formiminoglutamic-acid and Alcoholism

Topics: Absorption; Aged; Alcoholism; Anemia, Sickle Cell; Anticonvulsants; Arthritis, Rheumatoid; Biological Assay; Biological Transport; Bone Marrow; Carrier Proteins; Chemical Phenomena; Chemistry; Contraceptives, Oral; Female; Folate Receptors, GPI-Anchored; Folic Acid; Folic Acid Antagonists; Folic Acid Deficiency; Food Analysis; Formiminoglutamic Acid; Glutamate Formimidoyltransferase; Humans; Hydroxymethyl and Formyl Transferases; Infant; Infant Nutritional Physiological Phenomena; Infant, Newborn; Infections; Kidney Failure, Chronic; Malabsorption Syndromes; Malaria; Methotrexate; Neoplasms; Nervous System Diseases; Nutritional Requirements; Parenteral Nutrition, Total; Pregnancy; Pyrimethamine; Receptors, Cell Surface; Terminology as Topic; Thalassemia; Transferases; Trimethoprim

Topics: Alcoholism; Animals; Beer; Bone Marrow Cells; Erythropoiesis; Folic Acid; Folic Acid Deficiency; Formiminoglutamic Acid; Humans; Intestinal Absorption; Liver Diseases, Alcoholic; Nutrition Disorders; Peripheral Nervous System Diseases; Psychoses, Alcoholic; Tetrahydrofolates; Thrombocytopenia; Vitamin B 12; Vitamin B 12 Deficiency; Wine

The chronic administration of ethanol or brief exposure to nitrous oxide (N2O) decreases the activity of hepatic methionine synthase and disrupts normal metabolic processes that require folate and vitamin B12. This combination of drugs has clinical relevance since alcoholic patients often require surgery and receive N2O as a component of their anesthetic. To assess this clinical problem using a rodent model, rats were given a liquid ethanol diet (35% of calories as ethanol) and control rats were pair-fed a liquid diet with carbohydrate substituting for the caloric content of ethanol. After receiving liquid diets for 6 weeks, rats were exposed to 60% N2O/40% O2 for 6 hr. Urinary excretions of formic acid and formiminoglutamic acid (FIGLU) were used as indirect markers of folate status. In both the ethanol-fed and control groups, excretion of formic acid and FIGLU markedly increased the first day after N2O and returned towards background values by the second day after N2O exposure. Ethanol treatment alone decreased methionine synthase activities in liver, but not kidney or brain. Exposure to N2O further decreased methionine synthase activities, and recovery of methionine synthase activity after N2O occurred over a period of 4 days at the same rate in both the ethanol-fed and control groups. Ethanol treatment for 6 weeks combined with acute exposure to N2O did not deplete the rats of vitamin B12 in blood, liver, kidney, or brain. We conclude that in this animal model, chronic treatment with ethanol does not markedly exacerbate the disturbances in folate/vitamin B12 metabolism caused by brief exposure to N2O.

Topics: 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; Alcoholism; Animals; Folic Acid; Formates; Formiminoglutamic Acid; Liver; Male; Nitrous Oxide; Rats; Rats, Inbred Strains; Vitamin B 12

Forty-six male alcoholics hospitalized with polyneuropathy or intellectual impairment were studied after at least 2 wk of alcohol abstention. Neurological evaluation included neurophysiological examination of the sural nerve and tibial nerve, neurophysiological examinations, and CT-scanning of the brain. Alcohol and vitamin intakes were quantified by the interview method. Vitamin B-12 and folate status included examinations of peripheral blood and bone marrow aspirate, plasma vitamin B-12, plasma and erythrocyte folate, formiminoglutamic acid excretion test (FiGlu), methylmalonic acid excretion, and deoxyuridine suppression test (dU) on phytohemagglutinin-stimulated peripheral lymphocytes. The liver function was assessed by galactose elimination capacity and plasma clearance of antipyrine. There was no hematological sign of folate or vitamin B-12 deficiency. About 8% had low plasma folate, while neither erythrocyte folate nor plasma vitamin B-12 were decreased. However, half of the patients had functional folate deficiency as determined by abnormal FiGlu or dU. Compared to the remaining patients, those with abnormal FiGlu or dU had significantly more abnormal neurophysiological tests, and lower folate intake. There was no correlation between FiGlu or dU and the quantitative liver function tests. It is concluded that 1) folate deficiency may contribute to the development of alcoholic polyneuropathy, 2) the classical parameters for folate deficiency (blood concentrations, peripheral blood, and bone marrow examinations) are not reliable in diagnosing folate deficiency and 3) functional tests like FiGlu and dU are necessary to diagnose folate deficiency in alcoholics.

Topics: Adult; Alcoholism; Deoxyuridine; Folic Acid; Folic Acid Deficiency; Formiminoglutamic Acid; Hematologic Tests; Hepatic Encephalopathy; Humans; Liver Function Tests; Male; Middle Aged; Neurologic Examination; Peripheral Nervous System Diseases; Vitamin B 12; Vitamin B 12 Deficiency

A modification of the enzymic method of Tabor and Wyngarden for formiminoglutamate (FIGLU) estimation in urine is described. Alkaline degradation of FIGLU in blanks enhanced the sensitivity of the method. FIGLU excretion in 94 healthy persons indicated a sex and age dependence. Short term calorie restriction or fasting led to a decrease of FIGLU excretion while acute alcohol intoxication or chronic alcohol administration were accompanied by enhanced FIGLU excretion. It is suggested that decreased FIGLU excretion was due to histidine deficiency.

Topics: Adult; Age Factors; Aged; Alcoholic Intoxication; Alcoholism; Diet; Energy Intake; Fasting; Female; FIGLU Test; Formiminoglutamic Acid; Glutarates; Humans; Male; Middle Aged; Reference Values; Sex Factors

Topics: Alcoholism; Amino Acids; Anemia; Anemia, Pernicious; Chemical Phenomena; Chemistry; Deficiency Diseases; Folic Acid; Formiminoglutamic Acid; Glutamates; Histidine; Humans; Proteins; Urine