Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

70 patients with colic diverticular disease and 50 control subjects were compared. Sexes and ages were matched in the two groups. Significant higher frequencies of alcoholism (P < 0,00001), hyperlipidemia (P < 0,0001), impaired oral glucose tolerance test (P < 0,001), hyperuricemia (P < 0,01) and atherosclerosis (P < 0,000001) were noted in the diverticular group. Hypothesis about pathogenesis of diverticular disease are suggested.
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PMID:[Alcoholism, colic diverticular disease and metabolic disorders (author's transl)]. 23 42

In order to find out if there is an association between alcoholic heart disease and alcoholic liver disease, and to discover the prevalence and characteristics of anatomical findings in the heart at alcoholic subjects, a prospective study was realized during the autopsies of patients younger than 60 years old, who had died with alcoholic liver disease not associated with an obvious heart disease. A second group of subjects containing similar characteristics of the first group, only without a past history of alcoholism nor liver disease, were used as controls. The comparison between the two groups in respect to: age, nutritional status, macroscopic and microscopic findings of the heart, frequency and degree of atherosclerosis revealed no statistical difference. In conclusion, we submit that the subjects who had died from liver disease also presented myocardial alterations, but that these did not differe from those observed in the control subjects.
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PMID:[Primary alcoholic cardiac disease and alcoholic liver disease. Anatomopathological study]. 75 15

Moderate alcohol consumption is associated with a decreased risk of coronary artery disease. The mechanism of the putative protective effect of alcohol intake, however, remains elusive. Recent studies suggest that a ratio of apolipoprotein A-I/apolipoprotein B and Lp(a) are better indicators of the risk of atherosclerosis than total cholesterol and high density lipoprotein cholesterol. To assess the effect of alcohol on these analytes, we determined the concentration of Lp(a), apolipoprotein A-I, apolipoprotein B, total cholesterol, and high-density lipoprotein cholesterol, and calculated low-density lipoprotein cholesterol in serum of 12 patients meeting DSM-III-R criteria for alcohol dependence at the time of admission for treatment of alcohol withdrawal (before). The analyses were repeated after 4 weeks of supervised abstinence on a locked research unit (after). With abstinence, there was a significant increase in the concentration of Lp(a), the atherogenic index and the ratio of low-density to high-density lipoprotein cholesterol but a significant decrease in total cholesterol, high-density lipoprotein cholesterol, apolipoprotein A-I, and the apolipoprotein A-I/B ratio. Apolipoprotein B and low-density lipoprotein cholesterol showed no significant changes before and after alcohol abstinence. Thus, decreased Lp(a) and increased high-density lipoprotein cholesterol and apolipoprotein A-I may be factors mediating the putative protective effect of alcohol in coronary artery disease.
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PMID:The effect of alcohol withdrawal on serum concentrations of Lp(a), apolipoproteins A-1 and B, and lipids. 821 36

In order to evaluate whether plasma beta-thromboglobulin (as a marker of the degree of platelet function) in patients presenting clinically evident atherosclerosis is related to the presence or absence of different risk factors (smoking habit, arterial hypertension, hypercholesterolemia, diabetes, hypertriglyceridemia, obesity, hyperuricemia, alcoholism), 40 patients have been studied in whom mean beta-thromboglobulin levels was 54 +/- 25.56 ng/ml, which is very superior to levels considered normal. However, the presence of one or more risk factors did not lead to significant variations in b-thromboglobulin concentrations, and no differences were found either when each risk factor was considered separately. The positive correlation (r = 0.98; p less than 0.01) between beta-thromboglobulin and apo B levels is highlighted. The results suggest that platelet hyperfunction seems to be due to a greater extent to the atherosclerotic process rather than to the existence of a particular risk factor.
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PMID:[Beta-thromboglobulin levels and atherosclerosis. Its relationship with the presence of risk factors]. 153 62

In this paper, the authors tried to establish the association of alcoholism with arterial hypertension as well as with risk factors for atherosclerosis, which are invariably accompanying arterial hypertension, in engine-room personnel (N = 80), in other seamen of the "Jugolinija" (N = 119), and in the control group which was made up of employees of the Technical Department, Shipyard, "3. maj", Rijeka (N = 108). The chi 2-test showed a statistically significant difference in the prevalence of alcoholism, and the t-test a statistically significant difference in the daily consumption of alcohol between the two groups of seamen and the control group. The prevalence of alcoholism and the daily consumption of alcohol were higher in seamen. There were no such differences between the two groups of seamen. Similarly, arterial hypertension was more prevalent and systolic (SBP) and diastolic blood pressure (DBP) were higher in the two groups of seamen compared with the control group. Since, there were no significant linear correlations between the alcohol consumption and SBP and DBP, it could not be said that higher values of SBP and DBP were positively related to the greater consumption of alcohol in seamen as compared to the control group. No significant linear correlation was found between alcohol consumption and studied risk factors too. However, higher prevalence of arterial hypertension in alcoholics among the engine-room personnel suggested some association of the alcohol consumption with arterial hypertension.
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PMID:[Alcoholism, risk factors and prevalence of arterial hypertension in naval personnel]. 166 26

A wide-range complex of biochemical techniques was used to study metabolic processes in workers exposed to cobalt and ethanol. In practically healthy workers were found laboratory manifestations of hepato-biliary irritations, hyperpermeability of the hepatocytes' cytoplasmic membrane, cholestasis syndrome, initial manifestations of muscular dystrophy and minor signs of atherosclerosis risks. The biochemical shifts were like those in alcoholism cases. It was suggested that, under the existing technological conditions of cobalt-containing hard-facing alloys' powder processing, the action of ethanol increased the toxic effect of cobalt.
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PMID:[Metabolic status in workers engaged in the production of cobalt-containing powder compositions of hard alloys]. 179 96

In case-control study of 53 cases of intracerebral hemorrhage diagnosed by CT scan. Significant risk factors were chronic alcoholism (P less than 0.05), history of hypertension, fundus arteriosclerosis, aorta atherosclerosis, electrocardiogram (ECG) abnormalities, high blood triglycerides, hyperviscosity, hyper-plasma viscosity, hyperfibrinogenemia and increased VWF (P less than 0.01 or P less than 0.001). After principal component analysis hyperviscosity, hypertension, coronary heart disease, ECG abnormalities, chronic alcoholism, and increased VWF were selected as primary risk factors (accumulative contributed rates 59.84%). Alcoholism, EXG abnormalities, aorta atherosclerosis correlates significantly with haemorheology.
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PMID:[Risk factors of intracerebral hemorrhage. A case-control study]. 180 64

To study past histories of patients who died suddenly, we selected cases from all the summary death certificates in which death occurred within 24 hours from the onset of symptoms spanning 1984 to 1986 in Niigata prefecture with a population of 2.5 million. We then re-examined all information on the death certificates to determine the underlying causes. Sudden deaths due to cardiovascular diseases other than acute myocardial infarction and cerebrovascular accident (OCD) accounted for the largest proportion (51.4%). The proportion of death of unknown etiology increased with the decrease in age in both sexes aged 15 to 54 years, accounting for 67.8% in males and 51.1% in females. The number of cases with histories of diseases related to atherosclerosis (e.g. hypertension, old cerebrovascular accident, etc) increased with age in both sexes, accounting for 38.5% in males and 36.4% in females, both aged 75 years old and over. Except diseases related to atherosclerosis, the past histories accounted for 2.5% or greater were as follows: alcoholism (4.1%), psychiatric disorder (PSY, 2.9%) and valvular heart diseases (VD, 2.6%) in 15-54-year-old males; ischemic heart diseases (IHD, 9.4%), arrhythmia without organic heart diseases (ARR, 2.5%) and VD (2.5%) in 55-74-year-old male; IHD (11.4%), bronchial asthma (3.7%), common cold within one month (CC, 3.6%), cor pulmonale or its related diseases (3.0%) and ARR (2.6%) in male of 75 years old and over; PSY (8.7%), IHD (5.8%), VD (5.1%), pregnancy, delivery or related diseases (4.4%), chronic renal failure (3.6%) and CC (2.9%) in 15-54-year-old females; IHD (10.2%), VD (3.2%) and ARR (2.6%) in 55-74-year-old females; and IHD (11.8%) in females of 75 years old and over. When diseases related to atherosclerosis were included, half of the sudden death cases due to OCD had past histories of underlying cause. As descriptions of past histories are often incomplete, there were probably more cases with past histories. The results of this study indicate that investigation of past histories may aid in elucidating and preventing sudden death.
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PMID:[Past histories of sudden death without specific underlying disease]. 184 23

The most important pathophysiological and pathogenetic facts are: The lower autoregulation threshold of cerebral blood flow and hypoxidosis, blood pressure in bradycardia, cerebral fits and stroke marks in CT, carotid atherosclerosis; reduced cerebral metabolism in chronic alcoholism and Wernicke. Reversible hypoglycemic induced hemiplegia. Multiinfarct syndrome and cerebral degenerative process Alzheimer. Effect of treatment by Piracetam.
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PMID:[Pathophysiology, clinical aspects and therapy of pre- and postoperative disorders of cerebral circulation and function]. 198 1

Considerable progress has been made in recent years in our understanding of atherogenesis and, in particular, of how it relates to lipoprotein metabolism. In this conference, we attempt to re-evaluate the data on the relation between alcohol intake and coronary heart disease, emphasizing the effects of alcohol on lipoprotein metabolism. Epidemiologic data generally show an inverse correlation between coronary heart disease risk and moderate alcohol intake (variously defined but generally corresponding to 2 to 4 drinks per day). The potentially drastic effects of excessive alcohol intake on health, however, preclude any recommendation that patients increase their alcohol consumption. Equally, there may be no basis for prescribing moderate alcohol intake but, even here, the data are far from complete. The mechanism by which moderate alcohol intake "protects" remains unclear. Perhaps the best available hypothesis relates to the increased concentration of high-density lipoprotein (HDL) cholesterol associated with moderate alcohol intake. However, it should be stressed that we are still uncertain about the mechanisms linking a high HDL level to protection against coronary heart disease. If a high HDL level is only a marker (and not directly protective), raising HDL levels need not confer protection. Alcoholism, on the other hand, is associated with marked elevation of triglyceride-rich lipoproteins and is among the most common causes of hypertriglyceridemia. Moreover, once hepatic damage occurs, plasma HDL levels may actually be lower than normal. The determining point is that high alcohol intakes are associated with increased overall mortality. Until we know more about the metabolic and behavioral effects of alcohol and about its linkage to atherosclerosis, we have no basis for recommending either that patients increase their alcohol intake or that they start to drink if they do not already.
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PMID:Alcohol and atherosclerosis. 202 65


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