Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most common complications of cocaine ingestion are on the cardiovascular and central nervous systems and produce chest pain and generalized seizures. In humans, decreased levels of butyrylcholinesterase (BChE) (EC 3.1.1.8) have been associated with sustained effects of cocaine and life-threatening complications. Administration of purified human BChE has previously been demonstrated to protect against cocaine-associated cardiovascular toxicity in rats. A shift in the metabolism of cocaine as well as enhanced metabolism may be the underlying mechanism of the enzyme. Therefore, levels of the parent drug and four metabolites were determined in rat plasma after i.p. administration of a lethal cocaine dose, followed by i.v. administration of BChE. Plasma and brain concentrations of cocaine were lowered by 80% after BChE administration. Furthermore, the metabolic profile of cocaine in the plasma was altered. The concentration of ecgonine methylester was doubled although the concentration of ecgonine, a secondary metabolite of cocaine, was reduced. The level of benzoylecgonine was reduced by one-half while norcocaine was absent. Cocaine-associated effects upon the central nervous system were also shown to be reduced by administration of BChE to conscious rats. Furthermore, our studies in the cat have also shown that purified BChE shifts the metabolic profile of cocaine (1 mg/kg) to the pharmacologically inactive products ecgonine methylester and ecgonine. Pretreatment with BChE (0.27, 1.0, and 10.0 mg/kg) ameliorated the hypertensive effects of cocaine (1 mg/kg) by reducing the duration and the extent of BP elevation by 66%. Administration of the enzyme, 1 min after cessation of cocaine infusion, resulted in an immediate attenuation in the cocaine-induced broadening of the QRS complex. These results suggest that BChE could be an effective and rapid therapy for the treatment of life-threatening cocaine-induced cardiovascular effects in human while clearing the total body burden of cocaine.
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PMID:Therapeutic use of butyrylcholinesterase for cocaine intoxication. 926 11

A 46-year-old woman was admitted to our hospital with chest pain. Chest X-ray and CT revealed an anterior mediastinal mass as well as several small masses attached to the left chest wall. Thymoma was diagnosed by percutaneous biopsy. The serum level of anti-acetylcholine receptor antibody was 30.3 pmol/ml. At operation, the thymoma was found left in the anterior mediastinum, extending to the upper lobe of the lung. There were also numerous tumors of various size in the left parietal pleura. Thymectomy, partial resection of the upper lobe of the lung and pleurectomy were performed. One month later, she developed myasthenia gravis. After a complete remission of myasthenia gravis brought about by anti-choline esterase therapy, the patient was treated with irradiation. She has been well for more than five years after the operation but her serum anti-acetylcholine receptor antibody level is still higher than normal.
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PMID:[A case of thymoma with pleural dissemination which was treated by pleurectomy with patient survival without recurrence for more than five years]. 961 85

We report a 22 year old male who was admitted to our hospital with alleged history of consumption of monocrotophos poison and had presented with chest pain. His electrocardiogram (ECG) had showed ST segment elevation myocardial infarction and troponins were elevated. He also had low cholinesterase levels and was treated with pralidoxime and atropine and his condition improved. Cardiac catheterization showed patent coronaries. Acute coronary syndrome is a rare manifestation of organophosphorus compound (OPC) poisoning. The current case and subsequent review of literature tells us the need for close cardiac monitoring of all patients with OPC poisoning.
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PMID:Myocardial Infarction following Organophosphorus Compound Poisoning. 3131 37

Myasthenia gravis is an auto-immune disease that results in muscle weakness caused by antibodies released against acetylcholine receptors at the presynaptic membrane. Treatment options include acetylcholinesterase medications that cause a wide range of side-effects by increasing the concentration of acetylcholine at the synaptic cleft. One peculiar side effect seen is the precipitation of myocardial infarction caused by an excess of acetylcholine especially among elderly females. We present an interesting case of an 88-year-old female with a history of lung cancer newly diagnosed with paraneoplastic myasthenia gravis, started on treatment with prednisone 40 mg daily, and pyridostigmine 60 mg every six hours. She initially showed remarkable improvement in symptoms within a few hours, however, one day later, the patient developed sudden onset of chest pain radiating towards her left arm. A 12-lead electrocardiogram (EKG) showed diffuse ST-elevation in anterior leads and cardiac enzymes were found to be elevated. Pyridostigmine was stopped and the patient was started on heparin. The patient underwent cardiac catheterization which showed 50% stenosis in the right coronary artery (RCA) and 70% in the left anterior descending artery (LAD). The patient was monitored in the cardiac care unit (CCU) for 24 hours and later on discharged home on oral prednisone. It is a common practice to start treatment with anti-cholinesterase medications in newly diagnosed patients of myasthenia gravis, however, these medications can precipitate myocardial ischemia by coronary vasogenic spasm or by their arrhythmogenic effect. It is important to be aware of these outcomes while starting patients on these medications.
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PMID:Rare Case of Iatrogenic Myocardial Infarction Induced by Use of Pyridostigmine. 3295 56