Patients admitted for alcohol detoxification should receive intramuscular thiamine 200 mg for the first two days starting as quickly as possible, folate 1600 mcg daily, and magnesium 250 mg twice a day.  B-12 500 mcg daily is probably a good idea, but has been untested.  If patients show signs of alcohol withdrawal, oral chlordiazepoxide 50 mg. every hour until mild drowsiness is excellent for withdrawal. Thiamine 50 mg, folate 800 mcg., and magnesium 250 mg. twice daily should be continued even if the patient relapses into drinking.  Patients over age 50 should also take B-12.  Research suggests that everyone should probably take the folate and magnesium, although thiamine supplementation is probably needed only in detoxing and relapsed alcoholics and some patients with anorexia nervosa.

AST/ALT Ratio High In Advanced Alcoholic Liver Disease: In a study of 313 patients with alcohol dependence admitted for alcohol withdrawal (W), 78 patients with alcohol abuse or dependence admitted to surgical or medical wards with various primary somatic (S) diagnoses, and 48 consecutive patients with alcohol abuse or dependence admitted to surgical or medical wards for treatment of alcohol-related liver cirrhosis (C), there was a significant rise in the AST/ALT ratio from the W to the S patients, and from the S to the C patients. In the W group, the ratio was < or = 1.0 in 64% of the patients, and only exceptionally > or = 2. In the C group, 69% had a ratio > or = 2, and 8% a ratio < or = 1.0. The mean ratio was midway in the S group. In the C group, there was a progressive decline in aspartate (AST/ALT) ratios after admission. High AST/ALT ratio suggests advanced alcoholic liver disease. High AST/ALT ratio may indicate advanced alcoholic liver disease rather than heavy drinking. Nyblom H, et al. Sahlgrenska University Hospital, Gothenburg, Sweden. Alcohol Alcohol. 2004 Jul-Aug;39(4):336-9.

Chlordiazepoxide Great for Withdrawal: In a meta-analysis of 9 prospective controlled trials, sedative-hypnotic agents were more effective than neuroleptic agents in reducing duration of delirium and mortality, with a relative risk of death when using neuroleptic agents of 6.6. There was no significant differences among various benzodiazepines (e.g. chlordiazepoxide) and barbiturates. No deaths were reported in 217 patients from trials using benzodiazepines or barbiturates. Adequate doses should be used to maintain light somnolence for the duration of delirium. Management of alcohol withdrawal delirium. An evidence-based practice guideline. Mayo-Smith MF, et al. VA, Manchester, NH. Michael.Mayo-Smith@med.va.gov. Arch Intern Med. 2004 Jul 12;164(13):1405-12. Ed: Oral chlordiazepoxide (Librium) is actually faster acting than intramuscular.  Giving 50 mg doses every 60 minutes until mild drowsiness will eliminate the dangers of alcohol withdrawal.  Nursing should be careful not to give chlordiazepoxide to patients who are already mildly drowsy.

Folate Markedly Reduced in Alcoholics and Reduces High Homocysteine: In 40 chronic alcohol abusers and 44 healthy moderate drinkers, before alcohol withdrawal, derivatives of reactive oxygen metabolites (d-ROMs) were significantly higher (p<0.0001) in heavy drinkers: 368  vs 245 U.CARR. Plasma homocysteine were higher in alcoholics (p<0.0001): 18 vs 9.1 micromol/L. The patients showed markedly lower plasma folate than controls (p<0.0001): 4.1 ng/mL vs 8.8 ng/mL, but more similar vitamin B12 levels: 487 pg/mL 621 pg/mL. A negative correlation between homocysteine and folate was observed before withdrawal in alcoholics (p<0.038). Both serum thiols and homocysteinemia were decreased (p<0.0001 and p<0.022) after a week of alcohol withdrawal and folate administration. Folate seems to be a strong determinant of both plasma homocysteine and thiol concentrations. Pro-oxidant activity and methionine metabolism in chronic alcohol abusers: relationship to alcohol withdrawal and folate administration. Trotti R, et al. Pavia, Italy. rosa.trotti@mondino.it. Ed: Clearly, folate supplementation is important. B-12 500 mcg daily, in view of its similarly very low cost and lack of side-effects, might be a good idea, too.

Homocysteine When High Predicts Cognitive Deficits in Alcohol Withdrawal Patients: In 89 adults during early withdrawal treatment, patients with cognitive deficits showed significantly higher homocysteine serum levels (p = 0.004), while the difference in blood alcohol concentration was not significant. Cognitive deficits were best predicted by high homocysteine serum levels. Short-term cognition deficits during early alcohol withdrawal are associated with elevated plasma homocysteine levels in patients with alcoholism. Wilhelm J, et al. University of Erlangen-Nuremberg, Germany. J Neural Transm. 2005 Jul 6. Ed: Folate 800-1600 mcg or more should probably be given to all AWS patients.  In fact, the same is healthy for all everyone.

Homocysteine Damages the Brain: There is evidence from in vitro and in vivo studies that homocysteine induces neuronal damage and cell loss. Clinical evidence suggests a strong relationship between higher plasma homocysteine levels and brain atrophy in healthy elderly subjects as well as in elderly at risk of and with Alzheimer's disease. Chronic alcoholism leads to elevated plasma homocysteine levels. There is an association between brain atrophy and increased levels of homocysteine in chronic alcoholism. Homocysteine plays a role in a shared biochemical cascade involving overstimulation of N-methyl-D-aspartate (NMDA) receptors, oxidative stress, activation of caspases, DNA damage, endoplasmic reticulum and mitochondrial dysfunction. Homocysteine as a neurotoxin in chronic alcoholism. Bleich S, et al. University of Erlangen-Nuremberg, Germany. srtefan.bleich@psych.imed.uni-erlangen.de. Prog Neuropsychopharmacol Biol Psychiatry. 2004 May;28(3):453-64. Ed: Alcoholics should take folate and B-12 even if they relapse.  Besides, teaching them to be more health conscious is another step away from alcoholism.

Magnesium Depletion Linked to Severe Alcohol Withdrawal: In a study of 129 chronic alcoholics with alcohol withdrawal, hypomagnesemia was diagnosed in 42% with a severe, 19% with a moderate and 20% with weak withdrawal (p < 0.05). Hypomagnesemia in patients with chronic alcoholism in the course of alcohol withdrawal syndrome (AWS). Stasuikinene VP, et al. Russia. Ter Arkh. 2004;76(11):97-9. Ed: Magnesium 250 mg twice a day should probably be given to all AWS patients.  In fact, the same is healthy for all everyone.

Short-Term Detox Might Help: In a study of 479 admitted alcoholics, of whom 86% were interviewed 3 months after discharge, 60.5% of the intention-to-treat sample and 54% of the follow-up sample had relapsed. 28% had taken part in inpatient rehabilitation programs, and 26.5% had had at least one further inpatient withdrawal treatment. There were highly significant reductions in quantity of consumed alcohol, numbers of drinking days, and numbers of intoxication days. Multivariate analyses revealed that biographical, social, and treatment-related items were predictors of unfavorable outcome. A short length of stay was identified as a predictor of unfavorable health status after 3 months. Short-term effects of acute inpatient treatment of alcoholics. A prospective, multicenter evaluation study. Reker T, et al. Westfalische Klinik fur Psychiatrie, Munster. t.reker@wkp-muenster.de. Nervenarzt. 2004 Mar;75(3):234-41. Ed: This is not a controlled study.  Thus, it cannot be used as any proof of benefit.

Thiamine Defiency in Alcoholism May Damage the Cerebellum: Chronic alcohol consumption is frequently accompanied by cerebellar degeneration. A decrease in dentate nuclei intensity would indirectly indicate that iron accumulation, and therefore, oxidative stress may play a role in alcoholic cerebellar degeneration. In an MRI study of 45 alcoholics and 44 age and controls, dentate nuclei intensity was not significantly decreased in patients with chronic alcohol consumption (65.4 vs. 69.0)(p = 0.15). In contrast, vitamin B1 level correlated with cerebellar size in alcoholics even if the vitamin B1 concentration was within normal values (p = 0.028). Thiamine deficiency rather than direct neurotoxic effects of alcohol is the main causative factor for the development of alcoholic cerebellar degeneration. Vermal atrophy of alcoholics correlate with serum thiamine levels but not with dentate iron concentrations as estimated by MRI. Maschke M, et al. University Duisburg-Essen, Germany. matthias.maschke@uni-essen.de. J Neurol. 2005 Jun;252(6):704-11. Chronic alcohol consumption can result in thiamine deficiency by causing inadequate nutritional thiamine intake, decreased absorption of thiamine from the gastrointestinal tract, and impaired thiamine utilization in the cells. The major manifestations of thiamine deficiency in humans involve the cardiovascular (wet beriberi) and nervous (dry beriberi, or neuropathy and/or Wernicke-Korsakoff syndrome) systems. There has been a significant reduction in the prevalence of WKS in Australia since the introduction of thiamine enrichment of bread flour.

Thiamine 200 mg IM for Two Days Helped Patients Going Through Detox: Wernicke-Korsakoff syndrome (WKS) is most often seen in people who are alcohol dependent. Treatment with thiamin may rapidly resolve acute symptoms. However, much evidence suggests that identification of WKS on clinical examination is relatively insensitive when compared with diagnosis after death. In a 2-day DB PC study of 107 alcoholics going through detox and without the clinical triad of acute WKS, patients were given different doses of intramuscular thiamin for two consecutive days, ranging from 5 mg to 200 mg. A superior performance was found in the group that received the highest dose of thiamin, compared with the other four treatment groups. Thiamin treatment and working memory function of alcohol-dependent people: preliminary findings. Ambrose ML, et al. University of Melbourne, Australia. m.ambrose@psych.unimelb.edu.au. Alcohol Clin Exp Res. 2001 Jan;25(1):112-6.; 9 patients with no history of alcohol abuse but with acute signs of ophthalmoplegia or nystagmus and ataxia resolved within 48 h after intravenous thiamine. Precipitating events included vomiting 2, drastic weight-reducing diet 2, renal colic in a postpartum woman 1, colonic surgery 2 and chronic hemodialysis 1. In 2 patients there was no obvious precipitating event but their history was suggestive of a genetic predisposition. Eur Neurol. 2001;45(1):34-7. Rare anaphylactoid reactions have occurred with the use of parenteral thiamine.

Thiamine Deficiency Common, Not Riboflavin or B-6: In a study of alcoholics admitted for detoxification without evidence of significant brain damage, alcoholics known to have severe chronic brain damage (BDAM), and controls, 20% of alcoholics had an abnormally low thiamine activity and an abnormally high activation ratio, while 45% were abnormal in either one or both parameters. An additional 10% had an abnormally high activation ratio but normal ETK activity, as did 30% of the BDAM group. There was no evidence of riboflavin or pyridoxine deficiency in either of the patient groups. Individual susceptibility to Wernicke-Korsakoff syndrome and alcoholism-induced cognitive deficit: impaired thiamine utilization found in alcoholics and alcohol abusers. Heap LC, et al. Kings College, London, UK. Psychiatr Genet. 2002 Dec;12(4):217-24.

Beta-Blockers Should Be Started If Small Varices: Beta-blockers are extensively used to prevent variceal bleeding in patients with large esophageal varices. In a 5-year study of 161 patients with cirrhosis and small esophageal varices, 9 patients on nadolol and 29 on placebo had growth of esophageal varices: 20% versus 51% (P < 0.001). The cumulative probability of variceal bleeding was also lower in patients randomized to nadolol (P = 0.02). Survival was not different (P = 0.33). Adverse effects resulting in withdrawal of drug occurred in 9 in the nadolol group and one in the placebo group (P = 0.01). A placebo-controlled clinical trial of nadolol in the prophylaxis of growth of small esophageal varices in cirrhosis. Merkel C, et al. University of Padua, Italy. carlo.merkel@unipd.it. Gastroenterology. 2004 Aug;127(2):476-84.