Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 11-year-old boy was given halothane, nitrous oxide and oxygen, pancuronium 0.4 mg and suxamethonium 100 mg for induction of anaesthesia. In response to this a marked jaw stiffness occurred which lasted for two minutes and the anaesthesia were terminated. Four hours of apnoea ensued and he suffered generalized severe myalgia lasting for one week. He was found to have atypical plasma cholinesterase with a dibucaine number of 12, indicating homozygocity. This was verified by study of the family. The case shows that prolonged jaw rigidity and myalgia may occur after suxamethonium in patients with atypical cholinesterase despite pretreatment with pancuronium.
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PMID:Suxamethonium-induced jaw stiffness and myalgia associated with atypical cholinesterase: case report. 737 68

We have investigated the possibility of using the pre-operative measurement of cholinesterase activity to predict the postoperative development of myalgia following the administration of suxamethonium. Seventy-seven patients presenting for elective extraction of wisdom teeth were entered in the study. All patients received a standard anaesthetic regimen, including suxamethonium to facilitate tracheal intubation, and standardised postoperative analgesia. Myalgia was assessed postoperatively and no correlation between muscle pains and cholinesterase activity was found.
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PMID:Suxamethonium-induced muscle pains are not related to cholinesterase activity. 828 36

Pain relief mechanisms of needling to the pain-producing muscle, application of a static magnetic field or external qigong, and needling to the acupuncture point were investigated in an experimentally designed pain producing muscle of animals. Single isometric twitch height in situ was reduced gradually by 10 Hz tetanic stimulation for one hour of the gastrocnemius muscle of guinea pigs. This reduction of twitch height was recovered by injection of 0.3-1 ml saline to the artery of this muscle, or of injection of a vasodilator, isoproterenol dissolved in 0.1 ml saline. Hence, reduction of twitch height could be induced by reduction of circulation in the muscle and recovery of it could be induced be recovery of circulation. Since it is easily considered that a pain substance might be accumulated in a muscle under reduced circulation, and such an accumulated substance might be eliminated by recovery of circulation, the reduction of twitch height after tetanic stimulation could be estimated as the pain-producing muscle and recovery of twitch, as the pain relieving muscle. 1) Needling to the pain muscle, 2) application of a static magnetic field or external qigong to the muscle, and 3) needling to the acupuncture point recovered the reduced twitch height due to tetanic stimulation. Atropine abolished this effect induced by the above 1, 2 and 3 procedures. Hence, the cholinergic vasodilator nerve might be involved in the induction of this effect. A sciatic nerve cut did not influence the effect of 1), but abolished the effect of 3). Denervation and capsaicin abolished the effect of 1). Substance P and a calcitonin gene- related peptide (CGRP) recovered the reduced twitch height, and atropine blocked the effect of CGRP, but did not block that of substance P. The effect of 2) was equivalent to that of anticholinesterase. A rostral lesion of the contralateral anterior hypothalamus did not abolish the effect of 3, but a caudal lesion of this region did. Electrical stimulation of this region produced an effect similar to that of 3). From these results, it was concluded that muscle pain relief by these procedures might be induced by recovery of circulation due to the enhanced release of acetylcholine as a result of activation of the cholinergic vasodilator nerve endings innervated to the muscle artery. However, manners of activation of the cholinergic nerve was different in effects of 1), 2) and 3). 1) might be induced by axon reflex of the CGRP nerve, 2) might be induced by inhibition of cholinesterase and 3) might be induced by a somato-autonomic reflex. The reflex center of this might be in the anterior hypothalamus.
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PMID:Comparisons of pain relief mechanisms between needling to the muscle, static magnetic field, external qigong and needling to the acupuncture point. 891 86

Clinically, neuromuscular blockade is induced with either depolarizing or non-depolarizing relaxants. Suxamethonium is the only depolarizing relaxant still in use. It is hydrolysed in the plasma by pseudo-cholinesterase (plasma cholinesterase). In some patients and in particular diseases the plasma cholinesterase activity is low and hence the effect of suxamethonium prolonged. Suxamethonium is characterized by side-effects such as myalgia, fasciculations and increase in intraocular, intracranial and intragastric pressure. More serious adverse reactions are masseter muscle spasm and potassium release, in patients with some neuromuscular diseases and increase in extrajunctional acetylcholine receptors. As non-depolarizing muscle relaxants benzylisoquinolines and steroidal compounds are mainly used. Each relaxant has its own pharmacological characteristics. The effect of most relaxants depends on liver and renal function because the pharmacokinetic behaviour is strongly dependent on these organs. Also, acid base balance disturbances, change in temperature, and neurological diseases have an effect on the profile of the relaxants. A number of drugs (anaesthetics, antibiotics, antiepileptics, etc.) have an effect on neuromuscular transmission, and thus interact with the relaxants. Some non-depolarizing relaxants cause histamine release and cardiovascular effects.
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PMID:Neuromuscular transmission and its pharmacological blockade. Part 2: Pharmacology of neuromuscular blocking agents. 908 50

We report a patient with polymyositis (PM) associated with myasthenia gravis (MG). Both disorders had been controlled for around 15 years by oral prednisolone and a cholinesterase inhibitor following surgical removal of invasive thymoma and radiotherapy, but muscular weakness due to myalgia and an increase in serum levels of myogenic enzymes, mainly ascribable to the recurrence of PM, reappeared immediately after cessation of these drugs, which was done because the patient had multiple bone fractures and severe osteoporosis due to the long-term corticosteroid therapy. Oral tacrolimus was therefore tried, and produced an improvement in muscular symptoms in association with normalization of myogenic enzymes. PM associated with MG as in this patient might be the best indication for tacrolimus, considering its efficacy in MG, but this drug should also be actively considered as a therapeutic option in refractory cases of PM alone, particularly when either corticosteroids or other immunosuppressive agents are not usable.
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PMID:Efficacy of tacrolimus in treatment of polymyositis associated with myasthenia gravis. 1516 59

Organophosphate-induced delayed polyneuropathy (OPIDP) is a rare toxicity resulting from exposure to certain organophosphorus (OP) esters. It is characterised by distal degeneration of some axons of both the peripheral and central nervous systems occurring 1-4 weeks after single or short-term exposures. Cramping muscle pain in the lower limbs, distal numbness and paraesthesiae occur, followed by progressive weakness, depression of deep tendon reflexes in the lower limbs and, in severe cases, in the upper limbs. Signs include high-stepping gait associated with bilateral foot drop and, in severe cases, quadriplegia with foot and wrist drop as well as pyramidal signs. In time, there might be significant recovery of the peripheral nerve function but, depending on the degree of pyramidal involvement, spastic ataxia may be a permanent outcome of severe OPIDP. Human and experimental data indicate that recovery is usually complete in the young. At onset, the electrophysiological changes include reduced amplitude of the compound muscle potential, increased distal latencies and normal or slightly reduced nerve conduction velocities. The progression of the disease, usually over a few days, may lead to non-excitability of the nerve with electromyographical signs of denervation. Nerve biopsies have been performed in a few cases and showed axonal degeneration with secondary demyelination. Neuropathy target esterase (NTE) is thought to be the target of OPIDP initiation. The ratio of inhibitory powers for acetylcholinesterase and NTE represents the crucial guideline for the aetiological attribution of OP-induced peripheral neuropathy. In fact, pre-marketing toxicity testing in animals selects OP insecticides with cholinergic toxicity potential much higher than that to result in OPIDP. Therefore, OPIDP may develop only after very large exposures to insecticides, causing severe cholinergic toxicity. However, this was not the case with certain triaryl phosphates that were not used as insecticides but as hydraulic fluids, lubricants and plasticisers and do not result in cholinergic toxicity. Several thousand cases of OPIDP as a result of exposure to tri-ortho-cresyl phosphate have been reported, whereas the number of cases of OPIDP as a result of OP insecticide poisoning is much lower. In this article, we mainly discuss OP pesticide poisoning, particularly when caused by chlorpyrifos, dichlorvos, isofenphos, methamidophos, mipafox, trichlorfon, trichlornat, phosphamidon/mevinphos and by certain carbamates. We also discuss case reports where neuropathies were not convincingly attributed to fenthion, malathion, omethoate/dimethoate, parathion and merphos. Finally, several observational studies on long-term, low-level exposures to OPs that sometimes reported mild, inconsistent and unexplained changes of unclear significance in peripheral nerves are briefly discussed.
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PMID:Organophosphate-induced delayed polyneuropathy. 1604 3

We report seven patients with immune-mediated rippling muscle disease (iRMD) and AChR-antibody positive myasthenia gravis (MG) without germline caveolin-3 gene mutations. We describe the follow-up of two patients and the clinical features of five new patients (1 female, 4 male, aged 32 to 69 years). These presented with significant generalized, exercise-induced and electrically-silent muscle rippling with myalgia, combined with generalized MG. In two of the seven patients, MG appeared before iRMD. Mediastinal imaging excluded thymic alterations in all, although two had other coincident tumours. Myalgia and rippling were aggravated by acetylcholinesterase-inhibitor treatment. Generalized MG and iRMD were successfully treated with plasma exchange, steroids and azathioprine in the two patients followed long-term. Muscle morphology of five patients showed a minimal myopathic pattern with rare lymphohistiocytic infiltration. In four patients, sarcolemmal caveolin-3, and dysferlin immunofluorescence staining was moderately reduced in a mosaic pattern, but caveolin-3 protein on Western blots was clearly reduced only in two. Notably, electron microscopy showed that caveolae were almost completely lost at the sarcolemma in the three biopsies examined but not in endothelium. Antibodies targeting high molecular weight muscle proteins, likely associated with the neuromuscular endplate and sarcolemma, were found in the iRMD patients but also in age-matched MG patients without iRMD. Since the generalized MG and iRMD improved with immunosuppressive treatments, it is likely that both are caused by autoantibodies, but the target for pathogenic antibodies in iRMD requires further study.
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PMID:Immune-mediated rippling muscle disease with myasthenia gravis: a report of seven patients with long-term follow-up in two. 1920 78

Some experimental models suggest that the use of pralidoxime in carbamate toxicity is deleterious. Although pretreatment with atropine minimizes the adverse effect of pralidoxime reported in these models, concerns over the risks of pralidoxime in humans with carbamate poisoning continue. We present a unique case of carbamate toxicity treated successfully with pralidoxime alone. An 80-year-old woman with Alzheimer's dementia presented to the emergency department with 3-4 days of lightheadedness, vomiting, diarrhea, and bilateral lower extremity muscle pain. Extensive review of systems was otherwise negative. Her vital signs were BP, 207/85 mmHg; pulse, 101 beats/min; rectal temperature, 36.6( degrees )C; respirations, 18/min; and SpO(2), 95% breathing room air. Her bedside glucose measurement was 6.7 mmol/L. Physical examination revealed a confused, diaphoretic, ill-appearing woman with miosis and fasciculations of the tongue, eyelids, gastrocnemius and quadriceps bilaterally. The heart, lung, abdominal and head, eyes, ears, nose and throat examinations were otherwise unremarkable. Nine 5-cm(2) rivastigmine patches (9.5 mg/24-hour) were found adherent to her torso and lower extremities. The patches were immediately removed and underlying skin cleansed with soap and water. Laboratory values including complete blood count, basic metabolic panel, calcium, magnesium, phosphorus, troponin, coagulation studies and urinalysis were unremarkable. Due to the absence of pulmonary muscarinic findings, no atropine was administered. However, 1 g of pralidoxime was administered intravenously over 30 min to treat fasciculations. Within 30 min of this treatment, there was significant improvement in symptoms and resolution of fasciculations. She was admitted to the hospital, required no further pralidoxime therapy and was discharged after 3 days. Rivastigmine is a reversible (carbamate) cholinesterase inhibitor used to treat dementia. In overdose, cholinergic crisis is expected and in this case was precipitated by patch overuse. We believe there was a causal relationship between pralidoxime administration and the prompt resolution of symptoms and fasciculations. This case of apparently safe and effective pralidoxime use without concomitant atropine administration in a patient with carbamate toxicity reinforces recent data demonstrating the potential safety of pralidoxime in carbamate toxicity.
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PMID:Use of pralidoxime without atropine in rivastigmine (carbamate) toxicity. 1975 37

To assess health risks in agricultural workers associated with environmental exposure to pollutants released from a petroleum refinery and from traffic, we performed a cross-sectional study that included 119 randomly selected subjects divided in two groups. Group 1 included 60 agricultural workers living in a rural community near the petroleum refinery and a motorway overpass, whereas Group 2 consisted of 59 agricultural workers performing similar activities and living in a rural community with no exposure to industrial and traffic pollutants. Risk assessment included a questionnaire, blood pressure measurement, spirometry, laboratory tests, and toxicological analysis. The groups showed a similar prevalence of health problems, with exception of muscle pain in the extremities, headache, and fatigue, which were significantly more common in Group 1. Diastolic blood pressure was higher in Group 1, but not significantly (p=0.057). The same is true for blood carbon monoxide. Significantly higher in Group 1 were blood haemoglobin (p=0.001) and blood lead (p<0.001). Serum cholinesterase activity was similar in both groups. Our findings indicate the need of regular medical exams, ambient monitoring and environmental impact assessment in agricultural population in order to detect individuals at risk and to institute adequate preventive measures.
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PMID:Environmental and occupational health risks among agricultural workers living in a rural community near petroleum refinery and motorway in Skopje region. 2118 33

Both organophosphorus (OP) and carbamate insecticides inhibit acetylcholinesterase (AChE), which results in accumulation of acetylcholine (ACh) at autonomic and some central synapses and at autonomic postganglionic and neuromuscular junctions. As a consequence, ACh binds to, and stimulates, muscarinic and nicotinic receptors, thereby producing characteristic features. With OP insecticides (but not carbamates), "aging" may also occur by partial dealkylation of the serine group at the active site of AChE; recovery of AChE activity requires synthesis of new enzyme in the liver. Relapse after apparent resolution of cholinergic symptoms has been reported with OP insecticides and is termed the intermediate syndrome. This involves the onset of muscle paralysis affecting particularly upper-limb muscles, neck flexors, and cranial nerves some 24-96 hours after OP exposure and is often associated with the development of respiratory failure. OP-induced delayed neuropathy results from phosphorylation and subsequent aging of at least 70% of neuropathy target esterase. Cramping muscle pain in the lower limbs, distal numbness, and paresthesiae are followed by progressive weakness, depression of deep tendon reflexes in the lower limbs and, in severe cases, in the upper limbs. The therapeutic combination of oxime, atropine, and diazepam is well established experimentally in the treatment of OP pesticide poisoning. However, there has been controversy as to whether oximes improve morbidity and mortality in human poisoning. The explanation may be that the solvents in many formulations are primarily responsible for the high morbidity and mortality; oximes would not be expected to reduce toxicity in these circumstances. even if given in appropriate dose.
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PMID:Organophosphorus and carbamate insecticide poisoning. 2656 88


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