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At least 55 records · Page 3Linked to original sources
PubMed1981

N-hydroxymethyl derivatives of nitrogen heterocycles as possible prodrugs II: possible prodrugs of allopurinol, glutethimide, and phenobarbital.

Solid samples of 1-hydroxymethyl- and 1,5-dihydroxymethylallopurinol, 1-hydroxymethylglutethimide, and 1-hydroxymethylphenobarbital were prepared, and equilibrium constants for their formation from formaldehyde and allopurinol, glutethimide, or phenobarbital were calculated. The N-hydroxymethyl derivatives had higher water solubilities and faster dissolution rates than the parent drugs, and they appear to be potentially useful as prodrugs.

Allopurinol↗
PubMed1980

Enzyme induction and serum and lipoprotein lipids: a study of glutethimide in normal subjects.

1. Serum and lipoprotein cholesterol and triglycerides were measured before, during and after the administration of glutethimide (500 mg daily) for 21 days to six healthy volunteer subjects. 2. Evidence of enzyme induction was provided by significant rises in D-glucaric acid excretion and antipyrine clearance. 3. Concentrations of total serum cholesterol, very-low-density-lipoprotein-, low-density-lipoprotein and high-density-lipoprotein-cholesterol rose significantly during treatment. 4. The time course of these changes was delayed in comparison with the rise and fall in D-glucaric acid excretion. 5. There was no change in the triglyceride content of either whole serum or lipoprotein fractions at any time during the trial. 6. The study provides further evidence that enzyme-inducing agents cause a rise in certain lipid concentrations.

Adult↗
PubMed1984

Descriptive epidemiology of mortality in New Jersey due to combinations of codeine and glutethimide.

A review of records of the Toxicology Laboratory of the New Jersey State Medical Examiner's Office yielded a total of 36 deaths attributable to overdose of "hits," an oral combination of codeine and glutethimide, during 1980-1981. During the same period, 126 deaths due to heroin overdose and 46 deaths due to methadone overdose occurred. The majority of hits cases (77.8%) occurred in the Newark vicinity. Demographic features of persons who died of the three agents are presented, and some explanations are advanced for the unexpectedly high mortality due to the oral narcotic combination.

Adult↗
PubMed1979

"Barbiturate burns" caused by glutethimide.

A case of glutethimide overdose associated with skin lesions resembling burns is reported. These characteristic skin lesions are usually ascribed to barbiturates. Their aetiology, incidence, and association with other drugs and neurological disorders are discussed.

Adult↗
PubMed1975

Phenolic metabolite, 2-ethyl-2(4-hydroxphenyl)-glutarimide in human urine following chronic ingestion of glutethimide (Doriden).

Urine samples from comatose patients, identified as having taken large amounts of the drug, glutethimide, were analyzed using gas chromatography, mass spectrometry, thin layer chromatography, and nuclear magnetic resonance spectrometry in order to identify metabolites of the parent drug. The phenolic compound 2-ethyl-2-(4-hydroxphenyl)-glutarimide was fully characterized as a new metabolite in human urine. Also 2-ethyl-2-(3-methoxy-4hydroxyphenyl)-glutarimide was proposed as a new metabolite of the parent drug. Other polar metabolites of the parent drug were also detected and partially characterized.

Chromatography, Gas↗
PubMed1975

[A contribution to acute glutethimide (Elrodorm) intoxication].

Following a short discussion of hitherto known facts about glutethimid intoxications, two own cases are described. In these cases minimal amounts (2.5 and 5 g) caused haemorrhagic diatheses and acute insufficiency of the liver, which in one case were combined with acute renal insufficiency. Possible causes are discussed.

Adult↗
PubMed1988

Fatalities associated with an acute overdose of glutethimide (Doriden) and codeine.

Abuse of the oral combination of glutethimide (DORIDEN) and codeine, commonly referred to as "sets", in the northwest Pennsylvania area is reviewed. Nine fatalities have been reported in the Erie area from 1985-87 due to acute toxicity with this combination. The glutethimide/codeine combination reportedly produces a euphoric effect comparable to intravenous heroin but is longer lasting. Age of the victims ranged from 18 to 37 years. In all cases there was a history of chronic intentional "sets" abuse by the victims prior to death. The 9 fatalities due to this combination of prescription drugs is unusually high for this area considering the population and rural nature of the Erie community. Although the use of "sets" has been reported occasionally in other localized areas of the country, no other significant use has been reported in Pennsylvania.

Codeine↗
PubMed1985

Toxicological analysis of amobarbital and glutethimide from bone tissue.

Author examined cadaver organs and bone samples (sternum, rib) of drug poisoning cases. Following suitable procedures, active drug components (amobarbital, glutethimide, and so forth) were identified by gas chromatography/mass spectrometry (GC/MS). Based on results of quantitative GC analysis, relationships were sought between the active agent concentrations measured in the organs and the bone samples.

Adult↗
PubMed1983

Catatonia associated with glutethimide withdrawal.

Catatonia is a syndrome that is often considered as a subtype of schizophrenia, although studies have shown that it is most often associated with affective disorders. There are also many medical causes of catatonia. A case is presented in which glutethimide withdrawal seems the most likely explanation for catatonic symptoms.

Adult↗
PubMed1996

Isolation of N-vinylprotoporphyrin IX after hepatic cytochrome P450 inactivation by 3-[(arylthio)ethyl]sydnone in chick embryos pretreated with phenobarbital, glutethimide, dexamethasone, and beta-naphthoflavone: differential inhibition of ferrochelatase by N-vinylprotoporphyrin regioisomers.

Several xenobiotics caused hepatic porphyrin accumulation through mechanism-based inactivation of cytochrome P450(P450) and heme alkylation. Loss of iron from the alkylated heme results in formation of an N-alkylporphyrin, which is a potent inhibitor of ferrochelatase. N-Vinylprotoporphyrin IX (N-vinylPP) was identified in chick embryo liver after in ovo administration of 3-[(arylthio)ethyl]sydnone (TTMS). Pretreatment of chick embryos with beta-naphthoflavone, which causes a 90-fold increase in P450 1A levels, did not increase the formation of N-vinylPP after TTMS administration, showing that the heme moiety of P450 1A does not contribute to the formation of N-vinylPP. Increased amounts of N-vinylPP were isolated from dexamethasone-, phenobarbital-, and glutethimide-pretreated chick embryos, and it is possible that P450 2H and/or a P450 3A-like isozyme contributes to the formation of N-vinylPP. The ring B-substituted (NB) regioisomer of N-vinylPP constituted the lowest percentage of the total regioisomers (9-13%) in untreated and drug-induced chick embryos, thus supporting the concept that ring B of heme is occluded by a protein residue in the P450 active site. Previously, the finding that the NB regioisomer of N-ethylprotoporphyrin IX had one fifth the potency of the ring A-substituted (NA) regioisomer as a ferrochelatase inhibitor led to a proposal that an A-C ring tilt was important in N-alkylprotoporphyrins for ferrochelatase inhibition. The finding in the present study that the NA and NB regioisomers of N-vinylPP are equipotent does not support the above proposal. The ring C-substituted (NC) and ring D-substituted (ND) regioisomers of N-vinylPP had low potency.

Animals↗
PubMed1996

Chick embryo liver microsomal steroid hydroxylations: induction by dexamethasone, phenobarbital, and glutethimide and inactivation following the in ovo administration of porphyrinogenic compounds.

Metabolites of [4-(14)C]androstenedione (AD) and [4-(14)C]progesterone (PG) were separated and quantitated following incubation with hepatic microsomes from chick embryos. PG 2 alpha-hydroxylase and AD 7 alpha-hydroxylase, which are diagnostic markers in rat liver for cytochrome P450 (P450) 2C11 and 2A1/2, respectively, were not identified in chick embryo liver. PG 6 beta-hydroxylase and AD 6 beta-hydroxylase, diagnostic markers for P450 3A1/2 activity in rat liver, were identified in chick embryo liver, and we were able to show that radiolabeled 6 beta-hydroxyprogesterone and 6 beta-hydroxyandrostenedione, the metabolites of PG and AD 6 beta-hydroxylase, respectively, were homogeneous and identical with authentic standards. Dexamethasone, phenobarbital, and glutethimide were found to be significant inducers of PG and AD 6 beta-hydroxylases in chick embryo liver. The in ovo administration of the porphyrinogenic compounds 3,5-diethoxycarbonyl-1,4-dihydro-2,6-dimethyl-4-ethylpyridine (4-ethyl DDC) and 3-[2-(2,4,6-trimethylphenyl)-thioethyl]-4-methylsydnone (TTMS) caused inactivation of chick embryo hepatic PG and AD 6 beta-hydroxylases. Therefore, we suggest that PG and AD 6 beta-hydroxylases may serve as diagnostic markers for a P450 3A-like isozyme in the chick embryo, and that this isozyme is one of the targets for inactivation by 4-ethyl DDC and TTMS.

Animals↗
PubMed1976

Synthesis and characterization of alpha-phenyl-gamma-butyrolactone, a metabolite of glutethimide, phenobarbital and primidone, in human urine.

A novel metabolite, alpha-phenyl-gamma-butyfolactone has been isolated in urine samples of patients severely intoxicated by either glutethimide, phenobarbital, or primidone. This lactone was prepared synthetically and its spectral data and chromatographic properties were compared to those data obtained from the urine samples of drug overdosed victims. The results of these comparisons confirm the presence of this lactone in human urine following the ingestion of large amounts of the parent drug.

Glutethimide↗
PubMed1989

[Clinical observation on hypercortisolism treated with amino-glutethimide].

We reported the clinical results in 13 cases of hypercortisolism treated with amino-glutethimide (AG), which was developed by Tiantsin Research Institute of Medical Industry. Of the thirteen cases nine were confirmed by surgery and histology, and the others were diagnosed clinically. Clinical improvements have been achieved in ten of the thirteen cases over a therapeutic course of 8 to 12 wk with a daily dosage of 1.0 to 2.0 g of AG. Plasma and urinary corticosteroids, as well as plasma testosterone levels were significantly decreased after one-month treatment followed, however, by somewhat return and fluctuation. The high levels of blood glucose and serum insulin were declined after therapy consistent with the decrement of corticoids. Serum potassium levels in hypokalemic patients returned to normal after one month of therapy. Radial bone mineral contents in patients with low bone density returned or closed to normal after three-month treatment. The main side effects of AG are anorexia, nausea, drowsy, tierdness, skin rashes, etc, which are mild and transient. Adrenal hypofunction was seen in one case after treatment.

Adolescent↗