vitamin-k-semiquinone-radical and Alcoholism

Chronic alcoholics frequently have evidence of nutritional deficiency due to decreased intake, reduced uptake and impaired utilisation of nutrients. The alcoholic has increased nutrient requirements due to greater metabolic demands and the need for tissue repair. Chronic alcohol-related brain damage can often be a direct result of nutrient depletion, particularly of the vitamins thiamine, B12, nicotinamide and pyridoxine. Lesser degrees of brain damage are frequently unrecognised, and by the time a vitamin deficiency syndrome has developed and been diagnosed, irreversible damage has often occurred. The development of suitable computerised psychometric tests may allow earlier detection of brain malfunction associated with malnutrition, which can be reversed by nutrient repletion before permanent damage occurs. Circulating levels of vitamins can be a valuable guide to nutritional status, although care is needed when interpreting the results of such tests in the alcoholic. Sensitive microbiological and biochemical tests for assessing vitamin status in man have been available for some years, and in addition, new biochemical methods are constantly being developed. It is important that such methods are evaluated, and possibly adapted for clinical use where appropriate. Newer methods may have significant advantages over older, more established techniques. For thiamine and pyridoxine, for example, methods now exist to determine accurately circulating levels of the active forms of these vitamins, which could give more direct assessment of vitamin status than earlier methodology that uses indirect measurements, such as red cell enzyme activities. On the other hand, in the case of folate and B12, there has been a tendency to opt for the easy-to-perform radioassay techniques, when in fact the earlier microbiological methods offer greater sensitivity and probably also better accuracy. Technically difficult assays should not be disregarded if they can give information which is of greater clinical use than a simpler assay technique. Clinical laboratories should always bear in mind what their vitamin methods are actually measuring, particular consideration being given to whether metabolically inactive forms or analogues are determined in the assay. This can be of importance to the interpretation of vitamin data in the alcoholic, who often has problems forming active vitamins from their precursors.(ABSTRACT TRUNCATED AT 400 WORDS)

Topics: Alcoholism; Ascorbic Acid; Avitaminosis; Ethanol; Humans; Intestinal Absorption; Nutrition Disorders; Nutritional Requirements; Vitamin A; Vitamin B Complex; Vitamin D; Vitamin E; Vitamin K; Vitamins

Topics: Alcoholism; alpha-Tocopherol; Animals; Calcifediol; Factor VII; Humans; Hydroxycholecalciferols; Intestinal Absorption; Liver Diseases, Alcoholic; Prothrombin Time; Tocopherols; Vitamin D; Vitamin D Deficiency; Vitamin E; Vitamin E Deficiency; Vitamin K; Vitamin K 1; Vitamin K Deficiency

Levels of oxidative defenses and blood-clotting factors are normally reduced in newborns, increasing the risk of injury to developing brain structures around the time of birth. This early neonatal vulnerability corresponds to a timeframe in which the development of reward-related limbic structures is particularly active. Taking advantage of a serendipitous event in the history of treating newborns, we tested the hypothesis that vitamin K supplementation, administered to facilitate the synthesis of blood-clotting proteins within this critical timeframe, might also reduce the development of alcohol dependence later in life.. Subjects were approximately full-term male infants, selected from a large Danish birth cohort. Two thirds of the original 330 subjects in this study were high-risk sons of alcoholic fathers; 241 of the total completed the 30-year follow-up. Of subjects reported on for this article (N = 238), 44 received vitamin K supplementation at birth; 161 were considered high risk, and 66 were categorized as having lower birth weight (<6 lbs). A comprehensive series of measures was obtained on each subject before, during and shortly after birth as well as at 1 year of age. The Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised, diagnosis of alcohol dependence and a measure of lifetime problem drinking served as the 30-year outcome variables.. Vitamin K treatment, inherited risk and low birth weight each independently predicted alcohol dependence and problem drinking at age 30. Vitamin K treatment was associated with significantly lower rates of alcohol dependence and fewer symptoms of problem drinking.. Vitamin K treatment at birth might protect against the development of alcoholism in adults by reducing early postnatal hemorrhage and oxidative brain damage.

Topics: Adolescent; Adult; Alcoholism; Blood Coagulation Factors; Brain Damage, Chronic; Cerebral Hemorrhage; Child; Child of Impaired Parents; Child, Preschool; Cohort Studies; Denmark; Follow-Up Studies; Humans; Infant; Infant, Low Birth Weight; Infant, Newborn; Infant, Newborn, Diseases; Limbic System; Male; Oxidative Stress; Reward; Risk; Vitamin K

Purpura fulminans is a rare syndrome of progressive hemorrhagic necrosis of the skin that may present as a dermatologic emergency. It most commonly affects children during the convalescent phase of a streptococcal infection or a viral exanthem. In adults, it may be associated with sepsis or acquired causes. Its pathogenesis has challenged physicians for decades. It has been discovered that purpura fulminans is almost always associated with disseminated intravascular coagulation and can occur in subjects with inherited or acquired deficiencies of the protein C anticoagulant pathway. Patients with liver compromise may also be potential candidates for coagulopathies secondary to hepatic dysfunction and impaired protein synthesis. It is widely recognized that individuals who consume alcohol on a long-term basis may develop severe hepatotoxicity from ingestion of therapeutic doses of acetaminophen (500 to 1000 mg every 4 to 6 hours). We have observed a patient with chronic alcoholism in whom hepatotoxicity and purpura fulminans developed secondary to the ingestion of acetaminophen.

Topics: Acetaminophen; Adult; Alcoholism; Drug Therapy, Combination; Female; Heparin; Humans; Purpura; Skin; Vitamin K

There is evidence that vitamin K-deficiency during human pregnancy can be caused by the therapeutic use of warfarin or phenytoin. The pregnancy histories of three cases of Binder's syndrome are reported. One was associated with warfarin exposure, one with phenytoin exposure and one with alcohol abuse. It is proposed that Binder's syndrome can be caused by prenatal exposure to agents that cause vitamin K-deficiency. Sprague-Dawley rats were treated from postnatal day 1 to 12 weeks with daily doses of warfarin (100 mg/kg) and concurrent vitamin K1 (10 mg/kg). This regimen creates a net extra-hepatic vitamin K-deficiency. The treated rats developed with a distinct facial appearance characterized by a markedly reduced snout. Histological examination showed that the normally non-calcified septal cartilage was extensively calcified. It is proposed that normal growth of the septal cartilage is necessary for the development of the profile of the nose and midface and that normal growth will only take place while the septal cartilage is uncalcified.

Topics: Adolescent; Alcoholism; Aneurysm, Ruptured; Animals; Cartilage; Child, Preschool; Female; Humans; Infant; Intracranial Aneurysm; Male; Maxilla; Nasal Bone; Nasal Septum; Phenytoin; Pregnancy; Pregnancy Complications, Cardiovascular; Prenatal Exposure Delayed Effects; Rats; Rats, Sprague-Dawley; Thrombophlebitis; Vitamin K; Vitamin K Deficiency; Warfarin

Enzymatic and nonenzymatic mixed-function oxidase systems have been shown to generate an oxidant that catalyzes the inactivation of glutamine synthetase and other metabolic enzymes. Recent studies have shown that microsomes isolated from rats chronically fed ethanol generate reactive oxygen intermediates at elevated rates compared with controls. Microsomes from rats fed ethanol were found to be more effective than control microsomes in catalyzing the inactivation of enzymes added to the incubation system. The enzymes studied were alcohol dehydrogenase, lactic dehydrogenase, and pyruvate kinase. The inactivation process by both types of microsomal preparations was sensitive to catalase and glutathione plus glutathione peroxidase, but was not affected by superoxide dismutase or hydroxyl radical scavengers. Iron was required for the inactivation of the added enzymes; microsomes from the rats fed ethanol remained more effective than control microsomes in catalyzing the inactivation of enzymes in the absence or presence of several ferric complexes. The inactivation of enzymes was enhanced by the addition of menadione or paraquat to the microsomes, and rates of inactivation were higher with the microsomes from the ethanol-fed rats. The enhanced generation of reactive oxygen intermediates and increased inactivation of enzymes by microsomes may contribute toward the hepatotoxic effects associated with ethanol consumption.

Topics: Alcohol Dehydrogenase; Alcoholism; Animals; Enzyme Inhibitors; Ethanol; Ferric Compounds; Glutathione; Hydrogen Peroxide; L-Lactate Dehydrogenase; Male; Microsomes, Liver; Oxidation-Reduction; Oxygen; Paraquat; Pyruvate Kinase; Rats; Rats, Inbred Strains; Superoxide Dismutase; Vitamin K

Twenty male alcoholic subjects were studied initially within 1 day after stopping alcohol and again after about 1 week. Vitamin and mineral measurements were made on blood and abnormal prothrombin molecules quantitated for vitamin K status. Nine of the 20 patients received menadiol after the initial blood sample. Twelve of the alcoholics had significant elevations of abnormal prothrombin. Of these 12, all five who received vitamin K reduced the abnormal prothrombin levels toward normal but no change was observed in the seven who did not receive vitamin K. All nine patients receiving vitamin K lowered the abnormal prothrombin level significantly whereas there was no change in those 11 who did not receive vitamin K. The prothrombin time by the one-stage technique was normal in all patients. These data suggest that the production of abnormal prothrombin is frequently present in alcoholics and this may represent a subclinical vitamin K deficiency.

Topics: Adult; Alcoholism; Humans; Male; Middle Aged; Prothrombin; Vitamin K; Vitamin K Deficiency

The alcohol withdrawal syndromes are generally self-limited processes from which spontaneous recovery can be anticipated. To achieve this outcome, the various types of withdrawal must be managed in such a way as to prevent the occurrence of life-threatening situations. This begins with a good initial evaluation, followed by the appropriate pharmacologic and behavioral steps to control the severity of withdrawal symptoms and to manage complications. Once the withdrawal process is completed, the patient can then be entered into a long-term treatment program.

Topics: Acute Disease; Alcohol Withdrawal Delirium; Alcoholism; Benzodiazepines; Chloral Hydrate; Ethanol; Folic Acid; Gastrointestinal Hemorrhage; Hallucinations; Humans; Nutrition Disorders; Seizures; Social Support; Substance Withdrawal Syndrome; Thiamine; Vitamin K; Water-Electrolyte Imbalance

Alcoholic hepatitis is the precursor of cirrhosis. Susceptibility is independent of amount and duration of ethanol intake or of diet. Centrilobular hyalin, the key morphologic abnormality, sensitizes lymphocytes to secrete factors which may account (in part) for necrosis, liver cell destruction, increased collagen synthesis and development of cirrhosis. Diagnosis may be facilitated by detection of alcoholic hyalin antigen (AHAg) and antibody (AHAb) in serum of patients with alcoholic hepatitis. Treatment requires abstinence. Steroids have not reduced mortality rates. Measures to improve immunologic reactivity may be helpful. Persons unable to abstain should be enrolled in a surveillance group.

Topics: Alcoholism; Anemia; Animals; Diet; Ethanol; Hepatitis; Humans; Lymphocyte Activation; Macrophage Migration-Inhibitory Factors; Pyridoxine; Rabbits; Vitamin B 12 Deficiency; Vitamin K

Topics: Alcohol Withdrawal Delirium; Alcoholism; Chlorpromazine; Drug Therapy; Humans; Phenytoin; Psychoses, Alcoholic; Psychotic Disorders; Reserpine; Vitamin A; Vitamin K; Vitamins

Topics: Alcoholism; Antifibrinolytic Agents; Bilirubin; Blood; Drug Therapy; Hematologic Tests; Humans; Infusions, Parenteral; Liver Cirrhosis; Liver Cirrhosis, Alcoholic; Liver Function Tests; Prothrombin; Serum Albumin; Vitamin K; Vitamin K 1; Vitamins

Topics: Alcoholism; Anemia; Anemia, Macrocytic; Anorexia Nervosa; Ascorbic Acid; Avitaminosis; Celiac Disease; Deficiency Diseases; Diet; Diet Therapy; Female; Folic Acid; Humans; Infant; Infant, Newborn; Infant, Newborn, Diseases; Pregnancy; Pregnancy Complications; Sprue, Tropical; United Kingdom; Vitamin A; Vitamin B 12; Vitamin B Complex; Vitamin D; Vitamin K; Vitamins; Vomiting

Topics: Alcoholism; Anemia; Anemia, Hypochromic; Avitaminosis; Cholestyramine Resin; Common Bile Duct; Diet; Diet Therapy; Diuretics; Folic Acid; Folic Acid Deficiency; Gastrointestinal Hemorrhage; Humans; Hydrochlorothiazide; Ion Exchange Resins; Jaundice; Liver Cirrhosis; Liver Cirrhosis, Biliary; Postoperative Complications; Prothrombin Time; Vitamin B 12; Vitamin B Complex; Vitamin K

Topics: Alcohol Deterrents; Alcoholism; Apomorphine; Chlorpromazine; Diet; Diet Therapy; Disulfiram; Humans; Promazine; Psychoses, Alcoholic; Psychotic Disorders; Vitamin A; Vitamin K; Vitamins

Topics: Adrenal Cortex Hormones; Alcoholism; Arginine; Diet; Diet Therapy; Diuretics; Folic Acid; Glutamates; Humans; Lipotropic Agents; Liver Cirrhosis; Liver Cirrhosis, Alcoholic; Liver Extracts; Malates; Pterins; RNA; Spironolactone; Sulfonamides; Vitamin B Complex; Vitamin K

Topics: Alcoholism; Humans; Vitamin A; Vitamin K; Vitamins

Topics: Alcoholism; Ethanol; Humans; Vitamin A; Vitamin K; Vitamins

Topics: Alcoholism; Liver; Prothrombin; Vitamin K; Vitamin K 3

Topics: Alcoholism; Humans; Vitamin A; Vitamin K; Vitamins

Topics: Alcoholism; Humans; Vitamin A; Vitamin K; Vitamins

Topics: Alcoholism; Glucose; Humans; Vitamin A; Vitamin K; Vitamins