The impact of frailty on intra-hospital survival in older patients with COVID-19 infection: the importance of early identification. SEMI-COVID National Registry.

BACKGROUND: Emerging evidence suggests that frailty may be a significant predictor of poor outcomes in older individuals hospitalized due to COVID-19. This study aims to determine the prognostic value of frailty on intrahospital patient survival. METHODS: This observational, multicenter, nationwide study included patients aged 70 years and older who were hospitalized due to COVID-19 in Spain between March 1 and December 31, 2020. Patient data were obtained from the SEMI-COVID-19 Registry of the Spanish Society of Internal Medicine. Frailty was assessed using the Clinical Frailty Scale. The primary outcome was hospital survival. Cox proportional hazards models were used to assess predictors of survival. RESULTS: A total of 1,878 participants (52% men and 48% women) were included, with 1,351 (71.9%) survivors and 527 (28.1%) non-survivors. The non-survivor group had higher mean age (83.5 vs. 81 years), comorbidities (6.3 vs. 5.3 points on the Charlson index), degree of dependency (26.8% vs. 12.4% severely dependent patients), and frailty (34.5% vs. 14.7% severely frail patients) compared to survivors. However, there were no differences in terms of sex. Our results demonstrate that a moderate-severe degree of frailty is the primary factor independently associated with shorter survival [HR 2.344 (1.437-3.823; p<0.001) for CFS 5-6 and 3.694 (2.155-6.330; p<0.001) for CFS 7-9]. CONCLUSION: Frailty is the main predictor of adverse outcomes in older patients with COVID-19. The utilization of tools such as the Clinical Frailty Scale is crucial for early detection in this population.

Patterns of food avoidance in chronic fatigue syndrome: is there a case for dietary recommendations?

OBJECTIVES: To assess the dietary habits and food avoidance-behavior in patients with Chronic Fatigue Syndrome (CFS). METHODS: Cross-sectional pilot study with 28 patients diagnosed with severe CFS. Eating habits were assessed with a food frequency questionnaire and 3-day food records. We analyzed variables related to dietary restrictions induced by symptoms or external information. RESULTS: The most prevalent restrictions were for dairy products and gluten-containing grains, with 22 and 15 restricting patients, respectively. Patients reported different digestive symptoms, which did not improve with the use of exclusion diets. Thirteen patients had received information against the intake of certain foods through different sources. Six cases of grains restriction and 11 of dairy were compatible with a counseling-induced pattern of exclusion. CONCLUSIONS: There is not a homogeneous pattern of food avoidance. Dietary restrictions should be based on a proven food allergy or intolerance. Dietary counseling should be based on sound nutritional knowledge.

Growth hormone treatment for sustained pain reduction and improvement in quality of life in severe fibromyalgia.

Functional defects in growth hormone (GH) secretion and its efficacy as a complementary treatment have been suggested for fibromyalgia. This study investigated the efficacy and safety of low-dose GH as an add-on therapy in patients with both severe FM and low insulin-like growth factor 1 levels. A total of 120 patients were enrolled in a multicenter, placebo-controlled study for 18 months. They were randomly assigned to receive either 0.006 mg/kg/day of GH subcutaneously (group A, n=60) or placebo (group B, n=60) for 6 months (blind phase). The placebo arm was switched to GH treatment from month 6 to month 12 (open phase), and a follow-up period after GH discontinuation was performed until month 18. Standard treatment for fibromyalgia (selective serotonin re-uptake inhibitors, opioids, and amitriptyline) was maintained throughout the study. Number and intensity of tender points, Fibromyalgia Impact Questionnaire (FIQ) with its subscales, and EuroQol 5 dimensions test (EQ5D) with visual analogue scale (VAS) were assessed at different time points. At the end of the study, 53% of group A patients obtained fewer than 11 positive tender points, vs 33% of group B patients (P<.05). 39.1% vs 22.4% reached more than 50% improvement in VAS (P<.05). Group A patients showed significantly improved FIQ scores (P=.01) compared with group B. Although GH discontinuation worsened all scores in both groups during follow-up, impairment in pain perception was less pronounced in the GH-treated group (P=.05). In this largest and longest placebo-controlled trial performed in FM (NCT00933686), addition of GH to the standard treatment is effective in reducing pain, showing sustained action over time.

High prevalence of growth hormone deficiency in severe fibromyalgia syndromes.

CONTEXT: Fibromyalgia (FM) is characterized by widespread pain and fatigue and is considered a syndrome with different pathogenic mechanisms. Controversial data on GH axis disturbances have been published. Some preliminary trials have shown promising effects of GH therapy on tender points and quality of life in FM. AIM: The aim was to study the patterns of GH secretion/sensitivity in a cohort of severe FM patients. SETTING: The study was conducted in five tertiary hospitals. METHODS: A total of 493 FM women (1990 American College of Rheumatology criteria) recruited from five centers, having more than 16 tender points, Fibromyalgia Impact Questionnaire scores above 75, more than 1 yr of stable medication (serotonin reuptake inhibitors, amitriptyline, and opioids), and body mass index below 35 kg/m(2) underwent baseline IGF-I/GH determinations; an insulin tolerance test (ITT) and a modified IGF-I generation test were performed in those cases showing IGF-I of 150 microg/liter or less. RESULTS: A total of 169 of the 493 patients (34.2%) showed IGF-I of 150 microg/liter or less. Mean peak GH during ITT was 13.3 +/- 9.9 ng/ml in 127 patients in which the test was performed. In 22 of 127 (17.3%), ITT peak GH was 5 microg/ml or less, and in eight of them (6.3%), the peak GH was 3 ng/ml or less. Mean baseline GH (n = 127) was 1.47 +/- 2.58 ng/dl, and eight of 120 (6.8%) showed an insufficient IGF-I response (<50% over baseline) to the IGF-I generation test. CONCLUSION: FM patients show a high prevalence of GH axis dysfunction. A significant number of patients show biochemical patterns of GH deficiency as well as some degree of GH resistance and might be potential candidates for substitution treatment.

[Detecting adverse drug events during the hospital stay]. / Detección de acontecimientos adversos producidos por medicamentos durante la estancia hospitalaria.

INTRODUCTION: The principal objective was to determine the incidence rate of adverse drug events (ADEs) in hospitalised patients and evaluate the event prevention percentage. METHODS: Multi-centre, prospective observational study lasting four months, performed in five hospitals providing different levels of care. We included all adult patients who were admitted to one of the selected centres for longer than 48 hours and who required pharmacological treatment. ADEs were identified by direct observation and the use of previously defined alarm signals. The Karch-Lasagna scale was used to determine the causality relationship, and the Schumock and Thornton questionnaire adapted by Otero was used to evaluate ADE preventability. Preventable drug-induced adverse events were classified according to the taxonomy that the Ruiz-Jarabo 2000 group defined, and coordinated by ISMP-Spain. RESULTS: We included 1,550 patients, 159 of whom experienced at least one ADE (10.3 %). The preventability percentage was 51.6 %, which represented 5.3 % of the total sample. The endocrine system (34.8 %) and the cardiovascular system (20.7 %) were the most affected by preventable ADEs. Antibiotics were responsible for 16.5 % of all ADEs. 9.3 % of all preventable ADEs were triggered by use of opiates. The vast majority of preventable ADEs (36.3 %) resulted from omitting a necessary medication. Only 4.4 % of preventable ADEs are considered to be serious. CONCLUSIONS: There is a high incidence rate of ADEs during patients' hospital stay (10.3 %), and half of them (51.6 %) could have been prevented. Implementation of an automatic alarm system and certain best practices for problem spots along the care circuit will help detect and avoid preventable ADEs.

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.

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.

Effects of alcohol on the heart.

Some evidence suggests that light to moderate alcohol consumption protects against cardiovascular diseases. However, this cardioprotective effect of alcohol consumption in adults is absent at the population level. Approximately 20 to 30% of patients admitted to a hospital are alcohol abusers. In medical practice, it is essential that patients' levels of consumption are known because of the many adverse effects that might result in the course of routine care. Ethanol damage to the heart is evident if alcohol consumption exceeds 90 to 100 g/d. Heavy ethanol consumption leads to increased risk for sudden cardiac death and cardiac arrhythmias. In patients with coronary heart disease, alcohol use was associated with increased mortality. An early response to drinking was an increased ventricular wall thickness to diameter ratio, possibly proceeding with continuous drinking to alcoholic cardiomyopathy, which had a worse outcome compared with idiopathic dilative cardiomyopathy if drinking was not stopped or at least reduced (< 60 g/d). In the ICU, patients with chronic alcoholism have more cardiac complications postoperatively. These complications probably are caused by biventricular dysfunction, particularly with the occurrence of severe infections or septic shock, events that are three to four times more frequent among chronic alcoholics than occasional drinkers or nondrinkers. To prevent further complications from drinking and for long-term management of drinking, patients with alcohol abuse and heart failure should be treated in brief intervention and follow-up programs. Prognosis is good even in patients with New York Heart Association class IV heart failure caused by cardiomyopathy if complete abstinence is accomplished. Noncompliance to smoking and alcohol restrictions, which are amenable to change, dramatically increases the risk for hospital readmissions among patients with heart failure.

Heart mitochondrial respiratory chain complexes are functionally unaffected in heavy ethanol drinkers without cardiomyopathy.

BACKGROUND: Harmful effects of chronic ethanol intake on liver mitochondria have been clearly demonstrated; however, mitochondria from skeletal muscle are preserved, and the effect of ethanol on heart mitochondria remains controversial. We assessed individual enzyme activity of mitochondrial respiratory chain (MRC) complexes and membrane oxidative damage of heart mitochondria in active ethanol drinkers before the development of dilated cardiomyopathy. PATIENTS AND METHODS: Heart samples were obtained from otherwise healthy organ donor individuals with a sudden death of traumatic or neurological cause in whom hearts could not be used because of absence of matched receptors or size inadequacy. Detailed history of alcohol intake was achieved from the relatives. Citrate synthase activity was spectrophotometrically assayed, as well as absolute (nmol x min(-1) x mg protein(-1)) and relative (corrected by citrate synthase) activities of complex I, II, III, and IV of the MRC. Oxidative damage of myocardium membranes was assessed measuring the degree of lipid peroxidation by fluorescence using cis-parinaric acid as probe. RESULTS: We included 10 ethanol drinkers (age 53 +/- 13 years, 100% males, mean lifetime intake of 15.6 +/- 7.9 kg ethanol kg body weight(-1)) and 12 controls (age 60 +/- 10 years, 75% males). Mitochondrial content did not differ between the two groups. Absolute enzyme activities for ethanol drinkers and controls were, respectively, 145 +/- 75 and 130 +/- 50 for complex I (p = NS); 399 +/- 193 and 376 +/- 100 for complex II (p = NS); 719 +/- 288 and 714 +/- 308 for complex III (p = NS); and 475 +/- 139 and 570 +/- 160 for complex IV (p = NS). After correcting such activities by citrate synthase activity, we failed again to demonstrate differences between ethanol drinkers and controls. Lipid peroxidation of myocardium membranes was similar in both groups. CONCLUSIONS: Chronic ethanol drinkers without cardiomyopathy exhibit normal MRC activity in the heart and do not show increased oxidative damage in myocardial membranes.

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.

Ethanol inhibits skeletal muscle cell proliferation and delays its differentiation in cell culture.

Chronic ingestion of ethanol (EtOH) produces physiological and morphological alterations in skeletal muscle. The effects of EtOH on skeletal muscle have been studied in experimental animals or on biopsies from alcoholic patients. However, alterations in skeletal muscle from alcoholic patients could be secondary to the effects of EtOH on the nervous system. In this study, by assaying the action of EtOH on primary skeletal muscle cell cultures, we provide evidence of its direct effect on skeletal muscle proliferation and differentiation. The results indicate that EtOH: (1) significantly inhibits skeletal muscle cell proliferation at the beginning of the proliferation phase; (2) delays skeletal muscle differentiation, shown by the significant changes in the evolution of the percentage of the creatine kinase isozymes; (3) has no significant effect on skeletal muscle DNA or protein content during the proliferation phase.

Acute ethanol treatment decreases intracellular calcium-ion transients in mouse single skeletal muscle fibres in vitro.

Alcohol misuse frequently leads to muscle weakness, which may also occur in the setting of acute and chronic alcoholic myopathies. At the cellular level, ethanol has been found to interfere with signalling mechanisms in cardiac myocytes, skeletal myotubes, and smooth muscle cells. In this study, we focused on the effects of ethanol on the intracellular calcium ([Ca(2+)](i)) transients responsible for excitation-contraction (EC) coupling in isolated mouse skeletal fibres loaded with the fluorescent Ca(2+) indicator fura-2. Following electrical stimulation, ethanol caused a significant reversible dose-dependent reduction in [Ca(2+)](i) transient amplitude, already significant at 100 mM ethanol (P = 0.03), without modifying resting [Ca(2+)](i). Evaluating the potential loci for the effects of ethanol, we indirectly measured sarcolemmal Ca(2+) entry by monitoring Mn(2+)-quenching of intracellular fura-2 via the nitrendipine-sensitive Ca(2+) channels during electrical pacing. Ethanol at doses of 20 mM and greater caused a dose-dependent reduction in the rate of fura-2 quenching (all at P<0.05). Moreover, the intracellular pool of Ca(2+) releasable by caffeine was found to be reduced at a minimum of 300 mM ethanol (P = 0.05). We conclude that ethanol reduces the [Ca(2+)](i) transients underlying EC coupling in single mouse skeletal muscle fibres. This acute effect of ethanol was primarily due to an inhibitory effect of ethanol on sarcolemmal Ca(2+) influx via voltage-operated Ca(2+)-channels and, to a lesser extent, to a reduction in the Ca(2+) sarcoplasmic reticulum loading state. This inhibitory effect of ethanol may be implicated in the development of muscle weakness with alcohol consumption.

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 (

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.

Chronic alcohol consumption increases serum levels of circulating endothelial cell/leucocyte adhesion molecules E-selectin and ICAM-1.

A group of 30 chronic alcoholics without alcohol-related diseases and 30 controls (teetotallers) were selected to measure serum levels of endothelial adhesion molecules (AMs) (ICAM-1, VCAM-1, and E-selectin). ICAM-1 and E-selectin serum levels were higher in alcoholics, whereas VCAM-1 serum levels were similar in both groups. There was a significant correlation between daily alcohol intake and serum level of ICAM-1 (r = 0.49, P = 0.003) and E-selectin (r = 0.41, P = 0.02). A significant positive correlation between E-selectin and total lifetime dose of ethanol was also observed (r = 0.52, P = 0.003). These changes in serum levels of endothelial AMs of chronic alcoholics may reflect endothelial and/or immune activation, and could interfere with the reactions between immune cells and the endothelium.

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.

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.

Usefulness of CT and MR imaging in the diagnosis of acute Wernicke's encephalopathy.

OBJECTIVE: In this study, we analyzed the sensitivity and specificity of CT and MR imaging in the diagnosis of acute Wernicke's's encephalopathy. SUBJECTS AND METHODS: Three groups of subjects were studied: 15 patients with acute Wernicke's encephalopathy; 15 asymptomatic alcoholics; and 15 control subjects. Studies included clinical and laboratory examinations as well as CT and MR imaging of the brain. RESULTS: On CT scans, two patients with Wernicke's encephalopathy (13%) and no asymptomatic alcoholics showed low-density abnormalities in the paraventricular regions of the thalamus (p = .2414). On MR imaging, increased T2 signal of paraventricular regions of the thalamus was observed in seven patients (46%) with Wernicke's encephalopathy and one asymptomatic alcoholic (6%) (p < .01), and increased T2 signal of periaqueductal regions of the midbrain in six patients (40%) with Wernicke's encephalopathy and one asymptomatic alcoholic (6%) (p < .05). However, no significant differences were observed in the prevalence of mamillary body shrinkage between alcoholics with Wernicke's encephalopathy (six [40%]) and asymptomatic chronic alcoholics (four [27%]). The sensitivity of MR imaging in revealing evidence of this disease was 53% and the specificity, 93%. CONCLUSION: MR imaging is useful in confirming the diagnosis of acute Wernicke's encephalopathy. However, the absence of abnormalities on MR imaging does not exclude this diagnosis. CT proved not useful in the diagnosis of Wernicke's encephalopathy.