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Doctors of many specialties, including the family doctors, encounter the problems of alcohol abuse in their patients. Due to the fact that many symptoms of dangerous diseases can be masked by the fact of alcoholism, a brief doctor's visit has to be conducted with watchfulness, caution and care. Family doctors have some brief testes (such as CAGE test, AUDIT test), besides of precise anamnesis and blood chemistry, which make it easier to identify a patient with an alcohol problem. People with disabilities are more exposed to alcohol abuse since they often experience additional factors such as unemployment, social isolation and homelessness. All of the above factors foster the more frequent alcohol usage. In Poland the main treatment method of alcohol addiction is psychotherapy practiced in the rehab centers. The detoxification treatment is voluntary and free of charge even though the patients checking into those facilities are doing it against their will. They are forced to do so by entourage, family, spouse or risk of unemployment. Acamprozate is considered as a drug, run to extend abstaining from alcohol. In the past, therapy with disulfiram substance was common, but now, it is considered as unethical behaviour. In practice of medicine, a patient with alcohol addiction creates not onlya medical but also legal problems. Therefore keeping of detailed medical documentation is very important as it may become significant evidence in the future.
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CM enhances outcomes for CBT treatment of cocaine dependence, but disulfiram provided no added benefit to the combination of CM and CBT.
Fifty-nine couples with an alcoholic husband, after receiving weekly BMT couples sessions for 5-6 months, were assigned randomly to get or not get 15 additional couples relapse prevention (RP) sessions over the next 12 months. Outcome measures were collected before and after BMT and at quarterly intervals for the 30 months after BMT.
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Individual therapists in office practice are often considered to have limited effectiveness in treating alcohol and drug dependence. In this article the author describes network therapy, an approach developed to assure greater success in such treatment. It uses psychodynamic and behavioral therapy while engaging the patient in a support network composed of family members and peers. A cognitive-behavioral model of addiction, based on the role of conditioned withdrawal in relapse, is described. Related techniques for securing abstinence are then reviewed; they augment individual psychotherapy to help patients avoid relapse caused by the affective and environmental cues that precipitate drug seeking. The role of social cohesiveness as a vehicle for engaging patients in treatment is outlined next, along with a related technique for enhancing an addicted patient's commitment to the therapy. This is done by using the patient's family and peers as a therapeutic network to join the patient at intervals in therapy sessions. The network is managed by the therapist to provide cohesiveness and support, undermine denial, and promote compliance with treatment. The author presents applications of the network technique designed to sustain abstinence and describes means of stabilizing members' involvement. Applications of network therapy to ambulatory detoxification, disulfiram and naltrexone administration, relapse prevention, and contingency contracting are reviewed.
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Cancer stem cells may be responsible for acquired pan-chemoresistance. As a drug used in clinic, DS may be repurposed as a CSC inhibitor to reverse the acquired pan-chemoresistance.
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Hepatic enzymes connected with the formation and metabolism of free D-glucuronic acid were affected in rats after treatment with disulfiram or diethyldithiocarbamate (300 mg/kg, intragastrically, per day, 4 X). The activities of UDPglucose dehydrogenase, UDPglucuronic acid pyrophosphatase, UDPglucuronosyltransferase and L-gulonate dehydrogenase were enhanced, while those of glucose-6-phosphate dehydrogenase, beta-glucuronidase and D-glucuronolactone dehydrogenase were inhibited. These changes were more pronounced with disulfiram than diethyldithiocarbamate. Treatment with phenobarbital (80 mg/kg, i.p., per day, 4 X) enhanced UDP glucuronosyl-transferase, but brought about different effects on the other enzymes. Concurrent administration of phenobarbital with disulfiram or diethyldithiocarbamate led to potentiation or antagonism of the primary effects of each compound when given alone. The results suggest that activation of the D-glucuronic acid pathway may proceed in various ways, and that it is not necessarily followed by a simultaneous induction of the microsomal mixed-function oxygenase activity.
Acamprosate, disulfiram (DIS), naltrexone and nalmefene can be used in treating alcohol use disorders. The drugs are, however, underutilized.
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Alcohol--orally given in concentrations from 1 to 4 g/kg body-weight--leads to a reduction of mast cells in the guinea pig lung. At the same time a minor decrease of histamine concentration was observed. The incompatibility reaction with alcohol after disulfiram intake (DAR) shows an additional degranulation oft mast cells of the lungs and decrease of histamine-content. So far, there seems little difference between the influence of disulfiram alone and the DAR. Besides thrombocytes and basophile leucocytes, the mast cells of the lung are responsible for the release of histamine and serotonine during higher alcohol concentrations and alcohol-disulfiram-reactions. We think that the intolerance phenomena of humans after alcohol--f.e. in form of flush-reaction--is at least partly related to the concomitant influence oft mast cell-substances.
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Benzo[a]pyrene (BP) administered to female outbred ICR/Ha mice by oral intubation induced neoplasia in the forestomach after 30 weeks in more than 90% of treated animals. However, no tumors occurred at that site if 1% disulfiram was added to the experimental diet. This inhibition of tumor formation was paralleled by a large inhibition of macromolecular binding of [3H]BP and [14C]BP to RNA and protein in the forestomach. The inhibitory effect of specific binding was strongest in the RNA fraction isolated at 8,000 X g for 20 minutes (6 times that of the control) and weakest in the DNA fraction (no significant difference). The highest specific binding was measured in the RNA fraction isolated at 32,000 X g for 120 minutes and the lowest binding in the DNA fraction. The relative distribution of the BP binding was such that greater than 90% of the BP was bound to protein and less than 1% was bound to DNA. Of the total inhibition of BP binding to all the macromolecular species studied, that to protein constituted the largest component (95%). In contrast to the forestomach, no inhibitory effect of BP binding to DNA, RNA, or protein by disulfiram was found in the liver, which remained free of cancer under the experimental conditions employed.
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The injection of ethanol (70 mmol/kg body weight) into male Wistar rats fed ad libitum caused an increase within 15 min in the liver inorganic pyrophosphate (PPi) content from 0.012 +/- 0.001 mumol/g (wet weight) to 0.029 +/- 0.001 mumol/g. The injection of acetate (20 mmol/kg body weight) increased the liver PPi to 0.157 +/- 0.075 mumol/g in 15 min. The alcohol dehydrogenase inhibitor 4-methylpyrazole blocked the accumulation of acetate and the increase in PPi was prevented. Disulfiram, an inhibitor of aldehyde dehydrogenase, did not prevent changes in redox state, but the accumulation of acetate in the liver was decreased and the increase in liver PPi content was diminished (0.019 +/- 0.003 mumol/g). These data suggest that the increase in PPi observed after injection of ethanol may be due to the activation of the acetate produced during ethanol and acetaldehyde oxidation.
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An NAD(P)-dependent 3 alpha-hydroxysteroid dehydrogenase (EC 126.96.36.199) was purified to homogeneity from rat liver cytosol, where it is responsible for most if not all of the capacity for the oxidation of androsterone, 1-acenaphthenol and benzenedihydrodiol (trans-1,2-dihydroxycyclohexa-3,5-diene). The dehydrogenase has many properties (substrate specificity, pI, Mr, amino acid composition) in common with the dihydrodiol dehydrogenase (EC 188.8.131.52) purified from the same source [Vogel, Bentley, Platt & Oesch (1980) J. Biol. Chem. 255, 9621-9625]. Since 3 alpha-hydroxysteroids are by far the most efficient substrates, the enzyme is more appropriately designated a 3 alpha-hydroxysteroid dehydrogenase. It also promotes the NAD(P)H-dependent reductions of quinones (e.g. 9,10-phenanthrenequinone, 1,4-benzoquinone), aromatic aldehydes (4-nitrobenzaldehyde) and aromatic ketones (4-nitroacetophenone). The dehydrogenase is not inhibited by dicoumarol, disulfiram, hexobarbital or pyrazole. The mechanism of the powerful inhibition of this enzyme by both non-steroidal and steroidal anti-inflammatory drugs [Penning & Talalay (1983) Proc. Natl. Acad. Sci. U.S.A. 80, 4504-4508] was examined with several substrates. Most non-steroidal anti-inflammatory drugs are competitive inhibitors (e.g. Ki for indomethacin, 0.20 microM for 9,10-phenanthrenequinone reduction at pH 6.0, and 0.835 microM for androsterone oxidation at pH 7.0), except for salicylates, which act non-competitively (e.g. Ki for aspirin, 650 microM for androsterone oxidation). The inhibitory potency of these agents falls sharply as the pH is increased from 6 to 9. Most anti-inflammatory steroids are likewise competitive inhibitors, except for the most potent (betamethasone and dexamethasone), which act non-competitively. The enzyme is inhibited competitively by arachidonic acid and various prostaglandins.