The Experts below are selected from a list of 8310 Experts worldwide ranked by ideXlab platform
Peter Lehnert - One of the best experts on this subject based on the ideXlab platform.
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suppression of vagus mediated pancreatic polypeptide release by the μ opiate receptor agonist Loperamide in man
British Journal of Clinical Pharmacology, 2003Co-Authors: Rudolf L Riepl, Barbel Reichardt, Christoph J Auernhammer, Gerald Beier, Jochen Schopohl, Gunter K Stalla, Peter LehnertAbstract:1. Morphine suppresses the release of pancreatic polypeptide, a hormone under vagal cholinergic control. The intention of the study was to detect whether the mu-opiate receptor agonist Loperamide is also able to inhibit pancreatic polypeptide release, and to define its site of action. 2. In groups of healthy subjects (n = 6 each) stimulation of pancreatic polypeptide was assessed in five different tests: (i) insulin-hypoglycaemia; (ii) modified sham feeding; (iii) intravenous infusion of the cholecystokinin analogue ceruletide; (iv) injection of corticotropin releasing hormone; (v) infusion of the muscarinic acetylcholine agonist bethanechol. All tests were performed after oral application of either a placebo or Loperamide (16 mg), tests (ii) and (iii) were repeated with Loperamide in smaller doses (2 and 6 mg), with Loperamide plus naloxone, with naloxone alone, and with infusion of atropine. Plasma concentrations of pancreatic polypeptide were measured radioimmunologically. 3. Release of pancreatic polypeptide in test (i) to (iv) was completely blocked by 16 mg Loperamide, whereas bethanechol-stimulated release (test 5) was not influenced. Tests (ii) and (iii) showed that the inhibition was dose-dependent and could be attenuated by naloxone. The inhibitory effect of Loperamide was comparable with that of atropine. 4. We conclude that Loperamide causes a dose-dependent inhibition of pancreatic polypeptide release mediated by vagal-cholinergic pathways, but does not have an atropine-like peripheral action.
Josef Stehlik - One of the best experts on this subject based on the ideXlab platform.
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ventricular tachycardia associated with high dose chronic Loperamide use
Pharmacotherapy, 2015Co-Authors: Hannah L Spinner, Nick W Lonardo, Roja Mulamalla, Josef StehlikAbstract:Loperamide is an antidiarrheal medication deemed by the U.S. Food and Drug Administration as safe enough to be sold as an over-the-counter medicine. Unlike other μ-opioid receptor agonists, Loperamide acts specifically in the myenteric plexus in the gastrointestinal tract, making the potential for abuse low and reports of toxicity extremely rare. We present a case of a patient previously in good health who developed episodes of cardiac pauses, nonsustained ventricular tachycardia, and eventually runs of sustained ventricular tachycardia with hemodynamic instability. She required cardiopulmonary resuscitation, multiple cardioversions, and placement of a pacemaker. Her medical history was remarkable only for type 2 diabetes and chronic postcholecystectomy diarrhea. Metformin was the only prescription medication she was taking at the time of presentation. However, she reported that she had been taking an entire bottle of Equate brand Loperamide (144 mg) daily for ~2 years. Loperamide overdoses associated with ventricular arrhythmias have been reported, but this is the first case to describe a serious ventricular arrhythmia associated with long-term use of a high dose of Loperamide. Chronic overtreatment with Loperamide may induce life-threatening arrhythmias.
Victor W. Pike - One of the best experts on this subject based on the ideXlab platform.
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Effects of ketoconazole on the biodistribution and metabolism of [11C]Loperamide and [11C]N-desmethyl-Loperamide in wild-type and P-gp knockout mice.
Nuclear medicine and biology, 2010Co-Authors: Nicholas Seneca, Sami S. Zoghbi, H. Umesha Shetty, Edward Tuan, Pavitra Kannan, Andrew Taku, Robert B. Innis, Victor W. PikeAbstract:Introduction [11C]Loperamide and [11C]N-desmethyl-Loperamide ([11C]dLop) have been proposed as radiotracers for imaging brain P-glycoprotein (P-gp) function. A major route of [11C]Loperamide metabolism is N-demethylation to [11C]dLop. We aimed to test whether inhibition of CYP3A4 with ketoconazole might reduce the metabolism of [11C]Loperamide and [11C]dLop in mice, and thereby improve the quality of these radiotracers.
Rudolf L Riepl - One of the best experts on this subject based on the ideXlab platform.
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suppression of vagus mediated pancreatic polypeptide release by the μ opiate receptor agonist Loperamide in man
British Journal of Clinical Pharmacology, 2003Co-Authors: Rudolf L Riepl, Barbel Reichardt, Christoph J Auernhammer, Gerald Beier, Jochen Schopohl, Gunter K Stalla, Peter LehnertAbstract:1. Morphine suppresses the release of pancreatic polypeptide, a hormone under vagal cholinergic control. The intention of the study was to detect whether the mu-opiate receptor agonist Loperamide is also able to inhibit pancreatic polypeptide release, and to define its site of action. 2. In groups of healthy subjects (n = 6 each) stimulation of pancreatic polypeptide was assessed in five different tests: (i) insulin-hypoglycaemia; (ii) modified sham feeding; (iii) intravenous infusion of the cholecystokinin analogue ceruletide; (iv) injection of corticotropin releasing hormone; (v) infusion of the muscarinic acetylcholine agonist bethanechol. All tests were performed after oral application of either a placebo or Loperamide (16 mg), tests (ii) and (iii) were repeated with Loperamide in smaller doses (2 and 6 mg), with Loperamide plus naloxone, with naloxone alone, and with infusion of atropine. Plasma concentrations of pancreatic polypeptide were measured radioimmunologically. 3. Release of pancreatic polypeptide in test (i) to (iv) was completely blocked by 16 mg Loperamide, whereas bethanechol-stimulated release (test 5) was not influenced. Tests (ii) and (iii) showed that the inhibition was dose-dependent and could be attenuated by naloxone. The inhibitory effect of Loperamide was comparable with that of atropine. 4. We conclude that Loperamide causes a dose-dependent inhibition of pancreatic polypeptide release mediated by vagal-cholinergic pathways, but does not have an atropine-like peripheral action.
Santosh K Padala - One of the best experts on this subject based on the ideXlab platform.
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electrocardiographic changes in Loperamide toxicity case report and review of literature
Journal of Cardiovascular Electrophysiology, 2019Co-Authors: Todd Teigeler, Heather Stahura, Rizwan Alimohammad, Gautham Kalahasty, Jayanthi N Koneru, Michael I Ellenbogen, Kenneth A Ellenbogen, Santosh K PadalaAbstract:Introduction Loperamide, an antidiarrheal agent, is a µ-opioid receptor agonist increasingly abused to prevent opioid withdrawal or to produce euphoric effects. At supra-therapeutic doses, Loperamide can cause cardiac toxicity due to blockade of Na and IKr channels, resulting in wide QRS rhythms, severe bradycardia, prolonged QTc, polymorphic ventricular tachycardia, cardiac arrest, and death. There are limited data on the cardiotoxic effects of high dose Loperamide. Methods and results A case report of Loperamide toxicity is presented and then added to a contemporary review of the literature. In total, the presentation and management of 36 cases of Loperamide cardiotoxicity are summarized. The overall median daily dose (interquartile range) of Loperamide was 200 (134-400) mg. The median QRS duration was 160 (125-170) ms. The median QTc duration was 620 (565-701) ms. Ventricular tachycardia was experienced by 24/36 (67%) of patients, 20 of which were specified to be polymorphic. Treatment was supportive, providing advanced cardiopulmonary life support and aggressive electrolyte repletion. Isoproterenol infusion or overdrive pacing was employed in 19/36 (53%) of cases. The median time to electrocardiogram normalization or hospital discharge, whichever came first, was 5 (3.5-10) days. Conclusion Loperamide overdose is a toxidrome that remains underrecognized, and in patients with unexplained cardiac arrhythmias, Loperamide toxicity should be suspected. Prompt recognition is critical due to the delayed recovery and high risk for life-threatening arrhythmias.
