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Biomedical subjects

P Devenyi

Publications and source records attributed to P Devenyi.

At least 19 recordsLinked to original sources
PubMed1988

Bromocriptine in cocaine withdrawal--does it work?

Heavy cocaine use has been reported to lead to dopamine depletion in the brain, which in turn may be responsible for strong cocaine craving after withdrawal. Bromocriptine, a dopaminergic agonist, was used on that basis to prevent relapses in the withdrawal period. In an uncontrolled trial of 25 heavy cocaine users, measurements of pre- and post-bromocriptine serum prolactin levels-as indicators of inhibitory dopaminergic control-did not suggest dopamine depletion. Moreover, in 13 of these 25 patients, an assessment scale for craving and for other subjective discomforts indicated some improvement in only a slight majority, which is probably inseparable from placebo effect.

Adolescent↗
PubMed1987

Oral phenobarbital loading: a safe method of barbiturate and nonbarbiturate hypnosedative withdrawal.

We tested the efficacy and safety of oral phenobarbital loading, 120 mg/h until the end-point of mild intoxication is reached, for the treatment of hypnosedative withdrawal in 48 physically dependent patients, 14 of whom had a history of withdrawal seizures. None of the patients experienced seizures or any other symptoms of withdrawal during the study period, regardless of the phenobarbital half-life. The phenobarbital loading technique can be used in any hospital, not only those with access to specialized drug analysis laboratories. The method of treatment we describe allows the clinician to focus on issues such as rehabilitation instead of drug administration and manipulation of doses.

Administration, Oral↗
PubMed1986

Detection of an alcohol specific product in urine of alcoholics.

A simple procedure, using high performance liquid chromatography, was developed to detect and measure in urine an alcohol specific product, "ASP" indicative of chronic alcohol consumption. One day after hospital admission, the average amount of ASP in urine of alcoholics was 17 times higher than that of control subjects and 5 and 2 times higher after 7 and 14 days of abstinence, respectively. Urinary levels of ASP should be of value in the identification of chronic alcoholism.

Alcohol Drinking↗
PubMed1985

Prevention of alcohol withdrawal seizures with oral diazepam loading.

Twenty patients withdrawing from alcohol who had reliable histories of previous alcohol-withdrawal seizures and thus were at high risk for a subsequent seizure were treated in hospital with oral diazepam loading: 20 mg of the drug was given every hour to a minimum total of 60 mg. None of the patients had a seizure during the stay in hospital. We believe that phenytoin prophylaxis is not necessary in these circumstances. However, if the patient is already taking phenytoin, this drug should not be abruptly discontinued in the withdrawal period in favour of diazepam loading.

Adult↗
PubMed1984

High-density lipoprotein response to alcohol consumption and abstinence as an indicator of liver function in alcoholic patients.

A study of 36 alcoholic men admitted to hospital when intoxicated was undertaken to confirm the value of changes in the level of high-density lipoprotein cholesterol (HDL) as an indicator of liver function in patients with chronic alcoholism. In the patients without severe liver disease the HDL level was high after the recent consumption of alcohol and usually dropped by 0.2 mmol/L or more after 1 or 2 weeks of abstinence. In contrast, in the patients with severe alcoholic liver disease the HDL level was initially low and generally remained low after abstinence.

Alcohol Drinking↗
PubMed1983

Diazepam loading: simplified treatment of alcohol withdrawal.

Alcohol withdrawal therapy can be simplified with a loading dose of diazepam, taking advantage of the kinetic tapering afforded by the drug's long t 1/2s and its metabolites, and of the effectiveness of nonpharmacologic maneuvers. In a double-blind trial, 50 inpatients in moderate to severe alcohol withdrawal received 20 mg oral diazepam and supportive care (n = 25) or placebo and supportive care (n = 25) every 2 hr until they were asymptomatic. Fifty-six percent of patients responded to placebo within 5 +/- 2.9 hr (mean +/- SD), whereas 72% responded to initial diazepam within 6.3 +/- 3.9 hr. Patients treated with diazepam had more rapid and greater improvement than those treated with placebo. Patients who did not respond to six doses of diazepam received further (unblinded) diazepam, 20 mg, every 1 to 2 hr. All patients who did not initially respond (n = 18) improved after more diazepam. Thus all patients who received diazepam (n = 36), during the experimental phase or subsequently, were effectively treated. There were no adverse effects. The median number of 20-mg diazepam doses to treat alcohol withdrawal were three, given over a period of 7.6 hr (range = 1 to 12 and 0.33 to 45 hr). Complications occurred only in those who received placebo during the experimental phase, indicating that delay in therapy may be responsible for the appearance of complications in alcohol withdrawal.

Adult↗
PubMed1981

Low-molecular-weight polyethylene glycol as a probe of gastrointestinal permeability after alcohol ingestion.

Gastrointestinal permeability has been assessed previously by the excretion of PEG-400, which consists of inert molecules that are neither degraded nor metabolized and are excreted intact in the urine. We report here the effects of alcohol on gastrointestinal permeability using PEG-400. Ten grams of PEG-400 dissolved in 60 ml of water were given to 12 intoxicated alcoholics (mean blood alcohol: 2406 mg/liter). The mean urinary excretion of PEG-400 in the following 6 hr was 3.75 +/- 0.3 g SEM. When repeated after sobering up (mean elapsed time: 45 hr), all except one subject showed a decrease in PEG-400 excretion (mean: 2.08 +/- 0.2 g) (P less than 0.001). Similar experiments were conducted in two series with 12 normal controls. (1) In 7 subjects the administration on consecutive days of (a) PEG-400 (10 g) alone, (b) 10.2 g (0.42 mol) of ethanol plus PEG-400 (10 g), (c) PEG-400 (10 g) alone, and (d) PEG-400 (10 g) plus a diuretic (40 mg furosemide) resulted in the following values of PEG-400 excretion in urine: (a) 2.12 +/- 0.3 g; (b) 3.5 +/- 0.3 g, P less than 0.005; (c) 2.02 +/- 0.4, NS; and (d) 2.2 +/- 0.2 g, NS. (2) In the second experiment (5 subjects) the administration on subsequent days of (a) PEG-400 (10 g) + 0.42 mol of urea; (b) PEG-400 (10 g) + 19.2 g ethanol; (c) PEG-400 (10 g) + 0.42 mol of urea resulted also, as in the previous experiment, in increased urinary excretion of PEG-400 after the solution (b) containing ethanol (P less than 0.001). Peak serum levels of PEG-400 were (a) 0.094 +/- 0.01 g/liter; (b) 0.152 +/- 0.02 g/liter (P less than 0.05); and (c) 0.095 +/- 0.01 (P less than 0.05). The ratio of urea--creatinine clearance and urinary volumes were the same in the three periods. Therefore, PEG-400 excretion was not related to changes in urinary clearance or in volume, since the furosemide increased the volume but not PEG-400 excretion. It is concluded that ethanol increases the permeability of the gastrointestinal tract as measured by the PEG-400 test, both in chronic alcoholics during intoxication and in nonalcoholics after a small dose of ethanol. The permeability alteration is transient once ethanol ingestion stops.

Adult↗
PubMed1981

High-density lipoprotein cholesterol in male alcoholics with and without severe liver disease.

In a study of 26 male alcoholics, the subgroup without severe liver disease showed significant elevation in high-density lipoprotein cholesterol (HDL) in the immediate post-intoxication period: HDL levels decreased to control levels after one to two weeks of abstinence. Those patients with advanced liver disease failed to show this ethanol-induced rise in HDL. We were not able to correlate these observations with any variation in sex hormone levels, nutritional indices, age or quantity of alcohol intake. We concluded that ethanol consumption in alcoholics is associated with an increase in HDL levels, which is offset by the development of alcoholic liver disease.

Adult↗
PubMed1980

Alcohol and high-density lipoproteins.

High-density lipoproteins (HDL) have been shown to be negatively associated with coronary heart disease; some epidemiologic evidence also suggests that alcohol may protect against coronary heart disease, but other evidence shows the opposite. Alcohol ingestion and even alcoholism may be associated with higher serum HDL levels, but the levels tend to return to normal within 2 weeks with abstinence from alcohol. The relation between HDL and alcoholism, however, is complex, since in addition to alcohol itself several other factors have to be considered. Liver disease and cigarette smoking tend to decrease the serum HDL level in alcoholic persons, while certain hormonal and nutritional influences and the concomitant use of other microsomal-enzyme-inducing drugs may lead to increased HDL levels. On balance, while alcohol per se may increase the serum HDL level, alcoholism--particularly alcoholic liver disease--probably negates the HDL-related protection against coronary heart disease.

Alcohol Drinking↗