance. In addition to being a CYP2C9 substrate, fluvastatin demonstrates inhibitory effects on this isoenzyme in vitro and in vivo. In human liver microsomes, fluvastatin significantly inhibits the hydroxylation of 2 CYP2C9 substrates, tolbutamide and diclofenac. The oral clearances of the CYP2C9 substrates diclofenac, tolbutamide, glibenclamide (glyburide) and losartan are reduced by 15 to 25% when coadministered with fluvastatin. These alterations have not been shown to be clinically significant. There are inadequate data evaluating the potential interaction of fluvastatin with warfarin and phenytoin, 2 CYP2C9 substrates with a narrow therapeutic index, and caution is recommended when using fluvastatin with these agents. Fluvastatin does not appear to have a significant effect on other CYP isoenzymes or P-glycoprotein-mediated transport in vivo.
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PMID:Clinical pharmacokinetics of fluvastatin. 1136 92

While excessive ethanol consumption can result in higher rate of morbidity and mortality resulting from several diseases including cancer and cirrhosis, epidemiological studies suggest that moderate alcohol ingestion reduces the risk of cardiovascular diseases. However, the precise mechanisms by which moderate alcohol consumption protects against coronary heart disease (CHD) is not fully understood. Epidemiological studies suggest that alcohol consumption influences several risk factors for CHD including blood pressure, plasma cholesterol levels, platelet function, and fibrinolytic parameters, preventing both vascular thrombosis and occlusion. Turning to molecular and cellular levels, ethanol has been shown to act on several signal transduction mechanisms involve in the inhibition of smooth muscle cells proliferation and migration and in the activation of the release of vasoactive factors from vascular cells such as nitric oxide (NO). The latter is of importance since NO has been shown to possess antioxidant, antiaggregant properties, to regulate vascular tone and to inhibit both proliferation of smooth muscle cells and adhesion of leukocytes. Altogether, the above mentioned beneficial properties of moderate concentration of ethanol might help to explain the cardio- and vascular protection induced by ethanol. This review compels several bibliographic data concerning the cardiovascular effect of moderate alcohol consumption.
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PMID:[Moderate alcohol consumption and cardiovascular diseases]. 1176 41

There is abundant epidemiological and clinical evidence showing that light-moderate drinking is associated with a reduced risk of coronary heart disease (CHD), total and ischaemic stroke and total mortality in middle-aged and elderly men and women. The epidemiological evidence suggests a J- or U-shaped relationship between alcohol and CHD. However, the apparent benefits of moderate drinking on CHD mortality are offset at higher drinking levels by increasing risk of death from other types of heart diseases (cardiomyopathy, arrhythmia etc.), neurological disorders, cancer, liver cirrhosis, and traffic accidents. The plausible mechanisms for the putative cardioprotective effects include increased levels of high-density lipoprotein cholesterol, decreased levels of low-density lipoprotein cholesterol, prevention of clot formation, reduction in platelet aggregation, and lowering of plasma apolipoprotein(a) concentration. Thus, alcohol reduces the risk of coronary vascular diseases both by inhibiting the formation of atheroma and decreasing the rate of blood coagulation.
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PMID:Cardioprotective effects of light-moderate consumption of alcohol: a review of putative mechanisms. 1221 28

Information was gathered on the smoking habits of 187,783 white men between the ages of 50 and 69 between January 1 and May 31, 1952. The men were subsequently traced through October 31, 1955. 11,870 men died during this period. The total experience covered 667,753 man years. For microscopically proved cases of cancer and for the total cases reported as cancer it was found that the death rates were higher among regular cigarette smokers than among men who never smoked, that the mortality ratio increased with the number of cigarettes smoked each day, and that the death rates were higher among pipe and cigar smokers than among men who never smoked. 7316 deaths occurred among regular cigarette smokers; this was an excess of 2665 over the 4651 deaths that would have occurred had the age-specific death rates for smokers been equal to that for nonsmokers. Coronary disease accounted for 52.1% of the excess; lung cancer accounted for 13.5% of the excess; and cancer of other sites accounted for 13.5% of the excess. An extremely high association between cigarette smoking and death rates for men with lung cancer was found in both rural areas and large cities. Only 338 deaths were ascribed to pulmonary diseases other than lung cancer. Only 1120 (9.4%) of the 11,870 deaths were attributed to diseases other than cancer, cardiac, circulatory, and pulmonary diseases and accidents, violence, and suicide. Only 3 of the specific disease entities - gastric and duodenal ulcers and cirrhosis of the liver - showed a statistically significant degree of association with smoking habits. The most important finding of this study was the high degree of association between cigarette smoking and the total death rate.
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PMID:Smoking and death rates: report on forty-four months of follow-up of 187,783 men. 2. Death rates by cause. 1230 37

Non-alcoholic steatohepatitis (NASH), is a critical link in the chain of metabolic fatty liver disorders that spans steatosis to cryptogenic cirrhosis. It is the hepatic manifestation of the insulin resistance (or metabolic) syndrome, and provides a clue to understanding fibrotic progression of other chronic liver diseases, particularly hepatitis C. Non-alcoholic steatohepatitis is often the first clinical indication of insulin resistance, with its complications of high blood pressure, coronary heart disease and type 2 diabetes. Among those with risk factors, NASH is common: present in at least 20% of obese adults or children with or without type 2 diabetes, and at least 5% of those overweight. With emerging urbanization, increasing affluence and behavioral changes of physical inactivity and high fat/energy-excessive diet, type 2 diabetes has become common in Asia and the western Pacific rim. The rates range from 7-40%, which in countries like Japan represents a 3-20-fold increase (depending on age) over the last 20 years. The increase is associated with central adiposity, insulin resistance, hepatic steatosis and NASH. After cancer, cirrhosis from NASH is now the second most common age-related cause of death in type 2 diabetes. Reversing these trends must become a public health priority; the first awakenings were evident in Taiwan at the time of this meeting. In order to stimulate clinicians to think more about the importance of metabolic liver disease for development of cirrhosis, this review will cover clinical and laboratory features, natural history and an approach to diagnosis and management of NASH. Some emerging concepts on pathogenesis will be mentioned briefly, but the emphasis will be on the potency of lifestyle adjustments (physical activity and diet) to prevent or reverse fatty liver disorders.
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PMID:Non-alcoholic steatohepatitis: what is it, and why is it important in the Asia-Pacific region? 1254 95

Nonalcoholic fatty liver disease (NAFLD) refers to a wide picture of liver damage, ranging from steatosis to steatohepatitis, fibrosis and cirrhosis. The epidemiological studies demonstrated an association of NAFLD with obesity, type 2 diabetes and hyperlipidemia. Under this light the metabolic syndrome (MS), including NAFLD, obesity, central fat distribution, diabetes, dyslipidemia, hypertension and atherosclerotic cardiovascular disease (CVD) can be considered the link to explain the presence of vascular diseases in patients with NAFLD. In NHANES III, the authors demonstrated that the presence of MS was associated with increased risk of myocardial infarction, stroke or both. In a prospective study on 1209 Finnish middle-aged men without CVD or diabetes at baseline, Lakka showed that MS per se is associated with an increased risk of CVD and all-cause mortality. Finally the Atherosclerosis Risk in Communities (ARIC) confirmed that subjects with MS were 2 times more likely to have prevalent coronary heart disease. From a pathophysiological point of view, growing evidences implicate the oxidative stress as the unifying mechanism for many CVD risk factors. Under this light there is emerging evidence suggesting that there is a significant increase in vascular oxidative stress in patients with MS, with the presence of endothelial dysfunction in the early stage of the syndrome. Indeed, the inflammation process evidentiated in these patients is initiated at the endothelial level, stressing the key role of this active and dynamic tissue in the pathophysiological pathways. Under this light the endothelium can be considered as the last effector of a multi-syndrome and the main target of all the future studies focused on the underlying mechamisms of this complex network. Because of the potential serious public health impact, the comprehension of these patophysiological pathways will be crucial to design new preventive measures and therapeutic strategies.
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PMID:Hepatic steatosis and vascular disease. 1623 88

The article presents a critical analysis of the attempts of other authors to propagate the significance of Helicobacter pylori (HP) infection in the origin and development of a range of extragastric diseases and syndromes. From the position of evidence-based medicine, the author of the article discusses the possibility of HP participation in the development of such diseases as cholelithiasis, primary sclerosing cholangitis, pancreobiliary cancer, hepatic encephalopathy in hepatic cirrhosis, pancreatic diseases, inflammatory bowel diseases, atherosclerosis, coronary heart disease, allergic diseases etc. The author concludes that the attempts to associate the development of these diseases with HP infection are in general unfounded and not evidence-based. The author also adduces his own data on the role of the mucose microflora (other than HP) in the pathogenesis of duodenal ulcer relapses, and the effects of differentiated antimicrobial therapy, which are not less prominent than those of HP eradication.
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PMID:[Helicobacter pylori infection: extragastric effects and diseases (a critical analysis)]. 1675 61

The association between serum lipids and mortality has not previously been established in Thailand. Baseline data from the Electricity Generating Authority of Thailand (EGAT) cohort study, plus a resurvey of the cohort 15 years later were analyzed. Participants were employees of EGAT: 2,702 men and 797 women. Total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), and triglycerides (TG) were taken as predictive variables; age, sex, hypertension, diabetes, cigarette smoking, alcohol drinking, and body mass index were taken as confounders. Dependent variables were all-causes and specific causes of mortality over 17 years of follow-up. The major cause of death among men was cardiovascular disease (CVD); among women, it was cancer. Relative risks (RR) for specific causes of death, for a mmol/L increase in each lipid, were estimated after adjustment for confounding factors using Cox proportional hazards regression. TC and LDL-C were negatively associated with liver cirrhosis mortality, although it was likely that the low cholesterol concentration was a consequence of the disease. HDL-C was negatively associated with CVD mortality (RR = 0.59; 95% confidence interval [CI], 0.39-0.93), coronary heart disease (CHD) mortality (RR = 0.36; 95% CI, 0.17-0.75) and all cause-mortality (RR = 0.68; 95% CI, 0.54-0.87). TG was not associated with mortality. HDL-C is an important risk factor for CVD in middle-class urban Thais. Health promotion programs to improve lipid profiles, such as effective exercise campaigns and dietary advice, are required to increase HDL-C and to help prevent CVD and premature death in Thailand.
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PMID:Associations between serum lipids and causes of mortality in a cohort of 3,499 urban Thais: The Electricity Generating Authority of Thailand (EGAT) study. 1821 84


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