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)

A 34-year-old woman was admitted to our hospital because of ptosis, dysarthria, muscle weakness of upper limbs and skin lesions. At the age of 22 years, she was diagnosed as having systemic lupus erythematosus (SLE) due to the presence of arthritis and high titer of antinuclear antibody. On admission, the high antiacetylcholine receptor antibody titer, along with the positive tensilon test and electromyography established a diagnosis of myasthenia gravis (MG). The demonstration of anti-intercellular antibodies both in cutaneous tissue and blood confirmed the diagnosis of pemphigus. MRI showed hypertrophic thymus. After thymectomy, the myasthenic symptoms aggravated and SLE and pemphigus erythematosus relapsed despite anti-cholinesterase treatment with plasmapheresis. She was then placed on corticosteroid therapy with an improvement of her all symptoms. This very rare case of MG associated with SLE and pemphigus erythematosus suggests that these diseases share common immunological abnormalities.
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PMID:[A case of myasthenia gravis associated with systemic lupus erythematosus and pemphigus erythematosus]. 916 41

Pyridostigmine bromide (PB) is a reversible cholinesterase inhibitor used routinely in the treatment of myasthenia gravis and recently by the US Army as a prophylactic agent against potential nerve gas attack in the Persian Gulf War. Pyridostigmine has been implicated as one of several possible causative factors associated with Persian Gulf illnesses. To investigate toxic interactions between PB and other drugs, male ICR mice received contralateral ip injections of either a selected adrenergic drug or caffeine, followed 15 min later by PB. Representative isobolograms plotted for each drug interaction illustrate that a beta-adrenoceptor agonist (isoproterenol), selective beta 2-adrenoceptor agonists (salbutamol, terbutaline), alpha 1- and alpha 2-adrenoceptor antagonists (yohimbine, phentolamine, prazosin), as well as the stimulant caffeine, strongly potentiate the lethal effect of PB. Agents with agonist activity at both alpha- and beta-adrenoceptors (epinephrine, norepinephrine) additively increase PB-induced lethality. The potentiation of toxicity between PB and these agents was counteracted by pretreatment with atropine and atropine methyl nitrate. An alpha 2-adrenoceptor agonist (clonidine) and beta-adrenoceptor antagonists (propranolol, nadolol, acebutolol) did not increase PB-induced lethalities. These data demonstrate a toxic synergism between PB, several commonly used classes of adrenergic agents and caffeine when exposure occurs in different combinations. Future studies into the mechanism(s) of these interactions may bring into question the usage of PB as a protective agent in combat conditions as well as delineate any possible contributions of the drug to Persian Gulf illnesses.
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PMID:Potentiation of pyridostigmine bromide toxicity in mice by selected adrenergic agents and caffeine. 925 Nov 70

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 performed transient evoked otoacoustic emission (TEOAE) measurements on 29 ears of myasthenia gravis (MG) patients. The purpose of the study was to support the role of acetylcholine (ACh) in the efferent innervation of cochlear outer hair cells (OHCs). Another aim was to establish additional diagnostic tools for the early determination of MG. Initially, threshold audiometry and impedance measurements showed normal values on the ears examined. The main finding was that TEOAE values were significantly lower in MG patients than in healthy controls. Mestinon, a reversible cholinesterase inhibitor, resulted in a significant increase in mean values of TEOAEs, although these values were still lower than normal. The results suggest that in MG, acetylcholine receptor (AChR) autoantibodies inhibit the function of OHC AChRs. Thus, the TEOAE generated by the active movements of OHCs is decreased in MG. Mestinon prevents the degradation of ACh, and thus stimulates efferent function and increases TEOAE values. The results obtained in this study support the role of ACh in the efferent function of OHC, as well as the impaired function of hair cell AChRs in MG patients. Consequently, measuring TEOAEs may be useful in the early diagnosis of some forms of MG. These results reinforce the importance of collaboration between neurologists and otolaryngologists in the management of diseases with pathological neurotransmission.
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PMID:Otoacoustic emission in myasthenia gravis patients and the role of efferent activation. 987 40

Neuromuscular disorders can impose significant disability in patients by virtue of weakness, pain, and sensory and autonomic symptoms and deficits. For all of these disorders, supportive measures, appropriate physical therapy, and respiratory support are beneficial. Pain management can be accomplished by the use of antiepileptic medications, such as carbamazepine, phenytoin, valproic, and gabapentin. Tricyclic antidepressants can also be helpful for pain management and depression. Benzodiazepines and baclofen are helpful for management of spasticity. No specific treatment exists yet for the motor neuron disorders. In peripheral neuropathies, identifying and treating the cause is most important. In other neuropathies, such as in acute or chronic inflammatory demyelinating neuropathies, immunosuppression is indicated. Myasthenia gravis can be treated with cholinesterase inhibitors and immunosuppression. A specific treatment does not exist yet for muscular dystrophies. Immunosuppression is helpful in patients with inflammatory myopathies. Toxic myopathies can be treated by removing the causative agent and by supportive measures. Endocrine myopathies will respond to treatment of the primary endocrinopathy.
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PMID:Diagnostic algorithms for neuromuscular diseases. 992 72

Adult, acquired, idiopathic, autoimmune myasthenia gravis has a well-characterized IgG anti-acetylcholine striated-muscle receptor antibody. Removal by plasma exchange is effective, established therapy to augment anti-cholinesterase and immunosuppressive therapy and is the treatment of choice for myasthenia gravis crisis. We report 36 consecutive patients referred and accepted for plasma exchange, 32 of whom were in or entering myasthenia crisis, over a 10 year period. An average of 7.8 (range 1 to 16) plasma exchange procedures were done, with uniform, significant improvement, including extubation of 13 in myasthenic crisis and discharge from hospital in all. We conclude that this is the best treatment for myasthenia gravis crisis in hospital. From recent cases, most, if not all, crises can be prevented by IVIgG or plasma exchange as out-patients with use of corticosteroid and or azathioprine.
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PMID:Predictable recovery from myasthenia gravis crisis with plasma exchange: thirty-six cases and review of current management. 1035 56

We reported a 63-year-old woman, suffered from myasthenia gravis with thymoma who later developed subacute motor neuronopathy after thymectomy. She noticed distally dominant muscle weakness and atrophy of bilateral upper extremities without sensory loss 4 month after thymomectomy. Her muscle weakness did not improve by intravenous administration of anti-cholinesterase (Tensilon test). Electrophysiological examinations showed no decremental response of examined muscles during repetitive nerve stimulation, nor motor nerve conduction block nor demyelination of affected peripheral nerves. Laboratory study demonstrated positive anti-acetylcholine receptor, anti-nuclear and SS-A antibodies. On immunohistochemistry, the patient's sera positively stained human and rat anterior horn cell cytoplasm as well as axoplasm of spinal white matter and root nerve axon, suggesting the presence of anti-axon antibody, possibly against neurofilament or tubulin components. The biopsied muscle specimen showed neurogenic muscle changes, but with no evidence of vasculitis nor cellular infiltration. Therapeutic trial of plasmapheresis was effective for her muscle weakness. Further recovery of weakness and muscle atrophy of hand muscles was obtained by combined therapy of intravenous and oral corticosteroid administration and plasmapheresis. These clinical, electrophysiological and histological findings suggested that antibodies against neuronal component might be responsible for her motor neuronopathy associated with myasthenia gravis. The findings of our case study may support the idea that some cases of motor neuron disease are caused by auto-immune mechanism.
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PMID:[Subacute motor neuronopathy associated with myasthenia gravis and thymoma]. 1054 13

Ocular symptoms of 17 myasthenia gravis (MG) patients were examined by electronystagmographic registration of optokinetic nystagmus. The aim of this study was to replace the subjective methods used previously with a more reliable quantitative technique and thus assess ophthalmoplegia and diplopia, important initial symptoms in MG. Slow phase angular speed values of foveolar type optokinetic nystagmus in the horizontal plane at 10, 20 and 30 degrees/s target speed were determined. Measurements were performed before and after administration of Mestinon, a reversible cholinesterase inhibitor. Twelve healthy volunteers were examined as controls under standard conditions. Results showed significant differences between MG patients and control group. Slow-phase angular speed was significantly larger after Mestinon administration (p < 0.001). It is concluded, that the exhaustion of external ocular muscles in MG can be well characterized by the determination of the slow phase angular speed values of optokinetic nystagmus (OKN). The examination of OKN was also recommended for the evaluation of ocular symptoms in other neurological disorders.
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PMID:Electronystagmographic analysis of optokinetic nystagmus for the evaluation of ocular symptoms in myasthenia gravis. 1058 93

The authors have for the first time evaluated the basic parameters of the voice using computed voice analysis in patients with myasthenia gravis (MG). The aim of the study was to introduce an objective method suitable for the assessment of dysphonic symptoms, which predominate in bulbar, oculobulbar and generalized MG. Voice profile studies included the evaluation of the singing voice range, voice dynamics, maximum phonation time, and mean fundamental frequency and intensity during speech. The characteristic of the stroboscopic picture was also determined. Investigations were carried out before and after the intake of Mestinon, a reversible cholinesterase inhibitor, and healthy subjects were used as a control group. In MG, the voice range and dynamics are badly impaired, maximum phonation time is shortened, the mean fundamental frequency during speech is increased, while the intensity is decreased. Mestinon resulted in an improvement in all these parameters, however, they were still impaired in comparison to the control subjects. Most changes were found to be statistically significant. The authors emphasize the role of the otolaryngologist and objective phoniatric methods in the evaluation of MG and other myasthenia-like neurological diseases. The use of these methods for the assessment of phoniatric symptoms in neurological diseases is highly recommended.
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PMID:[Phoniatric studies in myasthenia gravis patients]. 1060 89

Outer hair cells (OHCs) are the source of otoacoustic emissions, following a tropomyosin-miosin-dependent contraction, which are regulated by the olivocochlear bundle via the release of acetylcholine (ACh). ACh acts on ACh receptors (AChR) located on the OHC post-synaptic membrane. In myasthenia gravis (M.G.) neuromuscular transmission is reduced due to the action of AChR autoantibodies. It has previously been shown that M.G. induces a reduction in transient evoked otoacoustic emissions (TEOAEs), which is reversed after administration of a cholinesterase (AChE) inhibitor. Distortion product otoacoustic emissions (DPOAEs) were recorded before and 60 min after oral administration of 60 mg pyridostigmine bromide in 25 patients with normal hearing affected by M.G. The results were compared with those from 25 age-matched normal controls. Mean values of DPOAE amplitude in myasthenic patients were significantly (p < 0.05) lower at all frequencies before drug administration. All patients showed an overall significant (p < 0.05) increase in DPOAE amplitude after drug administration, although without reaching the control values. Such a recovery was more evident and highly significant (p < 0.01) for middle and high frequencies and could be explained by a higher concentration of ACh receptors in the basal and middle cochlear turns. These data seem to confirm the role of ACh in the neurotransmission of the auditory efferent system and may represent a new in vivo model for the investigation of the physiology of this system.
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PMID:The role of cholinergic transmission in outer hair cell functioning evaluated by distortion product otoacoustic emissions in myasthenic patients. 1134 60


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