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Biomedical subjects

M J Smilkstein

Publications and source records attributed to M J Smilkstein.

26 records · Page 2Linked to original sources
PubMed1987

A case of MAO inhibitor/MDMA interaction: agony after ecstasy.

After ingesting 3,4-methylene-dioxy-methamphetamine (MDMA) and the monoamine oxidase (MAO) inhibitor phenelzine, a 50 year old male developed marked hypertension, diaphoresis, altered mental status, and hypertonicity lasting 5-6 hours. This clinical course is typical of interaction between MAO inhibitors and some sympathomimetics including amphetamines. Such interaction has not previously been described involving MDMA. Sympathomimetic-MAO inhibitor interactions can cause excessive release of endogenous bioactive amines (e.g. norepinephrine, serotonin). Hypertensive crisis, intracranial hemorrhage, hypertonicity, and severe hyperthermia have occurred due to sympathomimetic-MAO inhibitor interactions. MDMA shares structural and pharmacologic features with other agents capable of causing this interaction, and this case suggests that MDMA can cause significant toxicity in patients taking MAO inhibitors.

3,4-Methylenedioxyamphetamine↗
PubMed1985

Hyperbaric oxygen therapy for severe hydrogen sulfide poisoning.

The optimum therapy for hydrogen sulfide poisoning is unclear. Adjuncts used in the treatment of cyanide poisoning have been advocated because of the shared mechanism of toxicity between hydrogen sulfide and cyanide. Following success in cyanide poisoning, hyperbaric oxygen therapy (HBO) has been suggested for use in treating hydrogen sulfide poisoning. A case of severe hydrogen sulfide poisoning was successfully treated with HBO after standard therapy was apparently ineffective. HBO as a therapeutic adjunct in hydrogen sulfide poisoning and the rationale for its use are discussed.

Adult↗
PubMedDate not supplied

Falsely elevated salicylate levels due to diflunisal overdose.

A 33-year-old man ingested 14 g of diflunisal (Dolobid, a NSAID), 3 propoxyphene-acetaminophen tablets, and ethanol. Although salicylate ingestion was specifically denied, toxicology screening revealed markedly elevated salicylate levels (176 mg/dL, 100 mg/dL, 41 mg/dL at 4 1/2, 10 and 24 hours postingestion). Blood ethanol level was 450 mg/dL. There was no respiratory alkalosis, metabolic acidosis, or increased anion gap to suggest salicylate toxicity. The patient recovered fully. Comparison testing of the salicylate assay technique used in the case (TDx fluorescence polarization immunoassay) and another commonly used technique (Trinder colorimetric assay) revealed marked cross-reactivity between salicylate and diflunisal. Samples of known diflunisal concentration were tested using the TDx salicylate assay. Percent cross-reactivity [(reported salicylate concentration/actual diflunisal concentration) x 100] was found to be 130 to 152.8% over the concentration range tested. Cross-reactivity between diflunisal and salicylate using the Trinder colorimetric assay was 20 to 52.5% over the concentration range tested. Diflunisal is not metabolized to salicylate and thus this cross-reactivity represents a significant drug-laboratory interaction. Salicylate levels measured by these methods appear to be unreliable when diflunisal is present.

Adult↗
PubMedDate not supplied

Delayed cardiotoxicity following quinine overdose: a case report.

Quinine poisoning typically results in a constellation of non-life threatening symptoms which include tinnitus, deafness, nausea, vomiting, vision changes, headache, and hypotension. Cardiac conduction defects, dysrhythmias, and cardiovascular collapse have all been reported after overdose and generally occur within 8 hours of ingestion. We report a unique case of delayed cardiotoxicity following quinine ingestion. Toxicity included marked ventricular conduction abnormalities for which serum alkalinization appeared to be therapeutically beneficial, and torsades de pointes requiring overdrive pacing for termination.

Drug Overdose↗