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PubMedDate not supplied

[Social functioning of patients with alcohol dependence treated with disulfiram at the substance abuse treatment center].

The effect of disulfiram ("Anticol") treatment lasting from 7 to 12 months of 57 alcohol dependent out-patients was evaluated. The satisfactory results (i.e. patients remained abstinent and took the medication regularly) were observed in 30 patients. Those patients did not differ from others in regard to age, length of alcohol abuse, the severity of dependence, the genetic encumbrance , the features of alexithymia , and the membership of AA-clubs. The percentage of patients with positive treatment results was significantly higher among subjects with high self-motivation to treatment, among married subjects, and among those professionally active. The findings are similar to the recent American results where about a half of alcoholics showed positive effects of disulfiram treatment, especially those with high motivation to the treatment and with the stabile social position.

Adult↗
PubMed1991

[Fulminating hepatitis after treatment with naproxen and/or disulfiram?].

A 49 year old female was started on disulfiram. Six weeks later she was given naproxen because of epicondylitis. After 5 days' treatment with naproxen she complained of nausea, anorexia and jaundice. At admission, bilirubin was 452 mumol/l, aspartate aminotransferase (ASAT) 1925 U/I, alanine aminotransferase (ALAT) 2815 U/I and prothrombin time measured as Normotest was 27%. The patient developed a fulminant hepatitis and died in hepatic coma almost four weeks after the introduction of naproxen. Postmortem examination disclosed a small liver (1,100 g) and histological examination showed massive necrosis and collapse of the lobules. The naproxen was the most probable cause of death, but it is impossible to exclude disulfiram as causative agent.

Chemical and Drug Induced Liver Injury↗
PubMed1990

[Disulfiram implants. Lack of pharmacological and clinical effects].

The therapeutic rationale for using implanted disulfiram is possible inhibition of the liver enzyme acetaldehyde dehydrogenase, producing an acetaldehyde-mediated aversive reaction after intake of ethanol. Several studies using volunteers and patients in a double blind controlled study produced no evidence that a disulfiram implant (1 g) has any significant pharmacological or clinical action, except for a higher frequency of local surgical complications.

Alcoholism↗
PubMedDate not supplied

Trace element status in alcoholism before and during disulfiram treatment.

Trace element status was ascertained in 19 alcoholic patients under long-term treatment with disulfiram and in 12 alcoholic patients treated for the first time; the latter group was re-examined after four weeks of treatment. Both groups were compared to matched controls with a moderate alcohol intake. The copper/zinc ratio in serum was increased in the patients under long-term treatment, and a significant decrease occurred during the first four weeks of treatment in the second group. Blood lead was slightly increased in the second group, but not in the patients under long-term treatment. Blood cadmium was high in both groups, perhaps related to excessive tobacco smoking. Blood mercury concentrations were uniformly low. Urinary nickel excretion in the first group was above reference values, and an increase was seen in the second group during the treatment period. Although trace element concentrations in body fluids may not reflect tissue levels, the results support the notion that trace element balances are influenced by alcoholism and disulfiram treatment.

Adult↗
PubMed1987

Metabolism of biogenic aldehydes in human blood: effects of ethanol, acetaldehyde and disulfiram.

The metabolism of biogenic aldehydes was measured in different fractions of human blood. Isolated erythrocytes, leukocytes, platelets and plasma were incubated with the aldehydes derived from dopamine and serotonin (DOPAL and 5-HIAL, respectively). The disappearance of the aldehydes and the formation of the acid and alcohol metabolites were analysed using HPLC with electrochemical detection. When erythrocytes were incubated with 1 microM DOPAL or 5-HIAL only the acid metabolites were formed, whereas both acid and alcohol metabolites were formed in incubations with leukocytes or platelets. No metabolites were formed when the aldehydes were incubated with plasma. In incubations with erythrocytes, the oxidation of the aldehydes was totally inhibited in the presence of 50 microM disulfiram, whereas the formation of both acid and alcohol metabolites was inhibited in incubations with platelets. Disulfiram did not affect the metabolism of DOPAL or 5-HIAL in incubations with leukocytes. The oxidation of the aldehydes was inhibited by 50-70% in the presence of a 500-fold excess of acetaldehyde. Ethanol at a concentration of 10 mM did not affect the metabolism.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

[Disulfiram and acute liver damage].

Few serious side effects have been reported from use of disulfiram. In this article we present a case where therapeutic doses of disulfiram resulted in acute liver damage. We also found neurological symptoms, although such side effects from use of this drug are rare.

Acute Disease↗
PubMedDate not supplied

[The effect of disulfiram on lipid metabolism in the rat liver].

Administration of disulfiram (200 mg/kg intragastrically for 3 days) was followed by an increase in the rat liver contents of total phospholipid fraction, triacylglycerine, lisophosphatidylcholine and a decrease in the relative level of phosphatidylethanolamine. This was associated with a decrease in the involvement of the tracer from 14C-ethanol in triacylglycerines, total phospholipids, lisophosphatidylcholine and cardiolipin. Alcohol injection (a 20% solution intraperitoneally in a dose of 1 g/kg for 30 minutes) against the background of treatment with disulfiram leads, in addition to the above-mentioned changes, to an increase of phosphatidylcholine concentration, a decrease of specific radioactivities of cholesterol, diacylglycerine and sphyngomyelin.

Animals↗
PubMed1989

Disulfiram hepatotoxicity: a consideration of its mechanism and clinical spectrum.

Disulfiram-induced hepatotoxicity is a recognised entity despite the difficulty in determining its contribution to the damage when alcoholism itself is a frequent cause of liver disease. Less well characterised is the mechanism of disulfiram-induced hepatotoxicity and the high fatality rate associated with this entity. The clinical spectrum of the disease is reviewed and experimental data suggesting the mechanism of toxicity are presented. Failure to recognise this problem and to terminate therapy as soon as possible may result in death due to massive hepatic necrosis.

Alcoholism↗
PubMed1987

Inhibitory effect of disulfiram (Antabuse) on alcohol dehydrogenase activity.

We investigated the effect of disulfiram (Antabuse) on the activity of alcohol dehydrogenase (EC 1.1.1.1) in vitro. We observed a time-dependent inhibition of this dehydrogenase by disulfiram and diethyldithiocarbamate similar to that obtained for aldehyde dehydrogenase (EC 1.2.1.3). These results suggest a possible explanation for various side effects observed in the clinical use of Antabuse.

Alcohol Dehydrogenase↗
PubMed1979

Effect of dopamine-beta-hydroxylase inhibitor (disulfiram) on the response of adenohypophysis, serum ceruloplasmin and hypothalamic ascorbic acid to estradiol treatment.

The administration of tetraethylthiuramdisulfide (disulfiram, Antabus--inhibitor of dopamine-beta-hydroxylase) resulted in an inhibition of the response of anterior pituitary to estradiol (i. e. increase of weight and of binding capacity of anterior pituitary proteins to thyroxine). At the same time there was no inhibition of an increase of ceruloplasmin (polyphenoloxidase) level after estradiol, while a decrease of ascorbic acid in hypothalamus was fully prevented. It was concluded that disulfiram may inhibit dopamine-beta-hydroxylase activity and thus presumably protect the hypothalamic dopamine which further inhibits the response of anterior pituitary to estradiol either directly or through a dopamine dependent growth inhibiting factor.

Animals↗
PubMed1986

Disulfiram and bipolar affective disorder: a case report.

The authors describe a case of bipolar affective disorder associated with disulfiram therapy and its interaction with ethanol. They recommend caution when prescribing disulfiram for patients with personal and familial antecedents of affective illness.

Bipolar Disorder↗
PubMed1986

Supervised disulfiram in alcoholism.

Despite its well-documented specific effectiveness in controlled trials, the alcohol-sensitizing drug disulfiram (Antabuse) is not widely prescribed in Britain for the management of alcohol abuse and it often arouses hostile and irrational feelings. However, interest in it is reviving. This paper reviews the evidence for its effectiveness, emphasizes the importance of correct dosage and supervised administration and of viewing disulfiram as generally only one component of treatment. Its low toxicity--especially compared with alcohol--is emphasized and the main arguments of its opponents are examined.

Alcoholism↗
PubMed1984

Disulfiram implantation: a dose response trial.

Alcoholic volunteers (N = 120) were assigned at random to receive an 800 mg, 1200 mg, or 1600 mg subcutaneous disulfiram implant. Patients were followed for a 2-year period. Although all groups showed an increase in sobriety following implantation, there was no significant dose-response relationship. There were no significant between-group differences in the incidence of disulfiram-ethanol reaction.

Adult↗
PubMed1984

Control of the human head louse with disulfiram and benzyl benzoate emulsions. A laboratory study.

The effects of disulfiram, benzyl benzoate and DDT, all components of a common preparation (Tenutex) for the control of the head louse, were tested on louse eggs. A significant higher mortality of eggs was evident after treatment with (i) disulfiram, (ii) benzyl benzoate, (iii) these two substances mixed, and (iv) Tenutex. DDT in this concentration had no effect on the survival of the eggs. Long-time exposure to Tenutex and Tenutex without DDT significantly lowered the hatching frequency of eggs. Almost no hatching occurred after exposure for 24 hours. The survival of larvae hatched from eggs treated with Tenutex was lower than for those treated with Tenutex without DDT. DDT seemed to have an effect primarily on the survival of larvae. Newly hatched larvae were more sensitive to the two Tenutex preparations than older larvae.

Benzoates↗
PubMed1980

Disulfiram neuropathy.

Disulfiram (Antabuse) can produce neuropathy in daily doses of less than the usually recommended 500 mg. The four recent cases reported in this paper emphasize the need for greater recognition of this condition. Nerve biopsies showed axonal degeneration. The neuropathy is difficult to distinguish from that associated with ethanol abuse. Disulfiram neuropathy occurs after a variable latent period (mean 5 to 6 months) and progresses steadily. Slow improvement may occur when the drug's use is stopped; often there is complete recovery eventually.

Adult↗
PubMed1983

Ethanol-cephalosporin antibiotic interactions: an animal model for the detection of disulfiram (Antabuse)-like effects.

Disulfiram (Antabuse)-like reactions occurring in patients undergoing antibacterial therapy with certain cephalosporin antibiotics, and after ingestion of ethanol, are well documented. A murine model is described which may prove useful in the detection of compounds likely to produce this effect. Eight cephem compounds (moxalactam, cefamandole, cefmetazole, cefonicid, cefmenoxime, cefoperazone, cefotiam, ceforanide) each carrying an N-methyltetrazolethiol substituent in the 3-position of the dihydrothiazine ring of the parent antibiotic were capable of inducing a disulfiram-like reaction in the test animals. Evidence is presented which strongly suggests a direct relationship between N-methyltetrazolethiol and related heterocyclic thiols and the ability to induce this reaction.

Animals↗
PubMed1983

Fulminant hepatitis associated with disulfiram. Report of a case.

Disulfiram is used commonly as reinforcement in the treatment of chronic alcoholism. Although the drug is generally considered safe, there are reports of side effects including psychosis and hepatitis. We report a case of fatal fulminant hepatitis caused by the use of disulfiram in a man with previously normal hepatocellular function.

Acute Disease↗
PubMed1980

[The metabolism of halothane under the influence of thiopental, methohexital, etomidate, enflurane and disulfiram under clinical conditions (author's transl)].

The biotransformation of halothane is supposed to be the cause of the rare "halothane-hepatitis". Therefore an inhibition of the metabolism of Halothane is of some interest. We used bromide as a metabolite of Halothane and investigated the bromide level of the serum of patients after halothane anaesthesia by means of x-ray fluorescence spectrometry. The induction of anaesthesia with Thiopental, Methohexital and Etomidate had no influence on the bromide level. Likewise the influence of Enflurane on the metabolism of Halothane was not significant. An effective inhibitor in man is Disulfiram. The authors assume, that further information about the toxicity of Halothane metabolites can be gained through further studies of drugs like Disulfiram.

Adolescent↗