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Biomedical subjects

E Sacanella

Publications and source records attributed to E Sacanella.

At least 19 recordsLinked to original sources
PubMed2003

The effect of alcohol consumption on endothelial adhesion molecule expression.

Endothelial adhesion molecules (AM) play an important role in the pathogenesis of several diseases namely infections, neoplasms and chronic inflammatory diseases. Because alcoholic hepatitis and even atherosclerosis are considered as inflammatory diseases and ethanol may modulate inflammatory response, several researchers have investigated the link between ethanol consumption, endothelial AM and the development of both processes. In vitro, animal and human studies have analysed the effects of ethanol and non-alcoholic components of alcoholic beverages on inflammatory biomarkers of atherosclerosis such as monocyte and endothelial AM. These studies have shown that both ethanol and non-alcoholic components of alcoholic beverages, mainly polyphenols, reduce intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin expression of vascular endothelium, as well as monocyte adhesion to this endothelium. These data suggest that moderate alcohol intake has an anti-inflammatory effect on the cardiovascular system and reduces early serum markers of atherosclerosis. However, at higher doses ethanol may exert an inflammatory effect. In fact, chronic alcoholics exhibit significantly higher serum levels of endothelial AM than abstainers and moderate drinkers. In addition, an upregulation of E-selectin, ICAM-1 and VCAM-1 is also detected in liver biopsies obtained from patients with alcoholic hepatitis and cirrhosis. The clinical usefulness of the measurement of serum endothelial AM is discussed.

Alcohol Drinking↗
PubMed2002

Differential effects of moderate or heavy alcohol consumption on circulating adhesion molecule levels.

Epidemiological studies suggest that moderate but not heavy alcohol consumption provides protection against coronary heart disease. We assessed the relationship between alcohol consumption and serum levels of adhesion molecules involved in the pathogenesis of early atherosclerosis. One-hundred apparently healthy men with similar cardiovascular risk factors were divided into four groups according to ethanol intake. Moderate drinkers (20-40 g/day) showed lower serum intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) levels than abstainers (p < 0.05; both), as well as lower serum ICAM-1, VCAM-1 and E-selectin levels than heavy drinkers (p = 0.01; all). The latter also showed higher serum ICAM-1 and E-selectin levels than abstainers (p < 0.001; both). We conclude that moderate drinkers show a significant reduction of soluble endothelial adhesion molecule levels compared to abstainers and heavy drinkers, that may contribute to the protective effect of moderate alcohol consumption against atherosclerosis.

Adult↗
PubMed2001

Increased circulating leptin levels in chronic alcoholism.

BACKGROUND: Malnutrition seen in chronic alcoholics is partly due to reduced energy intake. Leptin is a peptide hormone implicated in the regulation of appetite and expenditure of energy. The prevalence and significance of abnormal circulating leptin levels in alcoholics, as well as the relationship of these levels with nutritional status, liver disease, and ethanol consumption, remain uncertain. METHODS: Serum leptin levels were measured in 60 active asymptomatic alcoholics, 20 active alcoholics with cirrhosis of the liver, 20 abstinent alcoholics, and 60 controls. Nutritional status and ethanol consumption also were assessed. RESULTS: In the control group, circulating leptin levels (mean 4.7+/-0.3 microg/liter) correlated with body fat stores. Despite showing a lower fat area of the arm, active alcoholics had significantly higher leptin levels than the controls (p < 0.001), regardless of the presence of cirrhosis. By contrast, none of the abstinent alcoholics showed hyperleptinemia. In the multivariate regression analysis, the fat area of the arm (p < 0.001), the lifetime ethanol consumption (p = 0.007), and the number of cigarettes smoked per day (p = 0.02) were found to be independent factors that influenced leptin levels in active alcoholics. After we adjusted for age, fat area of the arm, and tobacco consumption, a significant correlation was observed between lifetime consumption of ethanol and serum leptin concentrations (r = 0.36, p < 0.001). CONCLUSIONS: Circulating leptin levels are increased in a dose-dependent manner in chronic alcoholism, regardless of nutritional status or the presence of compensated liver disease.

Adult↗
PubMed2000

[Evaluation of functional capability after hospital admission of nonagenarian patients].

BACKGROUND: Hospitalisation in nonagenarians patients may causes functional decline. PATIENTS AND METHOD: The study sample included all nonagenarians patients admitted during three months in two teaching hospitals. RESULTS: We studied 125 patients (24 [19%] died). In the remaining 101 patients the previous Barthel index (BI) was 75, at admission 33 (p < 0.0001), and at discharge 43 (p < 0.001). The decline in BI at discharge was remarkable ( 32; p < 0.0001) and persisted after 3 months (12, p < 0.003). CONCLUSION: After three months of hospitalisation in nonagenarians patients persist a functional decline.

Aged↗
PubMed2000

Low-dose ethanol consumption allows strength recovery in chronic alcoholic myopathy.

Chronic skeletal myopathy may affect one third of chronic alcohol misusers. It is generally accepted that abstinence allows partial recovery, and that continued high-dose ethanol consumption progressively deteriorates muscle function. However, the effect of low-dose ethanol consumption in alcoholic myopathy has not been studied. We studied 58 chronic alcoholic male patients with biopsy-proven chronic alcoholic myopathy over 5 years. We evaluated ethanol intake, biochemical and nutritional parameters, and assessed muscle strength. Eighteen patients who remained abstinent showed marked improvement in muscle strength. As expected, the 19 patients who persisted in high-dose ethanol consumption further diminished in their muscle strength. In the 11 patients who maintained low-dose (</=60 g ethanol/day) 'controlled' drinking, muscle strength improved (p=0.003), despite no change in nutritional and exercise status. There is a dose-dependent recovery in muscle strength according to the degree of ethanol consumption, and moderate controlled drinking of up to 60 g ethanol/day still allows improvement in muscle strength.

Adult↗
PubMed2000

High ethanol intake and malnutrition in alcoholic cerebellar shrinkage.

To determine the influence of chronic ethanol intake and nutritional status on cerebellar shrinkage in alcoholism, we studied 12 undernourished patients with acute Wernicke's encephalopathy (WE), 12 undernourished and 24 well-nourished asymptomatic chronic alcoholics, and 24 age-matched well-nourished controls, using morphometric analysis of MRI scans with volumetry of the cerebellum. Alcoholics reported a mean daily intake of ethanol of 177+/-8 g over a period of 27+/-1 years. Most undernourished alcoholics and half of the well-nourished alcoholics, compared to one-tenth of the controls, showed a significant reduction in cerebellar volume (p< or =0.01, both). Alcoholics with cerebellar shrinkage (n=33) were older (p=0.05) and tended to report greater daily ethanol intake than alcoholics without cerebellar shrinkage (n=15), although not significantly so (p=0.09). Cerebellar volume correlated negatively with age in controls and asymptomatic alcoholics (r> or =0.52, p< or =0.01, both), with a significantly greater shrinkage for age in the latter (p=0.003). Logistic regression analysis showed that malnutrition (OR 6.6 [95%CI 1.7-25.6], p=0.005) and a daily ethanol intake of more than 140 g over ten years (OR 6.1 [95%CI 1.8-20.5], p=0.003) were independently associated with the development of cerebellar shrinkage.

Adult↗
PubMed2000

Diastolic function impairment in alcoholics.

BACKGROUND: Chronic excessive ethanol consumption exerts a deleterious effect on the myocardium. Although the effects of chronic alcoholism on systolic cardiac function are well known, diastolic involvement has been evaluated only partially. Therefore, we determined the presence of left ventricular diastolic impairment in chronic alcoholics and its relation with simultaneous systolic dysfunction. We also assessed the influence of ethanol consumption in diastolic impairment. METHODS: Thirty-five alcoholics with cardiomyopathy (ejection fraction < or = 50%) and 77 alcoholics with normal systolic function (ejection fraction > 50%) were evaluated. Assessment of New York Heart Association functional class, history of ethanol intake, technetium-99m radionuclide angiocardiography, and bidimensional Doppler echocardiography with evaluation of systolic and diastolic left ventricular function were performed. RESULTS: Diastolic function impairment was present in one third of the alcoholics without cardiomyopathy, compared with two thirds of the patients with cardiomyopathy (p < 0.01). A pseudonormalization phenomenon of diastolic function was observed in patients with more advanced systolic dysfunction (ejection fraction < 32%). The deterioration of the diastolic parameters correlated with ethanol consumption, regardless of age (r = 0.44, p < 0.001 for ratio of peak velocity of the transmitral flow in early diastole and peak velocity of atrial contraction flow, with lifetime dose of ethanol). CONCLUSIONS: There seems to be a dose-dependent effect of ethanol on systolic and diastolic heart function. Diastolic function impairment is present in one third of alcoholics with normal systolic function and is even more frequent when systolic dysfunction coexists.

Adult↗
PubMed1999

Upregulated expression of VLA proteins and CD29 in peripheral blood lymphocytes of chronic alcoholics without ethanol-related diseases.

To analyze adhesion molecule expression on peripheral blood mononuclear cells (PBMCs) and on different lymphocyte subpopulations (CD2+, CD8+, CD19+, and CD56+ subsets) in chronic alcoholism, 30 well-nourished chronic alcoholics without ethanol-related diseases and 30 matched controls were included in the study. Adhesion molecules that mediate adhesion to other cells and to extracellular matrix proteins, and whose cellular expression is modified during lymphocyte activation, were selected for study. A detailed clinical evaluation, laboratory analysis, nutritional assessment, and study of adhesion molecule expression was performed. A significant higher expression of CD29 (beta1-integrin) (p = 0.001), VLA-3 (p = 0.002), VLA-4 (p = 0.03), and VLA-5 (p = 0.001) were observed on PBMCs of chronic alcoholics, compared with control subjects, whereas no changes were observed in CD18 (beta2-integrin) and CD50 (ICAM-3) expression. The upregulation of CD29 and VLA proteins only affected T lymphocytes (CD2+/CD8+/CD4+ cells). These data confirm that T cells of chronic alcoholics are basally activated and that changes in adhesion molecule expression on PBMCs may be responsible of disturbances of adhesion processes in chronic alcoholics without ethanol-related diseases.

Adult↗
PubMed1998

Activated lymphocytes (CD25+ CD69+ cells) and decreased CD19+ cells in well-nourished chronic alcoholics without ethanol-related diseases.

To assess lymphocyte subsets and expression of activation antigens in peripheral blood lymphocytes (PBLs) in chronic alcoholism, a cross-sectional study with 30 well-nourished chronic alcoholics and 30 controls was performed. Studies included detailed clinical and laboratory evaluation, nutritional status assessment, and determination of lymphocyte subpopulations, as well as activation antigens. A significant decrease of B cells (CD19+) was observed in chronic alcoholics, compared with controls (p < 0.001). A significant increase of PBLs expressing CD69 and CD25 (p < 0.01, both) in chronic alcoholics was also detected, whereas CD71 expression was unaffected. In addition, T lymphocytes expressing HLA-DR were significantly higher in chronic alcoholics than controls (p < 0.05). The serum level of soluble interleukin-2 receptor was also significantly higher in the alcoholic group, compared with controls (p = 0.04). Moreover, the estimated total lifetime dose of ethanol consumed correlated positively with the percentage of PBLs expressing CD25 (r = 0.48; p = 0.01) and negatively with PBLs expressing CD71 (r = -0.39; p = 0.04). By contrast, the changes were not related to age, nutritional status, or the presence of other ethanol-related diseases. In conclusion, chronic alcoholics present a significant decrease of B cells and an "incomplete activation state" of PBLs that depends on the dose of ethanol consumed.

Adult↗
PubMed1998

Serum and muscle levels of alpha-tocopherol, ascorbic acid, and retinol are normal in chronic alcoholic myopathy.

Some authors have suggested a possible loss of antioxidant factors in alcoholic skeletal myopathy. To assess the relationship between ethanol consumption and serum and muscle levels of alpha-tocopherol, ascorbic acid, and retinol in chronic alcoholics with and without skeletal myopathy, a prospective cross-sectional study was performed in the Alcohol Unit of a 1000-bed university hospital. Twenty-five chronic male alcoholic patients (10 with skeletal myopathy) and 15 male controls of similar age were included. Evaluation of daily and lifetime ethanol consumption, assessment of anthropometric and protein nutritional parameters, and open biopsy of the left deltoid muscle were performed, as well as determinations of serum and muscle levels of retinol, alpha-tocopherol, and ascorbic acid by HPLC analysis. Ten of the 25 chronic alcoholic patients presented histological criteria of skeletal myopathy. Four alcoholics presented caloric malnutrition and three protein malnutrition. All of the muscle biopsies of the control group were entirely normal, as were their nutritional studies. The serum and muscular levels of alpha-tocopherol, ascorbic acid, and retinol were normal and were similar in both alcoholics and controls. Except for serum retinol, these values were also similar in alcoholic patients with or without skeletal myopathy. In the univariate analysis, we identified the total lifetime dose of ethanol (p < 0.003), the muscle arm area (p < 0.05), and serum levels of prealbumin (p < 0.03) and retinol-binding protein (p < 0.05) as factors influencing the development of alcoholic myopathy. However, in multivariate analysis, the total lifetime dose of ethanol was the only independent factor in relation to alcoholic myopathy (p < 0.003). Serum and muscle levels of the antioxidants alpha-tocopherol, ascorbic acid, and retinol do not influence the presence of skeletal myopathy in chronic alcoholic patients.

Adult↗
PubMed1998

Natural history of alcoholic myopathy: a 5-year study.

Chronic myopathy is a common complication of alcoholism, but its natural history has not been well described. We, therefore, studied muscle structure and function in a 5-year study of 30 chronic alcoholics who became abstinent and 20 who relapsed, and 40 control subjects. The mean strength of the abstaining alcoholics increased from 18.6 to 23.2 kg; but, after 5 years, they were still substantially weaker than controls. In a subset who showed histological myopathy, the strength of half of the patients remained two standard deviations below that of controls. Alcoholics who relapsed tended to become progressively weaker (21.7 kg vs. 18.2 kg) and develop histological evidence of myopathy. Thus, continued alcohol abuse was generally reflected in deterioration of muscle strength and the appearance of histological injury to muscle. Importantly, almost half of the sober patients did not recover to normal levels, indicating that alcoholic myopathy is only partially reversible. We also unexpectedly found that, in some alcoholics, a substantial reduction in the amount of alcohol consumed may be as effective as complete abstinence in improving muscle strength or preventing its deterioration.

Alcoholism↗
PubMed1997

Comparison of alcoholic cardiomyopathy in women versus men.

To compare the prevalence and cardiac status of male and female alcoholics with alcoholic cardiomyopathy during a 5-year period, all chronic alcoholics with dilated cardiomyopathy who had clinical symptoms of heart failure were included. Alcoholic cardiomyopathy was diagnosed in 10 chronic alcoholic women and in 26 men; the prevalence of alcoholic cardiomyopathy was similar in both sexes. No significant differences were observed in age, nutritional parameters, and clinical and radiologic data of heart failure between the 2 groups. Alcoholic women reported a significantly lower daily dose of ethanol (p = 0.002), a shorter duration of alcoholism (p = 0.017), and a lower total lifetime dose of ethanol consumption (p = 0.001), and had a lower New York Heart Association functional class than men. Women also had lesser ventricular dysfunction than men. In a multivariate analysis, left ventricular systolic dysfunction was related to the total lifetime dose of ethanol consumption (p <0.04), but not to gender. Finally, when patients were matched for left ventricular ejection fraction, women had consumed a lower total lifetime dose of ethanol than men (p <0.001). The prevalence of alcoholic women with dilated cardiomyopathy was found to be similar to that of alcoholic men, although women required a lower total lifetime dose of ethanol to develop the disease.

Adult↗
PubMed1997

Atrophy of the corpus callosum in chronic alcoholism.

To determine the prevalence of corpus callosum atrophy in chronic alcoholics and its relationship to cognitive function and brain atrophy, a prospective clinicoradiologic study was carried out in 28 right-handed male patients with chronic alcoholism and 14 age- and sex-matched right-handed control subjects. Clinical evaluation, neuropsychological testing and measurement of the midsagittal corpus callosum area and thickness (genu, truncus and splenium), as well as the frontal lobe index and the width of the cortical sulci on T1- and T2-weighted magnetic resonance images were performed. Compared to controls, alcoholics had significantly decreased corpus callosum area and thickness, mainly in the genu. Two-thirds had a corpus callosum area 2 SD below the mean of the control group. The sagittal area of the corpus callosum body correlated negatively with the degree of frontal and cortical atrophies (r = -0.5579 and -0.6853, respectively p < 0.01, both). Alcoholics with corpus callosum atrophy exhibited impairment of visual and logical memories (p < 0.05 both) and those with reduced thickness of the genu showed impairment of frontal lobe tasks (p < 0.05). The reduction of corpus callosum indices (age-corrected) also correlated with the total lifetime dose of ethanol consumed (r = 0.6107, p < 0.001), but was not related to nutritional status or electrolyte imbalance. Atrophy of the corpus callosum is common among alcoholic patients and may reflect the severity and pattern of cortical damage. The degree of this atrophy also correlated with the severity of ethanol intake.

Adult↗
PubMed1997

Brain impairment in well-nourished chronic alcoholics is related to ethanol intake.

To determine the influence of chronic ethanol intake on the central nervous system, we studied 40 asymptomatic, well-nourished, chronic alcoholics (mean age, 42.6 +/- 9.1 years) and 20 age-, sex-, and education-matched control subjects. Studies included neuropsychological testing, visual and short-latency auditory evoked potentials, and morphometric analysis of computed tomography scans. The mean daily ethanol consumption of the alcoholics was 204 gm over an average of 26.4 years. Compared to control subjects, chronic alcoholics exhibited a significant prolongation of the P100 latency of visual evoked potentials, and a prolongation and reduction in the amplitude of the latency of the V wave of short-latency auditory evoked potentials. These abnormalities were related to the lifetime dose of ethanol consumed. Brain morphometric analysis showed that alcoholics had a significantly greater degree of brain shrinkage with age, compared to control subjects. The cortical atrophy index correlated significantly with the lifetime ethanol consumption. Neuropsychological testing in alcoholics compared to controls revealed a significant impairment of frontal skills that was related to age, degree of scholarship, and the presence of frontal atrophy. In conclusion, well-nourished chronic alcoholics exhibited significant brain impairment, as demonstrated by neuropsychological testing, evoked potentials, and brain morphometric analysis, which was correlated with the lifetime dose of ethanol consumed.

Adult↗
PubMed1995

Significance of type II fiber atrophy in chronic alcoholic myopathy.

To determine the significance of type II fiber atrophy in alcoholic myopathy and its relationship with ethanol-related diseases a prospective study was carried out in 100 chronic alcoholics who showed clinical suspicion of skeletal myopathy. Measurement of muscle strength, laboratory analysis, nutritional assessment and open biopsy of deltoid muscle were performed in each case, as well as electrophysiological testing for peripheral neuropathy. Hepatic ultrasonography and liver biopsy, echocardiography and radionuclide cardiac scanning were carried out in selected subjects. According to histomorphometric analysis, type II fiber atrophy was found in 33 cases (33%), being selective for type II B fiber in 23 (70%). Skeletal myopathy was diagnosed in 61 cases, alcoholic cardiomyopathy in 26, peripheral neuropathy in 23 and cirrhosis in 12. Patients with type II fiber atrophy had a significantly higher total lifetime dose of ethanol, presented a greater incidence of skeletal myopathy and peripheral neuropathy, and exhibited significantly lower values of percentage of ideal body weight and lean body mass than their counterparts. However, the only independent factors for developing type II fiber atrophy were the coexistence of caloric malnutrition (p = 0.004) and the presence of skeletal myopathy (p = 0.043). Selective type II fiber atrophy is a non-specific finding in alcohol-induced muscle damage appearing, overall, in the patients with caloric malnutrition as well as in those with histologic evidence of myopathy.

Adult↗
PubMed1995

Relationship between cardiomyopathy and liver disease in chronic alcoholism.

Based on anecdotal impressions, there is a common clinical perception that alcoholics with liver disease do not develop cardiomyopathy and that those with alcohol-induced cardiac disease are spared cirrhosis. To determine the relationship between alcoholic cardiomyopathy and cirrhosis, we carried out a prospective cross-sectional study that included: (1) 30 alcoholic men with cardiomyopathy; (2) 30 alcoholic men without cardiomyopathy (left ventricular ejection fraction > 55%); (3) 20 actively drinking alcoholics with cirrhosis; (4) 15 abstaining alcoholics with cirrhosis; and (5) 15 nonalcoholics with cirrhosis of other etiologies. Cirrhosis was observed in 13 of 30 patients with alcoholic cardiomyopathy (43%), compared with 2 of 30 alcoholics without cardiomyopathy (6%) (P < .001). Ten of the 20 active alcoholics with cirrhosis (50%) showed evidence of dilated cardiomyopathy. Actively drinking alcoholics with cirrhosis had a significantly lower mean ejection fraction and shortening fraction, as well as a greater mean end-diastolic diameter and left ventricular mass than abstaining alcoholics with cirrhosis. Cardiac studies of patients with nonalcoholic cirrhosis were normal. We conclude that a positive correlation exists between alcoholic cardiomyopathy and cirrhosis. Alcoholics admitted solely for cardiomyopathy have a higher prevalence of cirrhosis than unselected alcoholics without heart disease. Actively drinking alcoholics admitted only for cirrhosis show impaired cardiac performance, whereas abstaining alcoholics with liver disease tend to manifest normal cardiac function.

Adult↗