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 mature Brangus bull received the recommended dose of chlorpyrifos and became dull and inappetent 3 days later. Clinical findings included weakness, dehydration, rumen stasis, and rumen distention with fluid and gas. Blood cholinesterase activity was 25% of normal. The bull's condition improved after treatment with pralidoxime, antimicrobials, electrolyte solutions, vitamins, and adsorbents. Five weeks later, the bull had gained weight, the blood cholinesterase activity was 70% of normal, and the results of a semen evaluation indicated he was a satisfactory potential breeder.
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PMID:Chlorpyrifos intoxication in a bull. 242 91

A 37-year-old man suffered from photosensitivity and urinary casts with serological findings of positive anti-DNA antibody, LE cells and false positive VD reaction in September of 1979. He developed general fatigue, dyspnea and diplopia with ptosis of bilateral eyelids in November of 1979, which were improved by the anti-cholinesterase drugs. In January of 1980, he had an attack of unconsciousness and his chest X-ray film showed several tumorous shadows in the anterior mediastinum and middle and lower lung fields. Treating him with chemotherapy of VEMP, the pulmonary shadows disappeared. However, he developed severe muscle weakness with an elevated CPK (430 mU/ml) and a myogenic EMG pattern along with an increased anti-acetylcholine receptor antibody (243 n Mol/l), dysphagia and eyelid-ptosis. He died in September of 1985 and his autopsy disclosed a malignant thymoma of mixed type in the anterior mediastinum and an atrophy and fibrosis with infiltration of inflammatory cells in the striated muscles.
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PMID:[An autopsy case of a patient with myasthenia gravis who showed various symptoms of collagen diseases and complicated with malignant thymoma]. 281 7

BMT has become an important therapy for many hematologic disorders. Following BMT, the recipient may develop GVHD when it appears that immunocompetent donor lymphocytes react to host antigens. Acute and chronic GVHD represent two distinct syndromes. Acute GVHD has not been associated with primary neurologic involvement. Polymyositis has been reported in 12 patients with chronic GVHD, with the most common underlying illness being aplastic anemia. The clinical, serologic, and muscle biopsy features of the myositis in GVHD have been similar to those observed in idiopathic polymyositis. Weakness was moderate to severe and responded to prednisone, sometimes with the addition of azathioprine. Prognosis depended upon the underlying disease and not on the severity of the myositis. MG occurs rarely in chronic GVHD. Most patients with MG and GVHD have had aplastic anemia; those with aplastic anemia are more likely to have anti-AchR prior to BMT. The clinical manifestations of GVHD MG have not differed from classic autoimmune MG; each patient had elevated antiacetylcholine receptor antibodies titers. All patients have responded well to cholinesterase inhibitors but have received other immunosuppressants. These observations suggest that aplastic anemia is an important host factor in the development of the autoimmune disorders seen with chronic GVHD, certainly of myositis and MG. Herpes zoster peripheral nerve infections have occurred in patients with chronic GVHD. One patient had mononeuritis multiplex. In both acute and chronic GVHD, CNS impairment is usually caused by metabolic encephalopathy or infection. Primary CNS involvement has not been recognized.
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PMID:Neurologic complications of graft-versus-host disease. 304 48

Carbaryl, a widely used insecticide, is reputed to have a wide safety margin. It can induce acute cholinesterase poisoning, which is rapidly reversible on discontinuation of exposure. Long-term sequelae from long-term exposure have not previously been described in humans. This report describes the experience of a 75-year-old man who had long-term excessive exposure to carbaryl and in whom a debilitating syndrome, including headaches, memory loss, proximal muscle weakness, muscle fasciculation, muscle cramps, and anorexia with marked weight loss, developed. At the time of diagnosis, serum pseudocholinesterase levels were low, and his major symptoms resolved on termination of exposure. Late clinical features were sleep apnea and progressive development of a peripheral neuropathy. The difficulty in diagnosing the cause of a group of relatively nonspecific symptoms raises the question of whether chronic carbaryl neurotoxicity might be occurring more frequently than previously suspected.
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PMID:Subacute neurotoxicity following long-term exposure to carbaryl. 308 76

To study the effect of occupational organophosphate exposure on neuromuscular function, 24 workers exposed to fenthion [0,0-dimethyl-0(4-methyl mercapto-3 methyl phenyl)phosphorothioate], whose mean age was 31.7 years (range 22-50) and mean duration of exposure to fenthion 8.5 years (range 1-19) were subjected to detailed clinical and neurophysiological evaluation after spraying. The neurophysiological tests included motor and sensory nerve conduction velocity; F response, H reflex and electromyographic neuromuscular synapse testing. Fenthion exposure was monitored by serum acetyl cholinesterase (AchE) levels. The observations were repeated after withdrawing the workers from fenthion exposure for 3 weeks to study the reversibility of the observed changes. There was no clinical evidence of peripheral neuropathy or muscle weakness. However, peroneal motor conduction velocity (p less than 0.05) terminal motor latency of median (p less than 0.1), and peroneal nerve (p less than 0.05); F minimal latency and H reflex latency (p less than 0.01) were significantly affected. Twenty-nine per cent of workers had repetitive muscle activity. Serum AchE levels also showed significant changes (p less than 0.01). The clinical significance of these subtle neurophysiological changes requires further investigation and follow-up.
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PMID:A study of nerve conduction velocity, late responses and neuromuscular synapse functions in organophosphate workers in India. 319 Apr 48

The clinical and laboratory features of moderate to severe organophosphate and carbamate toxicity in 37 infants and children are presented. Ingestion of an improperly stored liquid pesticide was the most common route of intoxication (76% of patients); five (14%) children became intoxicated after playing on carpets and floors of homes that had been sprayed or fogged by unlicensed exterminators. The transfer diagnoses were incorrect for 16 or 20 patients who were transferred to our center from another institution. Miosis (73%), excessive salivation (70%), muscle weakness (68%), and lethargy (54%) were the most common abnormal signs; 49% and 22% of patients had tachycardia and seizures, respectively, and 38% of children had respiratory insufficiency that required endotracheal intubation and mechanical ventilation. The results of erythrocyte and serum cholinesterase activity assays were concordant in 83% of patients. Thirty-four (92%) patients were treated with atropine and/or pralidoxime; three patients required only supportive care. Most patients had a prompt response to therapy; however, two patients with organophosphate toxicity required multiple doses of atropine during a 24-hour period; in both instances, the doses of atropine were subtherapeutic. There were no deaths. Pneumonitis and/or atelectasis developed in ten patients, including six who had ingested a petroleum distillate-containing insecticide.
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PMID:Organophosphate and carbamate poisoning in infants and children. 333 78

Organophosphates are the most common group of chemicals involved in poisoning in Sri Lanka. Usually, poisoning is by ingestion for suicidal purposes, although accidental poisoning is not uncommon. Poisoning due to absorption through intact or damaged skin is rare. A 32-year-old man was admitted to a peripheral hospital following assault with a 100-ml bottle of insecticide called Monocrotophos, an organophosphate. He had a 2-in. long laceration just above his left eyebrow and there was spilling of the liquid contained in the bottle over his head and face. The liquid was wiped off but the head or face was not washed. After about 3 h the patient developed symptoms and signs of early organophosphate poisoning which were treated with atropine and pralidoxime. On the 3rd day, while on therapy, the patient developed severe weakness of limbs and respiratory distress needing intubation and assisted ventilation. The patient was transferred to the neurology intensive care unit of the General Hospital, Colombo, on the eighth day. His serum potassium levels were low and an ECG showed prominent U waves in all leads. The plasma cholinesterase levels were within 37.5-50% of normal even on the 20th day indicating severe exposure.
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PMID:Respiratory failure from severe organophosphate toxicity due to absorption through the skin. 335 Apr 49

This histochemical study examined the effects of chronic methylmercury (MeHg) intoxication on the motor and sensory innervation of extensor digitorum longus muscles. Light microscopic examination of silver-stained axons in the intramuscular nerve bundles of MeHg-treated rats showed Wallerian-like degeneration and a reduction in the number of nerve fibers. Disrupted axons were predominantly sensory because 22.2% of spindle afferents (Ia) and 90.0% of Golgi tendon organ (Ib) sensory fibers were completely degenerated whereas less than 1% of motor endings were totally destroyed. Partial disruption occurred in the cholinesterase and motor terminals of 13.7% of endplates. Our results demonstrated greater vulnerability of sensory nerves than of motor nerves to MeHg-induced degeneration. Thus, the abnormal reflexes, ataxia, and muscle weakness following MeHg poisoning appear related to reduction of proprioceptive feedback from muscles and tendons in addition to the documented lesions in the central nervous system.
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PMID:Effects of methylmercury on the motor and sensory innervation of the rat extensor digitorum longus muscle. 358 15

The abductor digiti minimi of a patient had undergone partial denervation with some subsequent re-innervation. Cooling of the muscle caused a severe reduction in the EMG and force which accompanied either voluntary effort or tetanic nerve stimulation, but it had little effect on the response to single stimuli. The ineffectual attempts at voluntary contraction of the cooled muscle did, however, block the response to single nerve stimuli. Administration of cholinesterase inhibitors did not improve neuromuscular transmission in the cooled muscle, but usually made it worse. It is concluded that depolarisation block may contribute to the weakness of cooled denervated muscles.
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PMID:The effects of cold on a partially denervated muscle. 358 58

Cyclic phenyl saligenin phosphate (PSP) proved to be a potent delayed neurotoxin, eliciting clinical disease and lesions, and depressing neuropathy target esterase and plasma cholinesterase at much lower doses than the protoxicant tri-ortho-tolyl phosphate (TOTP). Using adult White Leghorn chickens, we noted qualitative similarities in clinical signs and peripheral nerve and spinal cord lesions elicited by PSP and the TOTP. Ataxia and weakness were prominent clinical effects. Lesions began as a distal axonopathy affecting larger myelinated fibers in spinal cord white matter and peripheral nerve. The latter were studied in detail. Major features of the lesion were intra-axonal collections of mitochondria, dense and lamellar bodies, and granular degeneration of neurofilaments. These led to Wallerian-like degeneration. Percentages of teased peripheral nerve fibers demonstrating such degeneration correlated with severity of clinical signs.
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PMID:Neuropathological effects of phenyl saligenin phosphate in chickens. 360 Dec 42


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