Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Pharmacokinetics of dextropropoxyphene in acute poisoning. 27 28

Dextropropoxyphene is a widely prescribed synthetic opiate-like drug of uncertain analgesic efficacy which, in acute overdosage, manifests all the features of opiate toxicity. It is rapidly absorbed and, in association with other central nervous system depressants such as alcohol or benzodiazepine drugs, may be rapidly fatal. Seriously overdosed patients are comatose with respiratory depression, vomiting, seizures and circulatory collapse; small pupils are a useful diagnostic marker. The first priority is to establish the airway and treat convulsions, if present. All the features of overdosage are then rapidly and safely reversed by the specific opiate antagonist naloxone given intravenously. High tissue concentrations and slow elimination of dextropropoxyphene metabolites make continued and intensive monitoring after resuscitation essential because sudden unpredictable deterioration may occur for up to 24 hours. Other more slowly toxic co-ingestants such as paracetamol (acetaminophen) are often present and should be detected and treated as necessary. Dextropropoxyphene poisoning is now probably one of the most common causes of self-poisoning death because, although there is an effective antidote, subjects frequently succumb before treatment can be made available.
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PMID:Dextropropoxyphene overdosage. Pharmacological considerations and clinical management. 634 64

Dextropropoxyphene overdose may be complicated by serious cardiovascular manifestations, including conduction abnormalities and collapse. We report two patients in whom cardiac toxicity developed. Cardiovascular depression seemed to be improved after naloxone infusion in these two cases. Possible mechanisms are briefly discussed.
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PMID:Adverse cardiac manifestations following dextropropoxyphene overdose: can naloxone be helpful? 783 61