Life threatening tongue angioedema associated with an angiotensin-converting enzyme inhibitor

We present a case with angioedema of the tongue, following 1 dose of an angiotensin-converting enzyme (ACE) inhibitor ingestion. A gradual progression of angioedema required tracheotomy despite aggressive medical treatment and illustrates the severity of this adverse reaction, Although ACE inhibitors are considered safe, emergency physicians should be alert for minor angioedema at presentation that may progress to life threatening airway compromise

The interaction of the diltiazem with oral and intravenous cyclosporine in rats

This study investigated the effect of diltiazem on the bioavailability of oral and intravenous cyclosporine (CsA) in rats. While control rats received normal saline, experimental groups received 60 or 90 mg/kg diltiazem orally for 3 days. Each group divided into 2 equal groups that received a single oral dose or i.v. injection of CsA. Pharmacokinetic parameters were analyzed by nonparametric analysis of variance. Pretreatment with 60 or 90mg/kg diltiazem decreased the area under the blood CsA concentration-time curve (AUC) of oral CsA compared to control group (54.5% and 65.5% for AUC(0.24). 57.6% and 62.2% for AUC(0-infinity), respectively, p<0.05)

Massive intracranial hemorrhage associated with the ingestion of dimethyl sulfoxide

Dimethyl sulfoxide (DMSO) has been wide used in the treatment of arthritis and certain inflammatory diseases, and is also considered an alternative remedy for cancer even if not supported by concrete evidence. This report illustrates the first case of a fatal complication following the illicit use of this agent. A 55-y-old man who reportedly ingested 500 mg acetaminophen and similar to I ml DMSO solution was brought to the emergency department after experiencing 2 tonic-clonic seizures. He had been diagnosed with lung mesotelioma with brain metastases which caused no neurologic deficit. The ingested DMSO was the first dose within the last 3 mo. Examination revealed right-sided hemiplegia. Unenhanced computed tomography of the head showed 3 hemorrhagic areas with blood-cerebrospinal fluid at the left parietal, occipital and frontal regions accompanied by a midline shift. Despite initial resuscitation, 2 units of fresh frozen plasma and antiedema treatment, the patient experienced cardiac arrest that did not respond to resuscitative measures. DMSO can cause massive intrametastatic hemorrhage, and neurologic deterioration can be profound in patients with metastatic brain lesions

Effect of the selective mitochondrial KATP channel opener nicorandil on the QT prolongation and myocardial damage induced by amitriptyline in rats.

Abstract Objectives The aim of this study is to evaluate the protective effect of nicorandil, a selective mitochondrial KATP channel opener, on QT prolongation and myocardial damage induced by amitriptyline. Methods The dose of amitriptyline (intraperitoneal, i.p.) that prolong the QT interval was found 75 mg/kg. Rats were randomized into five groups the control group, amitriptyline group, nicorandil (selective mitochondrial KATP channel opener, 3 mg/kg i.p.) + amitriptyline group, 5-hdyroxydecanoate (5-HD, selective mitochondrial KATP channel blocker, 10 mg/kg i.p.) + amitriptyline group and 5-HD + nicorandil + amitriptyline group. Cardiac parameters, biochemical and histomorphological/immunohistochemical examinations were evaluated. p &amp;lt; 0.05 was accepted as statistically significant. Key findings Amitriptyline caused statistically significant prolongation of QRS duration, QT interval and QTc interval (p &amp;lt; 0.05). It also caused changes in tissue oxidant (increase in malondialdehyde)/anti-oxidant (decrease in glutathione peroxidase) parameters (p &amp;lt; 0.05), myocardial damage and apoptosis (p &amp;lt; 0.01 and p &amp;lt; 0.001). While nicorandil administration prevented amitriptyline-induced QRS, QT, QTc prolongation (p &amp;lt; 0.05), myocardial damage and apoptosis (p &amp;lt; 0.05), it did not affect the changes in oxidative parameters (p &amp;gt; 0.05). Conclusions Our results suggest that nicorandil, a selective mitochondrial KATP channel opener, plays a protective role in amitriptyline-induced QT prolongation and myocardial damage. Mitochondrial KATP channel opening and anti-apoptotic effects may play a role in the cardioprotective effect of nicorandil. </jats:sec