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Faik Ahmet Ayaz - One of the best experts on this subject based on the ideXlab platform.
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pseudocholinesterase levels are not decreased in grayanotoxin mad honey poisoning in most patients
Journal of Emergency Medicine, 2012Co-Authors: Abdulkadir Gunduz, Suha Turkmen, Suleyman Turedi, Faik Ahmet Ayaz, Asim Kalkan, Ismet Durmus, Ahmet AyarAbstract:Abstract Background The symptoms of mad honey poisoning resemble those of cholinergic Toxidromes; however, it is not clear whether they share a common biochemical basis. Objectives The aim of this study was to investigate a possible resemblance between mad honey poisoning and cholinergic Toxidromes. Methods This is a descriptive study performed prospectively in patients presenting to a University Medical Faculty Emergency Medicine Department emergency service with mad honey poisoning over 1 year, from September 2008 to September 2009. Adult patients with clinical findings suggesting mad honey poisoning (i.e., bradycardia, hypotension, syncope, and vertigo) and with a history of honey consumption were enrolled. Pseudocholinesterase levels in blood samples taken from the mad honey-poisoned patients were analyzed to determine whether these were lower than normal pseudocholinesterase levels for adults (5400–13,200 U/L). Results The most common symptoms of the 30 patients enrolled in the study were vertigo and nausea. Low blood pressure and bradycardia were the most frequently observed physical examination findings. None of the patients enrolled had a history of disease that might cause low pseudocholinesterase. Mean pseudocholinesterase levels in our patients with mad honey poisoning were 7139.30 ± 2316.41 U/L (min–max: 1785–12,835). Blood pseudocholinesterase levels were within normal limits in 90% of patients and below normal in 10%. Conclusion A low pseudocholinesterase level was found in 3 (10%) of our 30 patients. These biochemical data do not support the hypothesis that mad honey poisoning should be regarded as cholinergic poisoning.
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clinical review of grayanotoxin mad honey poisoning past and present
Clinical Toxicology, 2008Co-Authors: Abdulkadir Gunduz, Suleyman Turedi, Robert M Russell, Faik Ahmet AyazAbstract:Grayanotoxin is a naturally occurring sodium channel toxin which enters the human food supply by honey made from the pollen and nectar of the plant family Ericaceae in which rhododendron is a genus. Grayanotoxin/mad honey poisoning is a little known, but well studied, cholinergic Toxidrome resulting in incapacitating and, sometimes, life-threatening bradycardia, hypotension, and altered mental status. Complete heart blocks occur in a significant fraction of patients. Asystole has been reported. Treatment with saline infusion and atropine alone is almost always successful. A pooled analysis of the dysrhythmias occurring in 69 patients from 11 different studies and reports is presented. The pathophysiology, signs, symptoms, clinical course, and treatment of grayanotoxin/mad honey poisoning are discussed. In the nineteenth century grayanotoxin/mad honey poisoning was reported in Europe and North America. Currently, documented poisoning from locally produced honey in Europe or North America would be reportable. Possible reasons for this epidemiologic change are discussed.
Abdulkadir Gunduz - One of the best experts on this subject based on the ideXlab platform.
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pseudocholinesterase levels are not decreased in grayanotoxin mad honey poisoning in most patients
Journal of Emergency Medicine, 2012Co-Authors: Abdulkadir Gunduz, Suha Turkmen, Suleyman Turedi, Faik Ahmet Ayaz, Asim Kalkan, Ismet Durmus, Ahmet AyarAbstract:Abstract Background The symptoms of mad honey poisoning resemble those of cholinergic Toxidromes; however, it is not clear whether they share a common biochemical basis. Objectives The aim of this study was to investigate a possible resemblance between mad honey poisoning and cholinergic Toxidromes. Methods This is a descriptive study performed prospectively in patients presenting to a University Medical Faculty Emergency Medicine Department emergency service with mad honey poisoning over 1 year, from September 2008 to September 2009. Adult patients with clinical findings suggesting mad honey poisoning (i.e., bradycardia, hypotension, syncope, and vertigo) and with a history of honey consumption were enrolled. Pseudocholinesterase levels in blood samples taken from the mad honey-poisoned patients were analyzed to determine whether these were lower than normal pseudocholinesterase levels for adults (5400–13,200 U/L). Results The most common symptoms of the 30 patients enrolled in the study were vertigo and nausea. Low blood pressure and bradycardia were the most frequently observed physical examination findings. None of the patients enrolled had a history of disease that might cause low pseudocholinesterase. Mean pseudocholinesterase levels in our patients with mad honey poisoning were 7139.30 ± 2316.41 U/L (min–max: 1785–12,835). Blood pseudocholinesterase levels were within normal limits in 90% of patients and below normal in 10%. Conclusion A low pseudocholinesterase level was found in 3 (10%) of our 30 patients. These biochemical data do not support the hypothesis that mad honey poisoning should be regarded as cholinergic poisoning.
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An Atropa belladonna L. poisoning with acute subdural hematoma
Human & Experimental Toxicology, 2011Co-Authors: Ulas Cikla, Suha Turkmen, Yunus Karaca, Ahmet Faik Ayaz, Suleyman Turedi, Abdulkadir GunduzAbstract:Atropa belladonna L. is a plant long known to cause poisoning. But no cases of acute subdural hematoma resulting from such poisoning have been reported so far. Care must also be taken in terms of acute pancreatitis and rhabdomyolysis in cases of such poisoning. The plant may sometimes be mistaken for the Caucasian blueberry, V. arctostaphylos L. At least one anti-cholinesterase Toxidrome finding was determined in all the nine cases of belladonna poisoning in this series. No elevated creatine kinase was reported in one case with acute subdural hematoma and hyperamylasemia.
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clinical review of grayanotoxin mad honey poisoning past and present
Clinical Toxicology, 2008Co-Authors: Abdulkadir Gunduz, Suleyman Turedi, Robert M Russell, Faik Ahmet AyazAbstract:Grayanotoxin is a naturally occurring sodium channel toxin which enters the human food supply by honey made from the pollen and nectar of the plant family Ericaceae in which rhododendron is a genus. Grayanotoxin/mad honey poisoning is a little known, but well studied, cholinergic Toxidrome resulting in incapacitating and, sometimes, life-threatening bradycardia, hypotension, and altered mental status. Complete heart blocks occur in a significant fraction of patients. Asystole has been reported. Treatment with saline infusion and atropine alone is almost always successful. A pooled analysis of the dysrhythmias occurring in 69 patients from 11 different studies and reports is presented. The pathophysiology, signs, symptoms, clinical course, and treatment of grayanotoxin/mad honey poisoning are discussed. In the nineteenth century grayanotoxin/mad honey poisoning was reported in Europe and North America. Currently, documented poisoning from locally produced honey in Europe or North America would be reportable. Possible reasons for this epidemiologic change are discussed.
Suleyman Turedi - One of the best experts on this subject based on the ideXlab platform.
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pseudocholinesterase levels are not decreased in grayanotoxin mad honey poisoning in most patients
Journal of Emergency Medicine, 2012Co-Authors: Abdulkadir Gunduz, Suha Turkmen, Suleyman Turedi, Faik Ahmet Ayaz, Asim Kalkan, Ismet Durmus, Ahmet AyarAbstract:Abstract Background The symptoms of mad honey poisoning resemble those of cholinergic Toxidromes; however, it is not clear whether they share a common biochemical basis. Objectives The aim of this study was to investigate a possible resemblance between mad honey poisoning and cholinergic Toxidromes. Methods This is a descriptive study performed prospectively in patients presenting to a University Medical Faculty Emergency Medicine Department emergency service with mad honey poisoning over 1 year, from September 2008 to September 2009. Adult patients with clinical findings suggesting mad honey poisoning (i.e., bradycardia, hypotension, syncope, and vertigo) and with a history of honey consumption were enrolled. Pseudocholinesterase levels in blood samples taken from the mad honey-poisoned patients were analyzed to determine whether these were lower than normal pseudocholinesterase levels for adults (5400–13,200 U/L). Results The most common symptoms of the 30 patients enrolled in the study were vertigo and nausea. Low blood pressure and bradycardia were the most frequently observed physical examination findings. None of the patients enrolled had a history of disease that might cause low pseudocholinesterase. Mean pseudocholinesterase levels in our patients with mad honey poisoning were 7139.30 ± 2316.41 U/L (min–max: 1785–12,835). Blood pseudocholinesterase levels were within normal limits in 90% of patients and below normal in 10%. Conclusion A low pseudocholinesterase level was found in 3 (10%) of our 30 patients. These biochemical data do not support the hypothesis that mad honey poisoning should be regarded as cholinergic poisoning.
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An Atropa belladonna L. poisoning with acute subdural hematoma
Human & Experimental Toxicology, 2011Co-Authors: Ulas Cikla, Suha Turkmen, Yunus Karaca, Ahmet Faik Ayaz, Suleyman Turedi, Abdulkadir GunduzAbstract:Atropa belladonna L. is a plant long known to cause poisoning. But no cases of acute subdural hematoma resulting from such poisoning have been reported so far. Care must also be taken in terms of acute pancreatitis and rhabdomyolysis in cases of such poisoning. The plant may sometimes be mistaken for the Caucasian blueberry, V. arctostaphylos L. At least one anti-cholinesterase Toxidrome finding was determined in all the nine cases of belladonna poisoning in this series. No elevated creatine kinase was reported in one case with acute subdural hematoma and hyperamylasemia.
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clinical review of grayanotoxin mad honey poisoning past and present
Clinical Toxicology, 2008Co-Authors: Abdulkadir Gunduz, Suleyman Turedi, Robert M Russell, Faik Ahmet AyazAbstract:Grayanotoxin is a naturally occurring sodium channel toxin which enters the human food supply by honey made from the pollen and nectar of the plant family Ericaceae in which rhododendron is a genus. Grayanotoxin/mad honey poisoning is a little known, but well studied, cholinergic Toxidrome resulting in incapacitating and, sometimes, life-threatening bradycardia, hypotension, and altered mental status. Complete heart blocks occur in a significant fraction of patients. Asystole has been reported. Treatment with saline infusion and atropine alone is almost always successful. A pooled analysis of the dysrhythmias occurring in 69 patients from 11 different studies and reports is presented. The pathophysiology, signs, symptoms, clinical course, and treatment of grayanotoxin/mad honey poisoning are discussed. In the nineteenth century grayanotoxin/mad honey poisoning was reported in Europe and North America. Currently, documented poisoning from locally produced honey in Europe or North America would be reportable. Possible reasons for this epidemiologic change are discussed.
Matthew D. Krasowski - One of the best experts on this subject based on the ideXlab platform.
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an infant with a prolonged sympathomimetic Toxidrome after lisdexamfetamine dimesylate ingestion
Journal of Medical Toxicology, 2016Co-Authors: Kelly E Wood, Matthew D. KrasowskiAbstract:Introduction Stimulant medications are approved to treat attention deficit hyperactivity disorder (ADHD) in children over the age of 6 years. Fatal ingestion of stimulants by children has been reported, although most ingestions do not result in severe toxicity. Lisdexamfetamine dimesylate, a once daily long-acting stimulant, is a prodrug requiring conversion to its active form, dextroamphetamine, in the bloodstream. Based on its unique pharmacokinetics, peak levels of d-amphetamine are delayed. We describe a case of accidental ingestion of lisdexamfetamine dimesylate in an infant.
Michael Mazurek - One of the best experts on this subject based on the ideXlab platform.
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neuroleptic malignant syndrome a neuroimmunologic hypothesis
Canadian Medical Association Journal, 2010Co-Authors: Rebecca Anglin, Patricia I. Rosebush, Michael MazurekAbstract:Neuroleptic malignant syndrome is a fulminant and life-threatening Toxidrome that occurs in an estimated 0.07% to 3.23% of patients treated with antipsychotic medication.[1][1],[2][2] Patients typically present with fever, rigidity, changes in mental status and autonomic instability, often after the
