J. Fernández‐Solà

Effect of Alcohol Abstinence on Blood Pressure Assessment by 24-Hour Ambulatory Blood Pressure Monitoring

Several studies have shown that cessation of alcohol drinking reduces blood pressure (BP). However, attempts to reproduce these findings by ambulatory BP monitoring (ABPM) have shown inconsistent results. The aim of the present study was to assess the effect of 1 month of proven abstinence from alcohol on the 24-hour BP profile in heavy alcohol drinkers. Forty-two men who were heavy drinkers (>100 g of pure ethanol per day) were consecutively admitted to a general ward for voluntary alcohol detoxification. On the day of admission, they received a total dose of 2 g/kg of ethanol diluted in orange juice in 5 divided doses, and a 24-hour ABPM was performed. A new 24-hour BP monitoring in the same environmental conditions was performed after 1 month of proven alcohol abstinence while the subjects were receiving the same amount of fluid but without the addition of alcohol. After 1 month of proven alcohol abstinence, BP and heart rate (HR) significantly decreased. The reduction was 7.2 mm Hg for 24-hour systolic BP (SBP) (95% CI, 4.5 to 9.9), 6.6 mm Hg for 24-hour diastolic BP (DBP) (95% CI, 4.2 to 9.0), and 7.9 bpm for HR (95% CI, 5.1 to 10.7). The proportion of alcoholic patients considered hypertensive on the basis of 24-hour BP criteria (daytime SBP >/=135 mm Hg or daytime DBP >/=85 mm Hg) fell from 42% during alcohol drinking to 12% after 1 month of complete abstinence. Abstinence did not modify either the long-term BP variability, assessed by SD of 24-hour BP, or its circadian profile. We conclude that abstinence in heavy alcohol drinkers significantly reduces BP assessed by 24-hour ABPM and that this reduction is clinically relevant. These results show that heavy alcohol consumption has an important effect on BP, and thus cessation of alcohol consumption must be recommended as a priority for hypertensive alcohol drinkers.

Effects of Alcohol Withdrawal on 24 Hour Ambulatory Blood Pressure Among Alcohol-Dependent Patients

BACKGROUND Although epidemiologic studies have reported an association between alcohol intake and high blood pressure (BP), the results of intervention studies have shown inconsistent results. We embarked on a study to determine whether different subgroups of alcohol-dependent patients may be identified in relation to the effect of alcohol on BP. METHODS Fifty alcohol-dependent men (mean age, 41.4 years) received 0.4 g of ethanol per kilogram of body weight every 4 hr in 200 ml of orange juice during 24 hr and the same amount of orange juice without ethanol during another 24 hr. Twenty-four hour ambulatory BP monitoring was performed during ethanol and orange juice intakes, as was hormonal and biochemical analysis. RESULTS Thirty-five (75%) alcohol-dependent men were normotensive and 15 (30%) hypertensive. Eighteen (51%) normotensive and 12 (80%) hypertensive subjects showed a significant decrease in 24 hr mean BP after ethanol withdrawal (mean decrease of 8.4 mm Hg [95% confidence interval, -11.2 to -5.7] and 12.5 mm Hg [confidence interval, -16.2 to -8.8], respectively) and were considered as sensitive to alcohol. The remaining alcohol-dependent subjects were considered as resistant to alcohol. Normotensive subjects sensitive to ethanol showed a significantly greater left ventricular mass and a significantly lower ejection fraction than those normotensive patients whose BP did not change after ethanol withdrawal (both p < 0.01). CONCLUSIONS More than three fourths of the hypertensive and more than half of the normotensive alcohol-dependent patients showed sensitivity to the pressor effects of ethanol. Impairment also was observed in heart function in normotensive patients sensitive to the pressor effects of ethanol.

22 – Gender Differences in Alcohol Pathology

This chapter discusses the gender differences in alcohol-induced disease. Women clearly exhibit some different responses to the pathological effects of alcohol consumption compared to men. The chapter explains differences in the health of men and women, exploring reductionist assumptions and biological sources of these differences. The pharmacokinetics of alcohol determines the time course of alcohol concentration in blood after the ingestion of an alcoholic beverage and the degree of the exposure of organs to its effects. It has been established that, on an average, women have a higher blood alcohol level than men for a similar intake of ethanol. The reason for this higher alcohol concentration in women is multi-factorial in origin, with body weight, small water volume, lesser first-pass gastric or hepatic effects, and other genetic and hormonal effects mainly being involved. This higher alcohol concentration produces differences in the pathological expression of alcohol-induced organ damage in women manifested by the involvement of several organs. With respect to cardiac damages, in preclinical alcohol-induced ventricular dysfunctions, women are more sensitive to the toxic effects of ethanol than men.

29 – Nutritional Status in Alcoholics

This chapter discusses the nutritional status in chronic alcoholics. The prevalence of malnutrition among chronic alcoholics varies from 5 to 80%, depending on the population studied. In the past, many cross-sectional studies included indigent skid rows subjects or patients with severe somatic complications—such as liver cirrhosis, hence, the general belief that alcoholics have advanced malnutrition. However, later studies have revealed that nutritional deficiencies are rare among middle-class alcoholics without significant somatic complications. Therefore, although chronic alcoholism continues to be the main cause of malnutrition in the Western countries, nutritional deficiencies are usually found among low-income and homeless alcoholic populations, or in those with ethanol-related complications—especially liver disease or neurological disorders. Moreover, alcoholism and malnutrition is discussed jointly with regards to the pathogenesis, the prognosis, and even the therapy of ethanol-related diseases. Experimental, epidemiological and clinical studies suggest that ethanol has a direct effect on most body tissues. Nevertheless, because not all heavy drinkers exhibit all types of ethanol-related complications, other factors such as—nutritional deficiencies, environmental circumstances or genetic predisposition may enhance or prevent the effects of ethanol on cells.

86 – Adhesion Molecules and Alcohol Consumption

This chapter gives an overview of the effects of ethanol consumption or ethanol exposure on adhesion molecule expression and function and its possible relationship with ethanol-related diseases. Adhesion molecules are proteins expressed on the cell surface, which participate in a myriad of physiological processes—such as organogenesis, immune response and angiogenesis. On the other hand, ethanol exposure/consumption is associated with changes in the cell function including changes in adhesion molecule expression or function. Previous studies have suggested that alcohol may alter cellular and tissue adhesion molecules, and thereby, alter the processes in which they are involved. Thus, frequent alcohol-related health problems such as infectious diseases (for example pneumonia) may be explained by disturbances in immune response in which adhesion molecules have a key role. Alcohol-related diseases such as alcoholic hepatitis may also be explained, at least partially, by an excessive immune response of circulating leukocytes against the liver tissue in which adhesion molecules on hepatic endothelium and their counter-receptors on leukocytes are up-regulated. Moderate alcohol consumption seems to be a protector against atherosclerosis; the modification of monocyte-endothelial interactions, which is an early event in atheroma plaque formation, may be another potential mechanism to explain the lower incidence of atherosclerosis in alcohol drinkers.

53 – Alcoholic Myopathy: Clinical Aspects

This chapter describes the clinical aspects of alcoholic myopathy. Ethanol consumption may cause acute and chronic deleterious effect on skeletal muscle, inducing muscle weakness, atrophy, and myocyte death. Acute myopathy has and sporadic presentation among binge consumers. Chronic alcoholic myopathy has a prevalence of 40–60% in a population of alcohol misusers. Muscle weakness, myalgia and swelling are the main features of acute myopathy. In chronic myopathy, the most relevant features are proximal progressive muscle weakness and atrophy. There are more subclinical cases, which can be detected evaluating muscle weakness by myometry. Skeletal muscle involvement in alcoholism is related to other systemic diseases—such as dilated cardiomyopathy, peripheral neuropathy, malnutrition and liver cirrhosis. Myocytolysis and Type II fiber atrophy are the most prominent features in alcoholic myopathy. Because of the lack of a specific histological pattern, the diagnosis of alcoholic myopathy requires a characteristic clinical pattern and careful exclusion of other causes of myopathy. The physiopathological mechanisms that determine the muscle damage induced by ethanol are still not completely understood. Studies have shown that ethanol has a toxic direct effect, that is, producing muscle damage by altering membrane fluidity, channels, pumps and ionic transients, depression of muscle contractility, and protein synthesis or mitochondrial function.