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At least 19 recordsLinked to original sources
PubMed1979

Entrance into brain of dextropropoxyphene and the toxic metabolite norpropoxyphene.

Several studies show that dextropropoxyphene after oral administration is intensively biotransformed to norpropoxyphene by first pass metabolism in the liver. While dextropropoxyphene is analgesic, cardiotoxic and shows CNS toxicity with convulsions and respiratory depression, norpropoxyphene is cardiotoxic to the same degree as dextropropoxyphene, but is without analgesic or CNS-toxic effects (Lund-Jacobsen, 1978). This principal difference between the effects of dextropropoxyphene and norpropoxyphene might be due to differences in penetration into the brain. We investigated the penetration of the two compounds in 14C-labelled moities into the brain of rats by the technique originally described by Oldendorf (1970). By this method the extraction of dextropropoxyphene was found extremely high, while it was much lower for the metabolite. The extraction percentage for dextropropoxyphene after 5 and 10 S was 350 +/- 34.1 and 164 +/- 15.2, respectively, while the values for norpropoxyphene was 62 +/- 6.2 and 44 +/- 4.1 (mean +/- S.E.M.), respectively. This difference may at least partly explain the missing CNS-symptoms with the metabolite.

Animals↗
PubMed1977

Fatal dextropropoxyphene poisoning in Northern Ireland. Review of 30 cases.

Data from 30 fatal cases of dextropropoxphene poisoning occurring in Northern Ireland over three years have been studied. All the victims had ingested more than therapeutic amounts, and many had also taken alcohol or other drugs. Most of the deaths were probably suicides. Death occurred very rapidly suggesting that the narcotic effects of dextropropoxyphene predominated, and this may explain the scarcity of clinical reports, It is suggested that many doctors are unaware of the danger of dextropropoxyphene in overdosage and that the problem of dextropropoxyphene poisoning in the United Kingdom has not been fully appreciated. This supposition, if correct, highlights the absence of a satisfactory early-warning system for serious drug effects including death.

Acetaminophen↗
PubMedDate not supplied

Accidental fatal drug poisoning with particular erference to dextropropoxyphene.

A rapid increase in fatal accidental dextropropoxyphene poisonings which is proportional to the increased use of the drug is reported. In 30 accidental poisonings dextropropoxyphene was responsible for 50% of the cases, and is the most common accidental medical poisoning at the present time. This is probably due to the unappreciated narrow margin between therapeutic and fatal dose and the simultaneous intake of alcohol which increases the resorbtion speed from the gastro-intestinal tract. In Denmark a slow-release preparation is frequently used. which is especially dangerous because of repeated dosage by the patient attempting to induce the therapeutic effect more quickly.

Adult↗
PubMed1977

Mefenamic acid and dextropropoxyphene with paracetamol as analgesics in the accident department.

A double-blind study was carried out in 48 patients with soft-tissue injuries to compare the effectiveness of mefenamic acid and dextropropoxyphene plus paracetamol in relieving acute post-injury pain. Patients received capsules containing either 250 mg mefenamic acid or 32.5 mg dextropropoxyphene hydochloride plus 325 mg paracetamol and were instructed to take up to 6 capsules daily as necessary. By the third post-injury day both preparations had controlled pain adequately and lessened local tenderness in most cases. There was no significant difference in response between the two patient groups. Two patients in each group stopped treatment because of gastro-intestinal intolerance, and a further 4 patients in each group reported troublesome side-effects.

Acetaminophen↗
PubMed1978

Pharmacokinetics of dextropropoxyphene in acute poisoning.

Dextropropoxyphene (DP) is a commonly used medicament for suicide attempts in Denmark. Death may occur from respiratory depression or cardiac arrest. Mechanical hyperventilation which induces hypocapnia seems to reduce the occurrence of cardiac complications. In an attempt to relate the clinical events to the plasma concentrations of DP and the major metabolite norpropoxyphene (NP) we studied patients with acute poisoning treated either for 48 h with induced hypocapnia by hyperventilation or under a conservative regime. Hypocapnia was found to lead to a significant increase in the plasma half-life of DP. Under conservative treatment the plasma half-life was 17.9 +/- 6.7 (S.D.) h (n = 6), while under induced hypocapnia the mean of values from 5 patients was 30.5 +/- 6.9 (S.D.) h. Maximum serum levels of DP and NP were, however, significantly higher in the intensively treated patients (n = 7) than in those treated conservatively (n = 9), though less marked for NP compared to DP (DP: 4.9 +/- 2.1/2.4 +/- 1.0 mumol/l, NP: 6.3 +/- 2.4/4.1 +/- 1.7 mumol/l). A concentration dependent renal clearance of NP was not demonstrable. Possible explanations are the following: 1) A change in disposition pattern blood/tissue of DP during hypocapnia. 2) A reduced metabolism DP to NP during hypocapnia. 3) A reduction in other routes of elimination.

Biotransformation↗
PubMed1977

Determination of dextropropoxyphene and norpropoxyphene in autopsy material.

A method for the simultaneous determination of dextropropoxyphene (DP) and its major metabolite norpropoxyphene (NP) in autopsy material, has been developed. By the extraction procedure used, NP is completely converted to its more stable amide form, which like DP, produces well-defined peaks, in the subsequent gas-liquid chromatographic determination. Thin-layer chromatography is used for additional identification of the two compounds. In 20 g of autopsy material, the detection limit is 0.3 mug/g of tissue or body fluid. The recovery of standards added to control blood samples (1.25 mug/g) was 65 +/- 10% (S.D.) for DP and 59 +/- 9% (S.D.) for NP (n = 54). The method is routinely used for determinations in blood, muscle, liver and urine.

Autopsy↗
PubMed1977

Dextropropoxyphene and norpropoxyphene in blood, muscle, liver and urine in fatal poisoning.

Post-mortem concentrations of dextropropoxyphene (DP) and its major metabolite norpropoxyphene (NP) were determined by combined gas-liquid chromatography and thin-layer chromatography in autopsy material from 53 cases of fatal DP poisoning collected over a 1-year period. Among 11 oral cases without simultaneous ethanol ingestion, the minimal lethal dose was less than 1.5 g DP chloride. The ranges of total drug concentrations (DP + NP) were 1.1-15 mug/g in blood, 1.3-23 mug/g in muscle, and 27-261 mug/g in liver. Among 21 oral cases were ethanol was detected in the blood, the minimal lethal dose was 0.7 g DP chloride (ethanol 2.41 mg/g) and the total drug concentrations was 0.7-12 mug/g in the blood, 1.3-8.4 mug/g in the muscle and 19-285 mug/g in the liver. The minimal lethal blood concentrations tended to decrease with increasing ethanol concentration. NP constituted roughly half of the total drug levels, somewhat less in muscle and more in the urine, and this pattern was not changed in connexion with ethanol ingestion. Other metabolites were not detected.

Autopsy↗
PubMed1976

Acute poisoning with dextropropoxyphene. Clinical symptoms and plasma concentrations.

Out of 14 cases of poisoning assumed to be due to dextropropoxyphene-containing drugs, propoxyphene and its main metabolite norpropoxyphene could be demonstrated in 11. The concentrations of the drugs were determined shortly after admission and then after 2, 4, 6 and 10 hours (in four cases also after 16 hours). The highest plasma concentration of propoxyphene, 0.74 mug/ml, was found in one case of fatal poisoning. Another patient with a plasma concentration of 0.51 mug/ml showed signs of severe respiratory depression but survived after respirator therapy. In the patients with lower plasma concentrations the poisoning had a benign course. In most cases the plasma concentration of norpropoxyphene exceeded that of propoxyphene even in the first blood sample.

Acidosis↗
PubMed1977

Propoxyphene overdosage: a study of cases involving analgesic preparations containing dextropropoxyphene.

Propoxyphene and paracetamol concentrations have been determined in blood, urine, liver blood and stomach contents from 17 post mortem cases in which Distalgesic (a propoxyphene and paracetamol compound preparation) was involved. Five patients admitted to hospital with suspected Distalgesic poisoning have also been investigated. In most cases the propoxyphene concentrations, but not the paracetamol concentrations, exceeded the minimum lethal levels reported. On the basis of our results it appears that of the constituents of Distalgesic, propoxyphene has a far more immediate and dangerous effect than paracetamol.

Acetaminophen↗