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:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is limited information regarding the management and outcomes of patients presenting with anticholinesterase pesticide poisoning in Australia. Patients presenting to a tertiary referral hospital with anticholinesterase exposures were identified by discharge coding. The medical records of each patient were retrospectively reviewed. Based on clinical outcome, patients were classified as severe or non-severe poisonings. Forty-one presentations were noted between 1990 and 2003. Eight patients (20%) had severe poisoning of which tachycardia, fasciculations with weakness and metabolic acidosis were common manifestations. The diagnosis was delayed in four patients due to the absence of a clear history, which did not influence patient outcomes or put hospital staff at risk of nosocomial poisoning. The median length of hospital stay was prolonged in severe poisonings (20 days) compared to 12 hours in other patients. Two cases of intermediate syndrome were attributed to fenthion and diazinon, and one case of delayed polyneuropathy to trichlorfon. Cholinesterase activities were performed in only 49% of presentations. The overall mortality was 2.4% (1 death) and the mortality in patients with severe poisoning was 12.5%. The incidence of anticholinesterase poisoning in Australia is low. These outcomes were favourable and comparable with other published data. Measures to enhance the knowledge of medical staff supplemented by validated treatment protocols should be developed. For less significant exposures, an emphasis on adequate documentation of cholinergic signs and cholinesterase activities is necessary for rapid triage and may also have potential forensic implications if not performed.
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PMID:Experiences of anticholinesterase pesticide poisonings in an Australian tertiary hospital. 1611 88

Accidental or intentional ingestion of carbofuran can produce a life-threatening syndrome that requires prompt diagnosis and treatment. This paper investigates unintentional carbofuran poisoning in farm workers. Thirteen patients were admitted to the emergency department with carbofuran poisoning between January 2002 and August 2004 (2 female, 11 male). The patients had been poisoned while mixing the liquid form of carbofuran with seeds. Their hands were red on admission. Complaints most commonly reported by the patients on admission were nausea, vomiting, headache, weakness, dizziness and blurred vision. The most commonly observed signs were tachycardia, tachypnea, salivation, miosis, elevated blood pressure, and fasciculation. Three patients were agitated and one was lethargic on admission. We reviewed the patients' medical charts retrospectively, as well as the demographic data, intoxication route, clinical and laboratory presentations, and outcomes. We made the diagnosis according to a compatible exposure history and clinical findings. The most commonly observed laboratory finding was hyperglycemia, which was found in 6 patients. Serum pseudocholinesterase level was low in only one patient. All the patients were cured and discharged from the hospital in good physical condition. Rapid onset, mild illness and quick recovery are typical characteristics of acute occupational carbofuran poisoning. We conclude that public health efforts should educate farm workers about the dangers of pesticide application so that its threat can be diminished.
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PMID:Carbofuran poisoning among farm workers. 1635 64

Neuromuscular junction (NMJ) disorders are characterized by fuctuating muscle weakness. Acquired myasthenia gravis is the most common NMJ disorder with an overall prevalence in United States estimated at 60,000. Depending on the site of neuromuscular transmission failure, NMJ disorders have been classified as: (1) presynaptic (e.g., Lambert-Eaton myasthenic syndrome), (2) synaptic (e.g., cholinesterase inhibitor toxicity), and (3) post-synaptic (e.g., myasthenia gravis). Electrodiagnostic techniques used for investigation of NMJ disorders include repetitive nerve stimulation (RNS) and single fiber electromyography (SFEMG). Recent literature widely explores the use of SFEMG in the diagnosis and monitoring of myasthenia gravis, but this technique has a lesser role in the daily clinical practice outside of academic institutions. RNS is not as sensitive as SFEMG, but it is the most widely used electrodiagnostic method in the evaluation of suspected neuromuscular transmission disorders. RNS is technically easier and does not require special technical training and skill as SFEMG. Repetitive nerve stimulation was utilized first by Jolly in 1895 using an electrical drum and faradic tetanization to demonstrate a "myasthenic reaction" (weakening muscle contractions). In 1941, decremental response following the repetitive nerve stimulation was described by Harvey and Masland. While the technology has improved tremendously since then, the RNS testing is still based on supramaximal repetitive nerve stimulation and the measurement of decremental (or incremental) responses.
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PMID:Use of repetitive nerve stimulation in the evaluation of neuromuscular junction disorders. 1645 51

Uro-neurological assessment was performed in four patients with small-fiber neuropathy due to amyloidosis (2 transthyretin-type/2 immunoglobulin light-chain-type). Voiding difficulties were due to detrusor weakness and impaired bladder sensation. In two patients cholinesterase inhibition treatment caused urge incontinence, indicating detrusor denervation supersensitivity. The underlying mechanisms of urinary dysfunction seem to involve postganglionic cholinergic and afferent somatic nerves.
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PMID:Urinary dysfunction and autonomic control in amyloid neuropathy. 1647 99

Methyl parathion - MP (C[8]H[10rsqbNO[5rsqbPS) is a restricted-use pesticide that has been widely used as an agricultural insecticide. It belongs to the class of organophosphate chemicals characterized by their ability to inhibit acetylcholinesterase activity. The main route of human exposure is inhalation, but dermal contact and inadvertent ingestion can also be substantial. Populations that are susceptible to MP exposure primarily are applicators, manufacturers and individuals living near application and/or disposal sites. Exposure has also been reported as a result of illegal indoor application. MP related health effects include headaches, nausea, night-waking, diarrhea, difficulty breathing, excessive sweating and salivation, incoordination, and mental confusion. Other symptoms including behavior problems, motor skill problems and impairment of memory recall have also been reported. The primary targets of toxicity are the hematopoietic system (serum cholinesterase inhibition), the cardiovascular system (cardiovascular lesions, abnormalities in heart rate and increase in heart-to-body ratio), the reproductive system (placental morphology, fibrosis and hemorrhage, and inhibition of DNA synthesis in seminiferous tubules), and the nervous system (headache, muscle weakness, insomnia, dizziness, and impaired memory). MP is believed to not have any carcinogenic effects. In an attempt to update its toxicologic profile, we hereby provide a critical review of MP-related environmental and toxicologic effects, with a special emphasis on their potential implications for public health.
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PMID:Environmental toxicology and health effects associated with methyl parathion exposure--a scientific review. 1681 98

A physiological adjuvant to neuroplasticity cannot put new knowledge into the brain - it can only augment behavioral rehabilitation, which does replace knowledge in the brain lost due to injury. Clinical trials of adjuvant agents should therefore incorporate behavioral engines: behavioral therapies that have a potent effect and minimize error variance due to variability in subject attributes and the administration of the therapy. We consider in some detail the attributes of behavioral engines with a particular focus on constraint induced movement therapy. Human trials of physiological adjuvants to neuroplasticity are predicated on discoveries from animal research. Because human trials are expensive and carry risk of injury, it behooves us to lay a comprehensive foundation for these trials with animal studies (also incorporating behavioral engines) and to carefully mesh animal and clinical work. We review in detail our own and others' work involving human subjects with brain lesions and animal models of brain injury using donepezil, a central acetyl cholinesterase inhibitor, d-cycloserine, a partial agonist at the NMDA receptor glycine site, d-amphetamine, and methylphenidate in an effort to elucidate the strengths and weakness of animal and human neurorehabilitation science with respect to this mesh between animal and human subject research. We consider modifications in current approaches that might more efficiently advance neurorehabilitation science.
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PMID:CIMT as a behavioral engine in research on physiological adjuvants to neurorehabilitation: the challenge of merging animal and human research. 1691 58

Two terrorist attacks with the nerve agent Sarin affected citizens in Matsumoto and Tokyo, Japan in 1994 and 1995, killing 19 and injuring more the 6000. Sarin, a very potent organophosphate nerve agent, inhibits acetylcholinesterase (AchE) activity within the central, peripheral, and autonomic nervous systems. Acute and long-term Sarin effects upon humans were well documented in these two events. Sarin gas inhalation caused instantaneous death by respiratory arrest in 4 victims in Matsumoto. In Tokyo, two died in station yards and another ten victims died in hospitals within a few hours to 3 months after poisoning. Six victims with serum ChE below 20% of the lowest normal were resuscitated from cardiopulmonary arrest (CPA) or coma with generalized convulsion. Five recovered completely and one remained in vegetative state due to anoxic brain damage. EEG abnormalities persisted for up to 5 years. Miosis and copious secretions from the respiratory and GI tracts (muscarinic effects) were common in severely to slightly affected victims. Weakness and twitches of muscles (nicotinic effects) appeared in severely affected victims. Neuropathy and ataxia were observed in small number (less than 10%) of victims, which findings disappeared between 3 days and 3 months. Leukocytosis and high serum CK levels were common. Hyperglycemia, ketonuria, low serum triglyceride, hypopotassemia were observed in severely affected victims, which abnormalities were attributed to damage of the adrenal medulla. Oximes, atropine sulphate, diazepam and ample intravenous infusion were effective treatments. Pralidoxime iodide IV reversed cholinesterase and symptoms quickly even if administered 6 h after exposure. Post Traumatic Stress Disorder (PTSD) was less than 8% after 5 years. However, psychological symptoms continue in victims of both incidents. In summary, both potent toxicity and quick recovery from critical ill conditions were prominent features. Conventional therapies proved effective in Sarin incidents in Japan.
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PMID:Sarin experiences in Japan: acute toxicity and long-term effects. 1696 40

Myasthenia gravis (MG) is an autoimmune disorder of neuromuscular transmission, usually recognized with ocular complaints or generalized muscle weakness. However, among the 1520 MG cases that had been diagnosed and treated in our hospital in the last 15 years (1990-2005), we have identified 7 MG patients whose initial and prominent complaint was dysphonia and all had been misdiagnosed elsewhere. The diagnoses were confirmed with fibrolaryngoscope and voice analysis employed before and after a positive neostigmine (anticholinesterase) test. Electromyography with repetitive stimulations, single-fiber electromyography, and laboratory and radiographic evaluations were also conducted for diagnosis. A surprisingly low seropositivity rate of anti-acetylcholine-receptor antibodies (1/7) and anti-MuSK (Muscle Specific Kinase) antibodies (0/6) were found in these dysphonia MG patients. A cholinesterase inhibitor (ChEI) and immunosuppressive therapy were applied for treatment. Extended thymectomy was applied to MG patients with thymus hyperplasia or thymic tumor. Significant improvement was found in all 7 cases after these treatments. We have developed a sere of diagnostic protocol for this rare type of laryngeal MG, and discussed the clinical implication of our data. In summary, dysphonia or laryngeal disorder can be the only prominent manifestation of MG in rare cases, which should be taken into consideration during the diagnosis to patients with exclusive laryngeal complaints.
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PMID:Dysphonia as a primary manifestation in myasthenia gravis (MG): a retrospective review of 7 cases among 1520 MG patients. 1746 37

Myasthenia gravis (MG) is a rare, autoimmune neuromuscular junction disorder. Contemporary prevalence rates approach 1/5,000. MG presents with painless, fluctuating, fatigable weakness involving specific muscle groups. Ocular weakness with asymmetric ptosis and binocular diplopia is the most typical initial presentation, while early or isolated oropharyngeal or limb weakness is less common. The course is variable, and most patients with initial ocular weakness develop bulbar or limb weakness within three years of initial symptom onset. MG results from antibody-mediated, T cell-dependent immunologic attack on the endplate region of the postsynaptic membrane. In patients with fatigable muscle weakness, the diagnosis of MG is supported by: 1. pharmacologic testing with edrophonium chloride that elicits unequivocal improvement in strength; 2. electrophysiologic testing with repetitive nerve stimulation (RNS) studies and/or single-fiber electromyography (SFEMG) that demonstrates a primary postsynaptic neuromuscular junctional disorder; and 3. serologic demonstration of acetylcholine receptor (AChR) or muscle-specific tyrosine kinase (MuSK) antibodies. Differential diagnosis includes congenital myasthenic syndromes, Lambert Eaton syndrome, botulism, organophosphate intoxication, mitochondrial disorders involving progressive external ophthalmoplegia, acute inflammatory demyelinating polyradiculoneuropathy (AIDP), motor neuron disease, and brainstem ischemia. Treatment must be individualized, and may include symptomatic treatment with cholinesterase inhibitors and immune modulation with corticosteroids, azathioprine, cyclosporine, and mycophenolate mofetil. Rapid, temporary improvement may be achieved for myasthenic crises and exacerbations with plasma exchange (PEX) or intravenous immunoglobulin (IVIg). Owing to improved diagnostic testing, immunotherapy, and intensive care, the contemporary prognosis is favorable with less than five percent mortality and nearly normal life expectancy.
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PMID:Myasthenia gravis. 1798 28

Myasthenia gravis (MG) with antibodies against the muscle-specific tyrosine kinase (MuSK abs) is often a severe disease requiring aggressive treatment. Various immunosuppressive (IS) regimens have been employed; the efficacy of plasma exchange is unanimously recognized, while the indication for thymectomy is controversial. We evaluated the response to therapy in 57 MuSK-positive patients (12 M/45 F) comparing our experience with other authors' results. Disease severity and response to treatment were graded according to MG Foundation of America; follow-up ranged from 0.5-29 years. Owing to both MG severity and the unsatisfactory response to cholinesterase inhibitors, most patients (54/57) needed IS treatment, and 35 received one or more courses of plasma exchange and intravenous immunoglobulin. At the end of follow-up, the rate of complete remission was 8.8%, and IS treatment had been withdrawn in only 10/54 patients. The extent of therapeutic response varied considerably. With conventional IS therapy (prednisone alone or in combination with azathioprine or cyclosporine), most patients achieved good control of their disease, but 30% of them were left with permanent facial and bulbar weakness. In patients with refractory disease, the use of mycophenolate mofetil and rituximab proved very effective, as also reported by other authors. In our and others' experience, MuSK-positive MG markedly improves with IS therapy, although, in comparison with the AChR-positive disease, it is characterized by a lower remission rate, as a higher proportion of patients remain dependent on treatment. Thymectomy is mostly considered scarcely effective; however, at present, no firm conclusions can be drawn on its role in the treatment of this form of MG.
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PMID:Response to therapy in myasthenia gravis with anti-MuSK antibodies. 1856 56


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