Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

EEG studies were done in 19 patients comatose due to severe hepatic insufficiency associated with porto-caval shunting. The neurological deficits were graded in 5 stages and related to the abnormal EEG-pattern observed in 38 records. With deepening of coma, alpha-frequencies were gradually replaced by theta- and delta-activities. The frequency of theta- and delta-runs decreased with neurological deterioration. Triphasic waves (typical and/or atypical) were seen in 26% of the records. Typical triphasic waves were found to be limited to stage 3 of coma, whereas atypical forms appeared in earlier and later stages. After infusions of L-Valin, a transient improvement and disappearance of triphasic waves was observed, but no significant effect could be established on the final course of the disease. Sleep-like potentials and the reactivity to external stimuli decreased in deep stages of coma. Severe EEG abnormalities were correlated to low cholinesterase and high lactid acid blood level, but no correlation was found to the level of ammonia.
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PMID:[Electroencephalographic changes in coma due to hepatic insufficiency with porto-caval shunt (author's transl)]. 11

In the group of 107 patients poisoned by carbon monoxide (18 patients), ethanol (10), barbiturates (18), glutehimide (10), tranquilizers (19), organic solvents (10),salicylates (3), organochlorines (8), and sulfonamides (5)--the activities of 8 serum enzymes were determined for 6 consecutive days of treatment, the enzymes being as follows: aminotransferases, cholinesterase, alkaline phosphatase, lactate, alpha-hydroxybutyrate, glutamate, and sorbitol dehydrogenase. The antipyrine half-life was also assayed. It has been shown that the poisonings by particular groups of poisons do not bring about characteristic changes in the activity of enzymes that might be of any diagnostic value. The intensity of changes was connected withe depth and duration of toxic coma. Most frequently an increase ensued in the activity of AspAt and AlAt in the third 24-hrs period, and an increase in the activity of SDH in the first 24-hrs period. In the group under examination there were 26 drug abusers in whom a shortening of the antipyrine half-life was discovered. They were less responsive to toxic doses of drugs, and the enzymatic changes in them were less distinct. No changes in the activity of tested enzymes, which are characteristic of toxicomania, were found.
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PMID:The usefulness of the enzymatic tests in acute poisonings. 124 89

A 32-year-old woman who had ingested 300 ml of a potent cholinesterase inhibitor insecticide (Fonofos) with suicidal intent became progressively comatose and finally suffered respiratory arrest. Tracheal intubation, mechanical ventilation, vigorous gastric lavage and intravenous administration of atropine and obidoxime brought about complete clinical recovery within 24 hours of ingestion of this potentially fatal dose of Fonofos.
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PMID:[Poisoning with cholinesterase inhibitors]. 168 7

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

Benzodiazepines (BDZ) interact with specific receptors (R), whose activation improves Cl- -channel gating by the GABA receptor (GABA-R). Neurones, whose GABAergic input has a certain level of activity, will be more inhibited in the presence of BDZ (primary target neurones for BDZ). Secondarily, neurones dependent on the activity of primary target neurones will also be effected. Drugs that interact with GABAergic functions (except the BDZ-R) or with the function of primary or secondary target neurones may inhibit some or all BDZ effects; these are nonspecific BDZ antagonists (e.g. GABA-antagonists, cholinesterase inhibitors, naloxone, methylxanthines). Specific BDZ antagonists inhibit the action of BDZ by blocking competitively the BDZ-R. Ro 15-1788 is the best investigated specific BDZ antagonist. Virtually devoid of any pharmacological action by itself, the compound blocks all typical effects of BDZ. It is well tolerated also in man and will find application in anaesthesiology to shorten the sedative and muscle relaxant effect of BDZ and in emergency services to reverse comatose states after BDZ overdosage. Recently drugs have been found that produce effects opposite to the BDZ tranquilizers by inducing a conformation of the BDZ-R which depresses GABA-mediated Cl- -channel gating. The effects of these inverse agonists (e.g. proconvulsant , convulsant, anxiogenic) are blocked by pure competitive BDZ-R blockers, such as Ro 15-1788.
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PMID:Antagonists of benzodiazepines. 614 9

A 3-year-old boy was admitted to hospital following rapid-onset coma. Laboratory tests demonstrated hyperglycemia, glycosuria and keto-acidosis. Organophosphorus poisoning was the cause of the coma since he had been in contact with Parathion, serum cholinesterase activity was undetectable and his condition returned to normal under atropine therapy.
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PMID:Organophosphate poisoning presenting as diabetic ketoacidosis. 665 79

Disease secondary to heroin abuse constitutes a rarity in Spain. While there had been no previous cases in earlier years four young heroin addicts were admitted to the Hospital "1st de Octubre" for severe medical complications of their addiction within the last twelve months. Two patients were admitted in deep coma due to drug overdose, being cardiac arrhythmias and pulmonary edema the main associated complications. Cardiac rhythm disturbances are due to a heightened vagal tone, either secondary to inhibition of acetylcholine hydrolysis or to hypoxia, hypercapnia, and acidosis, factors that diminish cholinesterase activity and act synergistically to increase vagal tone. Pulmonary edema secondary to heroin overdose is non-cardiogenic and probably due to hypoxia added to the local action of heroin on the alveolocapillary membrane. The goal of therapy in such cases is to obtain an appropriate alveolar ventilation, the use of continuous positive pressure ventilation being required when there is pulmonary edema. The third patient had staphylococcal pneumonia with multiple abscess formation secondary to venous septic embolization originated peripherally where the drug was injected. Finally, the fourth patient was admitted because of a clinical and biochemical picture of HBsAg negative acute viral hepatitis, having suffered a similar clinical picture three years previously.
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PMID:[Severe medical sequelae in heroin addicts]. 720 89

Three patients with cholinesterase inhibitor poisoning have been presented. The patients were in a deep coma and, in one of them, artificial mechanical respiration was instituted. All three cases were treated by a procedure combining hemodialysis and hemoperfusion with Amberlite resin (XAD-4), and the clinical picture improved over a short period of time. After the end of procedure, the platelet count was approximately 41% of normal. Some aspects of these intoxications are discussed.
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PMID:Combined hemoperfusion and hemodialysis treatment of poisoning with cholinesterase inhibitors. 803 30

We report a 60-yr-old woman with schizophrenia, who manifested a neuroleptic malignant (NM)-like syndrome after acute organophosphate poisoning (OPP). She attempted suicide by ingesting 40% emulsions of DMTP (S-2,3-dihydro-5-methoxy-2-oxo-1,3,4-thiadizol-3-yl-methyl O,O-dimethyl phosphorodithioate) 100 ml. On admission, she was unconscious and demonstrated convulsions, depressed respiratory movements, miosis and profuse salivation. Plasma cholinesterase concentration (842 IU.L-1) was very low and OPP was diagnosed. She was treated with gastric lavage, atropine and pralidoxime (PAM). By the seventh day after admission, symptoms of OPP disappeared and serum ChE had recovered to a sub-normal level. On the 13th day, she demonstrated coma, high fever (41.0 degrees C) and lead-pipe rigidity. Serum CPK was increased (1631 IU.L-1). Dantrolene sodium iv was administered for three days. Body temperature began to decrease in 24 hr, and her consciousness, muscle rigidity and other neurological symptoms returned to normal by the 16th day after admission. She was discharged from the hospital without sequelae 55 days after admission. We conclude that OPP can predispose to an NM-like syndrome and that dantrolene may be effective in the management.
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PMID:Neuroleptic malignant-like syndrome: a complication of acute organophosphate poisoning. 859 Apr 92

Carbofuran is a carbamate that functions as a cholinesterase inhibitor. Accidental or intentional ingestion can produce a life-threatening syndrome that requires prompt diagnosis and treatment. We describe a case of intentional carbofuran ingestion that resulted in coma, respiratory failure from acute respiratory distress syndrome (ARDS), and cortical blindness.
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PMID:Human sequelae of severe carbamate poisoning. 952 4


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